目录号 | 产品详情 | 靶点 | |
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T37187 | |||
Lysosphingomyelin is an endogenous bioactive sphingolipid and a constituent of lipoproteins.1,2It is produced by the removal of the acyl group from sphingomyelin by a deacylase and acts as a precursor in the biosynthesis of sphingosine-1-phosphate . D-erythroLysosphingomyelin is an agonist of the S1P receptors S1P1, S1P2, and S1P3(EC50s = 167.7, 368.1, and 482.6 nM, respectively, for the human receptors).3It is also an agonist of the orphan receptor ovarian cancer G protein-coupled receptor 1 (ORG1) that induces calcium accumulation in cells overexpressing OGR1 (EC50= ~35 nM).4Levels of D-erythrolysosphingomyelin are increased in skin isolated from patients with atopic dermatitis, as well as postmortem brain from patients with Niemann-Pick disease type A, but not type B.2,5L-threolysosphingomyelin is also an S1P1-3agonist (EC50s = 19.3, 131.8, and 313.3 nM, respectively).3This product is a mixture of D-erythroand L-threolysosphingomyelin. [Matreya, LLC. Catalog No. 1321] 1.Ito, M., Kurita, T., and Kita, K.A novel enzyme that cleaves the N-acyl linkage of ceramides in various glycosphingolipids as well as sphingomyelin to produce their lyso formsJ. Biol. Chem.270(41)24370-24374(1995) 2.Nixon, G.F., Mathieson, F.A., and Hunter, I.The multi-functional role of sphingosylphosphorylcholineProg. Lipid Res.47(1)62-75(2008) 3.Im, D.-S., Clemens, J., Macdonald, T.L., et al.Characterization of the human and mouse sphingosine 1-phosphate receptor, S1P5 (Edg-8): Structure-activity relationship of sphingosine1-phosphate receptorsBiochemistry40(46)14053-14060(2001) 4.Meyer zu Heringdorf, D., Himmel, H.M., and Jakobs, K.H.Sphingosylphosphorylcholine-biological functions and mechanisms of actionBiochim. Biophys. Acta1582(1-3)178-189(2002) 5.Rodriguez-Lafrasse, C., and Vanier, M.T.Sphingosylphosphorylcholine in Niemann-Pick disease brain: Accumulation in type A but not in type BNeurochem. Res.24(2)199-205(1999) | |||
T37766 | |||
Transdermal Peptide is a 11-amino acid peptide, binds to Na+/K+-ATPase beta-subunit (ATP1B1), and enhances the transdermal delivery of many macromolecules. Transdermal Peptide (TD1) binds to ATP1B1, and mainly interacts with the C-terminus of ATP1B1 in yeast and mammalian cells. The interaction affects the expression and localization of ATP1B1 and epidermal structure, but can be antagonized by the exogenous competitor ATP1B1 or be inhibited by ouabain. Inhibition of Transdermal Peptide binding to ATP1B1 causes decreased delivery of macromolecular drugs across the skin[1]. [1]. Wang C, et al. Role of the Na(+)/K(+)-ATPase beta-subunit in peptide-mediated transdermal drug delivery. Mol Pharm. 2015 Apr 6;12(4):1259-67. | |||
T83848 | |||
VnP-16是一种合成肽段,对应vitronectin的氨基酸270-281,vitronectin是一种具有细胞附着、迁移和扩散等多功能作用的糖蛋白。该肽段在9.1 µg/cm2浓度下应用于细胞板时,能促进人类成骨细胞的附着和扩散,此效应可通过β1整合素的siRNA敲除被逆转。VnP-16诱导人类皮肤来源的间充质前体细胞和MC3T3-E1小鼠颅骨成骨前体细胞的成骨作用。在体内,VnP-16减少IL-1α诱导的骨质流失并减少小鼠颅骨中破骨细胞的数量。它还在卵巢切除引起的骨质疏失小鼠模型中增加骨矿物质密度并减少松质骨流失。 | |||
T83693 | |||
Magainin 2是一种从非洲爪蟾(X. laevis)皮肤中分离出的阳离子肽,具有宿主防御和抗菌活性。该化合物对细菌E. coli、K. pneumoniae、S. epidermidis、S. aureus及真菌C. albicans表现出活性(MICs分别为5、10、10、50和80 µg/ml)。Magainin 2(20 µM)能降低猕猴桃花粉的萌发率和平均管长。在被单纯疱疹病毒1型(HSV-1)或2型(HSV-2)感染的Vero细胞中,它可减少病毒复制(EC50s分别为22.16和19.8 µM),同时不影响细胞活性,其50%细胞毒性浓度值(CC50)大于100 µM。 | |||
T64692 | |||
Complement component C3 plays a particularly versatile role in this process by keeping the cascade alert, acting as a point of convergence of activation pathways, fueling the amplification of the complement response, exerting direct effector functions, and helping to coordinate downstream immune responses[3]. In C3-/- mice alcohol-induced liver steatosis is absent or strongly reduced after chronic or acute alcohol exposure. This suggests that the complement system and its component C3 contribute to the development of alcohol-induced fatty liver and its consequences[4].AMY-101 TFA (Cp40 TFA) is a peptidic inhibitor of the central complement component C3 (KD: 0.5 nM). It shows a favorable anti-inflammatory activity in models with COVID-19 severe pneumonia with systemic hyper inflammation[5].a daily subcutaneous dose of AMY-101 (4 mg/kg bodyweight) was protective against NHP periodontitis, suggesting that patients treated for systemic disorders (e.g., paroxysmal nocturnal hemoglobinuria) can additionally benefit in terms of improved periodontal condition[6].Plasma concentrations of both C3 and Cp40 were measured periodically and complete saturation of plasma C3 was confirmed. No differences in hematological, biochemical, or immunological parameters were identified in the blood or tissues of animals treated with Cp40 when compared to those injected with vehicle alone. Further, skin wounds showed no signs of infection in those treated with Cp40.Cp40 treatment was associated with a trend toward accelerated wound healing when compared with the control group. In addition, a biodistribution study in a rhesus monkey indicated that the distribution of Cp40 in the body is associated with the presence of C3, concentrating in organs that accumulate blood and produce C3[7]. | |||
T36618 | |||
Rupatadine (UR-12592) is a potent dual PAF/H1 antagonist with Ki of 0.55/0.1 uM(rabbit platelet membranes/guinea pig cerebellum membranes).IC50 value:Target: PAF/H1 antagonistin vitro: Rupatadine competitively inhibited histamine-induced guinea pig ileum contraction (pA2 = 9.29 +/- 0.06) without affecting contraction induced by ACh, serotonin or leukotriene D4 (LTD4). It also competitively inhibited PAF-induced platelet aggregation in washed rabbit platelets (WRP) (pA2 = 6.68 +/- 0.08) and in human platelet-rich plasma (HPRP) (IC50 = 0.68 microM), while not affecting ADP- or arachidonic acid-induced platelet aggregation [1]. The IC50 for rupatadine in A23187, concanavalin A and anti-IgE induced histamine release was 0.7+/-0.4 microM, 3.2+/-0.7 microM and 1.5+/-0.4 microM, respectively whereas for loratadine the IC50 was 2.1+/-0.9 microM, 4.0+/-1.3 M and 1.7+/-0.5 microM. SR-27417A exhibited no inhibitory effect [2].in vivo: Rupatadine blocked histamine- and PAF-induced effects in vivo, such as hypotension in rats (ID50 = 1.4 and 0.44 mg/kg i.v., respectively) and bronchoconstriction in guinea pigs (ID50 = 113 and 9.6 micrograms/kg i.v.). Moreover, it potently inhibited PAF-induced mortality in mice (ID50 = 0.31 and 3.0 mg/kg i.v. and p.o., respectively) and endotoxin-induced mortality in mice and rats (ID50 = 1.6 and 0.66 mg/kg i.v.) [1]. rupatadine treatment improved the declined lung function and significantly decreased animal death. Moreover, rupatadine was able not only to attenuate silica-induced silicosis but also to produce a superior therapeutic efficacy compared to pirfenidone, histamine H1 antagonist loratadine, or PAF antagonist CV-3988 [3]. [1]. Merlos M, et al. Rupatadine, a new potent, orally active dual antagonist of histamine and platelet-activating factor (PAF). J Pharmacol Exp Ther. 1997 Jan;280(1):114-21. [2]. Queralt M, et al. In vitro inhibitory effect of rupatadine on histamine and TNF-alpha release from dispersed canine skin mast cells and the human mast cell line HMC-1. Inflamm Res. 2000 Jul;49(7):355-60. [3]. Lv XX, et al. Rupatadine protects against pulmonary fibrosis by attenuating PAF-mediated senescence in rodents. PLoS One. 2013 Jul 15;8(7):e68631. | |||
T38002 | |||
LEO 39652 is a dual-soft PDE4 inhibitor with IC50s of 1.2 nM, 1.2 nM, 3.0 nM and 3.8 nM for PDE4A, PDE4B, PDE4C and PDE4D, respectively. LEO 39652 also inhibits TNF-α with an IC50 value of 6.0 nM. LEO 39652 is used for topical research of Atopic dermatitis (AD) [1]. LEO 39652 shows unbound in vitro potency when measured as LPS induced TNF-α release in human peripheral blood mononuclear cells (PBMC), incubated in serum free medium. LEO 39652 shows a relatively high binding to human serum albumin[2]. LEO 39652 is inactivated both in blood and liver (dual-soft) while stabled in the skin[1].Pharmacokinetic AnalysisLEO 39652 exhibits total clearance (rats 930, minipigs 200 and monkey 300 mL/min/kg) and ratio to total AUC (rats 4, minipigs 6 and monkey 6 %) following intravenous administration (rats 0.075, minipigs 0.5 and monkeys 2.0 mg/kg)[1]. [1]. Jens Larsen, et al. Discovery and Early Clinical Development of Isobutyl 1-[8-Methoxy-5-(1-oxo-3 H-isobenzofuran-5-yl)-[1,2,4]triazolo[1,5- a]pyridin-2-yl]cyclopropanecarboxylate (LEO 39652), a Novel Dual-Soft" PDE4 Inhibitor for Topical Treatment of Atopic Dermatitis. J Med Chem. 2020 Dec 10;63(23):14502-14521.[2]. Stefan Eirefelt | |||
T38844 | |||
MK-8245 trifluoroacetate is a liver-targeting inhibitor of stearoyl-CoA desaturase (SCD) with IC50 of 1 nM for human SCD1 and 3 nM for both rat SCD1 and mouse SCD1, with anti-diabetic and anti-dyslipidemic efficacy. IC50 value: 1 nM (hSCD1) Target: SCD1 in vitro: MK-8245, a phenoxy piperidine isoxazole derivative, has been identified as a potent and liver-specific SCD inhibitor. It contains a tetrazole acetic acid moiety, which is the key molecule for OATPs recognition and liver-targeting. MK-8245 displays similar potencies against human, rat and mouse SCD1 with IC50 values of 1 nM for human SCD1 and 3 nM for both rat SCD1 and mouse SCD1. MK-8245 exhibits a significant SCD inhibition in the rat hepatocyte assay which contains functional, active OATPs with IC50 of 68 nM, while being only weakly active in the HepG2 cell assay which is devoid of active OATPs with IC50 of ~1 μM. MK-8245 displays highly selective activity for the Δ-5 and Δ-6 desaturases (i.e., >100000 μM vs rat and human Δ5D and Δ6D as assessed in the HepG assay. in vivo: Administration of MK-8245 at 10 mg/kg in mice exhibits a tissue distribution profile concentrated in the liver. It shows a liver-to-Harderian gland ratio of 21, suggesting a high degree of liver-targeting compared to a systemically distributed compound with liver-to-Harderian gland ratio of 1.5. Oral dosing of MK-8245 in mice, rats, dogs, and rhesus monkeys demonstrates that MK-8245 is distributed mainly to the liver, with low exposure in tissues associated with potential adverse events. The liver-to-skin ratios are >30:1 in all four species. Administration of MK-8245 to eDIO mice before the glucose challenge improves glucose clearance in a dose-dependent manner with ED50 of 7 mg/kg. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-02035 | ASPRV1 Protein, Human, Recombinant (His & Myc) | Human | in vitro E. coli expression system | ||
ASPRV1 Protein, Human, Recombinant (His & Myc) is expressed in in vitro E. coli expression system.
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TMPJ-00667 | DEFB4A Protein, Human, Recombinant | Human | E. coli | ||
β-Defensin 4A is a membrane-active cationic peptide that functions in inflammation and innate immune responses. There are at least 30 β-Defensins, which are distinguished from α-Defensins by the connectivity pattern of their three intermolecular disulfide bonds. Members of the Defensin family are highly similar in protein sequence. This gene encodes Defensin, DEFB4;, which has broad-spectrum antimicrobial activity and may play an important role in innate epithelial defense. They are highly expressed in skin and tonsils, and to a lesser extent in trachea, uterus, kidney, thymus, adenoid, pharynx and tongue. β-Defensin 4A has low expression in salivary gland, bone marrow, colon, stomach, polyp and larynx. No expression in small intestine. The 45 amino acid mature human BD3 shares 38% and 33% amino acid sequence identity with mouse and rat BD3, respectively.
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TMPY-02959 | IL-20 Protein, Human, Recombinant | Human | E. coli | ||
IL20/Interleukin-20 belongs to the IL-10 family. It is a cytokine structurally related to interleukin 10. IL20/Interleukin-20 can be detected in skin, trachea, and other tissues. It is produced by activated keratinocytes and monocytes and transmits an intracellular signal through two distinct cell-surface receptor complexes on keratinocytes and other epithelial cells. It has been shown that interleukin-20 transduces its signal through signal transducer and activator of transcription 3 (STAT3) in keratinocytes. It may be involved in epidermal function and psoriasis. It also regulates the proliferation and differentiation of keratinocytes during inflammation, particularly inflammation associated with the skin. Also, IL20/Interleukin-20 also causes cell expansion of multipotential hematopoietic progenitor cells. A specific receptor for this cytokine is found to be expressed in skin and upregulated dramatically in psoriatic skin, suggesting a role for this protein in epidermal function and psoriasis.
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TMPY-01859 | LYPD3 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Ly6 / PLAUR domain-containing protein 3, also known as GPI-anchored metastasis-associated protein C4.4A homolog, Matrigel-induced gene C4 protein, MIG-C4, and LYPD3, is a cell membrane protein that contains two UPAR/Ly6 domains. Human LYPD3 contains two UPAR/Ly6 domains. LYPD3 is expressed in the placenta, skin, and urothelium. It is found in suprabasal keratinocytes of chronic wounds. Weak expression of LYPD3 is found in the esophagus and peripheral blood mononuclear cells. It is found in the majority of primary and metastatic transitional cell carcinomas (TCCs) and as well in breast cancer tissues, but not in adjacent normal tissues. High expression of LYPD3 is found in the tumor component of some noninvasive superficial lesions and invasive and metastatic urothelial cancers. LYPD3 is up-regulated in migrating keratinocytes during epithelisation of incisional skin wounds. LYPD3 supports cell migration. It may be involved in urothelial cell-matrix interactions. It may also be involved in tumor progression
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TMPY-02731 | SPINK4 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Serine protease inhibitor Kazal-type 4, also known as Peptide PEC-6 homolog and SPINK4, is a secreted protein that contains one Kazal-like domain. SPINK4 is a member of the SPINK protein family. The gene family of serine protease inhibitors of the Kazal type (SPINK) are functional and positional candidate genes for celiac disease (CD). SPINK1 plays an important role in protecting the pancreas against excessive trypsinogen activation. It is a potent natural inhibitor of pancreatic trypsin activity. SPINK1 mutations are associated with the development of acute and chronic pancreatitis and have been detected in all forms of chronic pancreatitis. SPINK2 functions as a trypsin/acrosin inhibitor and is synthesized mainly in the testis and seminal vesicle where its activity is engaged infertility. The SPINK2 protein contains a typical Kazal domain composed by six cysteine residues forming three disulfide bridges. SPINK9 was identified in human skin. Its expression was strong in palmar epidermis, but not detectable or very low in non palmoplantar skin.
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TMPJ-00162 | IL-1 alpha/IL-1A Protein, Human, Recombinant (hFc) | Human | Human Cells | ||
Interleukin-1 alpha (IL1α) is a cytokine member of the interleukin-1 family. IL-1 consists of two distinct forms: IL1α and IL1β that recognize the same cell surface receptors but are distinct proteins with approximately 25% amino acid sequence identity. IL1α is constitutively produced by epithelial cells and plays an essential role in maintenance of skin barrier function. Upon stimulation, a wide variety of cells including osteoblasts, monocytes, macrophages can be induced to express IL1α. IL1α possesses a wide range of metabolic, physiological, haematopoietic activities, and is critically involved in the regulation of the immune responses and inflammatory responses.
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TMPJ-00562 | PDGF-BB Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Platelet-Derived Growth Factor Subunit B (PDGFB) belongs to the PDGF/VEGF growth factor family. Platelet-derived growth factor is a potent mitogen for cells of mesenchymal origin. PDGFB can exist either as a homodimer (PDGF-BB) or as a heterodimer with the platelet-derived growth factor alpha polypeptide (PDGF-AB), where the dimers are connected by disulfide bonds. As growth factor,it plays an essential role in the regulation of embryonic development, cell proliferation, cell migration, survival and chemotaxis. It is required for normal proliferation and recruitment of pericytes and vascular smooth muscle cells in the central nervous system, skin, lung, heart and placenta. PDGFB also plays an important role in wound healing.
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TMPJ-00261 | TGF beta 2 Protein, Mouse/Rat, Recombinant | Mouse,Rat | Human Cells | ||
Transforming growth factor beta 2 (TGF-β2) is a member of TGF-beta superfamily that shares a characteristic cysteine knot structure. Mice with TGF-β2 gene deletion show defects in development of cardiac, lung, craniofacial, limb, spinal column, eye, inner ear and urogenital systems. All TGF-β isoforms signal via the same heteromeric receptor complex, consisting of a ligand binding TGF-β receptor type II (TβR-II), and a TGF-β receptor type I (TβR-I). Signal transduction from the receptor to the nucleus is mediated via SMADs. TGF-β expression is found in cartilage, bone, teeth, muscle, heart, blood vessels, haematopoitic cells, lung, kidney, gut, liver, eye, ear, skin, and the nervous system.
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TMPY-01008 | VEGFD Protein, Human, Recombinant (His) | Human | HEK293 | ||
Vascular endothelial growth factor D (VEGF-D), also known as C-fos induced growth factor (FIGF), belongs to the platelet-derived growth factor/vascular endothelial growth factor (PDGF/VEGF) family. FIGF protein is active in angiogenesis, lymphangiogenesis, and endothelial cell growth. FIGF protein is secreted as a non-covelent homodimer in an antiparallel fashion. Human FIGF protein is expressed in adult lung, heart, muscle, and small intestine, and is most abundantly expressed in fetal lungs and skin. FIGF protein is structurally and functionally similar to VEGF-C. Therefore, FIGF protein binds and activates VEGFR-2 (Flk1) and VEGFR-3 (Flt4) receptors, and may particularly be involved in cancers, such as breast cancer, epithelial ovarian carcinoma and so on.
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TMPJ-01204 | TPSAB1 Protein, Human, Recombinant (His) | Human | Human Cells | ||
Tryptases are serine proteases with trypsin-like specificity. Together with chymases and Cathepsin G, tryptases are important players in mast cell mediation of inflammatory and allergic responses. Tryptase alpha/beta-1(TPSAB1), also known as mast cell protease 7 (MCPT7), it exhibits anticoagulant activity due to its ability to degrade fibrinogen in the presence of a diverse array of protease inhibitors in plasma. The two Isoform 1 and isoform 2 are expressed in lung, stomach, spleen, heart and skin; in these tissues, isoform 1 is predominant. Isoform 2 is expressed in aorta, spleen, and breast tumor, with highest levels in the endothelial cells of some blood vessels surrounding the aorta, as well as those surrounding the tumor and low levels, if any, in mast cells. Isoform 2 cleaves large substrates, such as fibronectin, more efficiently than isoform 1, but seems less efficient toward small substrates. It may play a role in innate immunity.
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TMPJ-01065 | Noggin/NOG Protein, Mouse, Recombinant (His) | Mouse | Human Cells | ||
Noggin is a secreted homodimeric glycoprotein that is an antagonist of bone morphogenetic proteins (BMPs). Mouse Noggin cDNA encodes a 232 amino acid (aa) residue precursor protein with 19 aa residue putative signal peptide that is cleaved to generate the 213 aa residue mature protein which is secreted as a homodimeric glycoprotein. Secreted Noggin probably remains close to the cell surface due to its binding of heparin-containing proteoglycans. Noggin binds some BMPs such as BMP4 with high affinity and others such as BMP7 with lower affinity. It antagonizes BMP bioactivities by blocking epitopes on BMPs that are needed for binding to both type I and type II receptors. Noggin is expressed in defined areas of the adult central nervous system and peripheral tissues such as lung, skeletal muscle and skin. During culture of human embryonic stem cells (hESC) or neural stem cells under certain conditions, addition of Noggin to antagonize BMP activity may allow stem cells to proliferate while maintaining their undifferentiated state, or alternatively, to differentiate into dopaminergic neurons.
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TMPY-01371 | IL-17RA Protein, Human, Recombinant (His) | Human | HEK293 | ||
Interleukin-17 receptor (IL-17R), also known as Interleukin-17 receptor A (IL-17RA) and CD217 antigen (CD217), is a cytokine receptor that binds interleukin 17. IL-17R/IL-17RA (CD217) is a proinflammatory cytokine secreted by activated T-lymphocytes. It is a potent inducer of the maturation of CD34-positive hematopoietic precursors into neutrophils. IL-17R/IL-17RA (CD217) is a ubiquitous type I membrane glycoprotein that binds with low affinity to interleukin 17A. Interleukin 17A and its receptor IL-17RA play a pathogenic role in many inflammatory and autoimmune diseases such as rheumatoid arthritis. Like other cytokine receptors, this receptor likely has a multimeric structure. Defects in IL-17R/IL-17RA (CD217) are the cause of familial candidiasis type 5 (CANDF5). CANDF5 is a rare disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails, and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans.
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TMPY-00423 | FGFR2 Protein, Human, Recombinant (alpha IIIb, hFc) | Human | HEK293 | ||
FGFR2, also known as CD332, belongs to the fibroblast growth factor receptor subfamily where amino acid sequence is highly conserved between members and throughout evolution. FGFR2 acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. It is required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. FGFR2 plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. It also promotes cell proliferation in keratinocytes and imature osteoblasts, but promotes apoptosis in differentiated osteoblasts. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal CD332 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1. Defects in CD3322 are the cause of Crouzon syndrome, Jackson-Weiss syndrome, Apert syndrome, Pfeiffer syndrome, Beare-Stevenson cutis gyrata syndrome, familial scaphocephaly syndrome, lacrimo-auriculo-dento-digital syndrome and Antley-Bixler syndrome without genital anomalies or disordered steroidogenesis.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-01305 | OSMR Protein, Human, Recombinant (His) | Human | HEK293 | ||
Oncostatin-M specific receptor subunit beta also known as the oncostatin M receptor (OSMR) and Interleukin-31 receptor subunit beta (IL-31RB), is one of the receptor proteins for oncostatin M. OSMR is a member of the type I cytokine receptor family. IL-31RB/OSMR heterodimerizes with interleukin 6 signal transducer to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the interleukin 31 receptor, and thus transduces oncostatin M and interleukin 31 induced signaling events. Mutations in IL-31RB/OSMR have been associated with familial primary localized cutaneous amyloidosis. Defects in IL-31RB/OSMR are the cause of amyloidosis primary localized cutaneous type 1 (PLCA1), also known as familial lichen amyloidosis of familial cutaneous lichen amyloidosis. PLCA1 is hereditary primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening (lichenification) that may be exacerbated by chronic scratching and rubbing. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.
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TMPY-00972 | FGFR2 Protein, Human, Recombinant (His & hFc) | Human | HEK293 | ||
FGFR2, also known as CD332, belongs to the fibroblast growth factor receptor subfamily where amino acid sequence is highly conserved between members and throughout evolution. FGFR2 acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. It is required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. FGFR2 plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. It also promotes cell proliferation in keratinocytes and imature osteoblasts, but promotes apoptosis in differentiated osteoblasts. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal CD332 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1. Defects in CD3322 are the cause of Crouzon syndrome, Jackson-Weiss syndrome, Apert syndrome, Pfeiffer syndrome, Beare-Stevenson cutis gyrata syndrome, familial scaphocephaly syndrome, lacrimo-auriculo-dento-digital syndrome and Antley-Bixler syndrome without genital anomalies or disordered steroidogenesis.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-02335 | OSMR Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Oncostatin-M specific receptor subunit beta also known as the oncostatin M receptor (OSMR) and Interleukin-31 receptor subunit beta (IL-31RB), is one of the receptor proteins for oncostatin M. OSMR is a member of the type I cytokine receptor family. IL-31RB/OSMR heterodimerizes with interleukin 6 signal transducer to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the interleukin 31 receptor, and thus transduces oncostatin M and interleukin 31 induced signaling events. Mutations in IL-31RB/OSMR have been associated with familial primary localized cutaneous amyloidosis. Defects in IL-31RB/OSMR are the cause of amyloidosis primary localized cutaneous type 1 (PLCA1), also known as familial lichen amyloidosis of familial cutaneous lichen amyloidosis. PLCA1 is hereditary primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening (lichenification) that may be exacerbated by chronic scratching and rubbing. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.
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TMPY-01727 | GLA/alpha-Galactosidase A Protein, Human, Recombinant (His) | Human | HEK293 | ||
Alpha-galactosidase A, also known as Alpha-D-galactoside galactohydrolase, Alpha-D-galactosidase A, Melibiase and GLA, is a member of the glycosyl hydrolase 27 family. GLA is used as a long-term enzyme replacement therapy in patients with a confirmed diagnosis of Fabry disease. Defects in GLA are the cause of Fabry disease (FD) which is a rare X-linked sphingolipidosis disease where glycolipid accumulates in many tissues. The disease consists of an inborn error of glycosphingolipid catabolism. FD patients show systemic accumulation of globotriaoslyceramide (Gb3) and related glycosphingolipids in the plasma and cellular lysosomes throughout the body. Clinical recognition in males results from characteristic skin lesions (angiokeratomas) over the lower trunk. Patients may show ocular deposits, febrile episodes, and burning pain in the extremities. Death results from renal failure, cardiac or cerebral complications of hypertension or other vascular disease. Deficiency of GLA leads to the accumulation of glycosphingolipids in the vasculature leading to multiorgan pathology. In addition to well-described microvascular disease, deficiency of GLA is also characterized by premature macrovascular events such as stroke and possibly myocardial infarction.
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TMPY-03357 | FGFR2 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
FGFR2, also known as CD332, belongs to the fibroblast growth factor receptor subfamily where amino acid sequence is highly conserved between members and throughout evolution. FGFR2 acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. It is required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. FGFR2 plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. It also promotes cell proliferation in keratinocytes and imature osteoblasts, but promotes apoptosis in differentiated osteoblasts. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal CD332 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1. Defects in CD3322 are the cause of Crouzon syndrome, Jackson-Weiss syndrome, Apert syndrome, Pfeiffer syndrome, Beare-Stevenson cutis gyrata syndrome, familial scaphocephaly syndrome, lacrimo-auriculo-dento-digital syndrome and Antley-Bixler syndrome without genital anomalies or disordered steroidogenesis.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-01146 | Insulin Receptor Protein, Human, Recombinant (long isoform, His) | Human | HEK293 | ||
INSR (Insulin receptor), also known as CD22, is a transmembrane receptor that is activated by insulin. INSR belongs to the protein kinase superfamily and exists as a tetramer consisting of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha and beta subunits are encoded by a single INSR gene, and the beta subunits pass through the cellular membrane. As the receptor for insulin with tyrosine-protein kinase activity, INSR associates with downstream mediators upon binding to insulin, including IRS1 (insulin receptor substrate 1) and phosphatidylinositol 3'-kinase (PI3K). IRS-1 binding and phosphorylation eventually lead to an increase in the high-affinity glucose transporter (Glut4) molecules on the outer membrane of insulin-responsive tissues. INSR isoform long and isoform short are expressed in the peripheral nerve, kidney, liver, striated muscle, fibroblasts and skin, and is found as a hybrid receptor with IGF1R which also binds IGF1 in muscle, heart, kidney, adipose tissue, skeletal muscle, hepatoma, fibroblasts, spleen, and placenta. Defects in Insulin Receptor/INSR are the cause of Rabson-Mendenhall syndrome (Mendenhall syndrome), insulin resistance (Ins resistance), leprechaunism (Donohue syndrome), and familial hyperinsulinemic hypoglycemia 5 (HHF5). It may also be associated with noninsulin-dependent diabetes mellitus (NIDDM).
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TMPY-00843 | IL-25/IL17E Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Interleukin-25 (IL-25) is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. IL-25 is a member of the IL-17 family of cytokines. However, unlike the other members of this family, IL-25 promotes T helper (Th) 2 responses. IL-25 also regulates the development of autoimmune inflammation mediated by IL-17–producing T cells. IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin (TSLP)–activated dendritic cells (DCs), homeostatic cytokines, or T cell receptor for antigen triggering. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. A plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells had been provided.
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TMPY-00855 | IL-25/IL17E Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Interleukin-25 (IL-25) is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. IL-25 is a member of the IL-17 family of cytokines. However, unlike the other members of this family, IL-25 promotes T helper (Th) 2 responses. IL-25 also regulates the development of autoimmune inflammation mediated by IL-17–producing T cells. IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin (TSLP)–activated dendritic cells (DCs), homeostatic cytokines, or T cell receptor for antigen triggering. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. A plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells had been provided.
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TMPY-01403 | VNN1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Pantetheinase, also known as Pantetheine hydrolase, Vascular non-inflammatory molecule 1, Vanin-1, and VNN1, is a cell membrane protein which belongs to the CN hydrolase family and BTD/VNN subfamily. Vanin-1 contains one CN hydrolase domain. It is widely expressed with higher expression in spleen, kidney and blood. It is overexpressed in lesional psoriatic skin. Vanin-1 is also a member of the Vanin family of proteins which share extensive sequence similarity with each other, and also with biotinidase. The family includes secreted and membrane-associated proteins, a few of which have been reported to participate in hematopoietic cell trafficking. No biotinidase activity has been demonstrated for any of the vanin proteins, however, they possess pantetheinase activity, which may play a role in oxidative-stress response. Vanin-1 is an epithelial pantetheinase that provides cysteamine to tissue and regulates response to stress. Vanin-1 is expressed by enterocytes, and its absence limits intestinal epithelial cell production of proinflammatory signals. Vanin-1 regulates late adhesion steps of thymus homing under physiological, noninflammatory conditions. The early impact of vanin-1 deficiency on tumor induction was directly correlated to the amount of inflammation and subsequent epithelial proliferation rather than cell death rate. Vanin-1 molecule was shown to be involved in the control of thymus reconstitution following sublethal irradiation.
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TMPY-04815 | C1 inhibitor Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
Plasma protease C1 inhibitor, also known as C1-inhibiting factor, C1-INH, C1 esterase inhibitor, SERPING1 and C1IN, is a serine proteinase inhibitor (serpin) that regulates activation of both the complement and contact systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). Owing to its ability to modulate the contact and complement systems and the convincing safety profile, plasma-derived C1 inhibitor is an attractive therapeutic protein to treat inflammatory diseases other than HAE. Deficiency of C1 inhibitor results in hereditary angioedema, which is characterized by recurrent episodes of localized angioedema of the skin, gastrointestinal mucosa or upper respiratory mucosa. C1 inhibitor may prove useful in a variety of other diseases including septic shock, reperfusion injury, hyperacute transplant rejection, traumatic and hemorrhagic shock, and the increased vascular permeability associated with thermal injury, interleukin-2 therapy and cardiopulmonary bypass.
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TMPJ-00042 | TSLP Protein, Human, Recombinant | Human | E. coli | ||
Thymic stromal lymphopoietin (TSLP) is a novel member of the hemopoietic cytokine family that promotes the development of B cells and shares overlapping activity with IL-7. The human TSLP protein comprises a 28 amino acids (aa) signal sequence and 131 aa mature region. Human TSLP has two isoforms lfTSLP and sfTSLP produced by alternative splicing . lfTSLP is expressed in a number of tissues including heart, liver and prostate, and sfTSLP (63aa) is predominantly expressed in keratinocytes of oral mucosa, skin and in salivary glands. In aa sequence level, Human TSLP displays about 43% identity with mouse TSLP.TSLP is a cytokine that functions mainly on myeloid cells; it induces the release of T cell-attracting chemokines from monocytes and enhances the maturation of CD11c(+) dendritic cells.TSLP has proliferative effects on the myeloid cell line and may initiate asthma or atopic dermatitis responses by directly activating mast cells . TSLP signals cells via the interleukin-7 receptor-α chain (IL-7Rα),shared with IL-7, together with the TSLP receptor (TSLPR) subunit. Recent studies indicate that TSLP and its receptor are novel therapeutic targets for rheumatoid arthritis,for increased intraarticular TSLP concentrations in patients has caused chemotaxis and activation of arthritogenic T cells.
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TMPY-04356 | GSK3B Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
GSK3B is a serine-threonine kinase, belonging to the glycogen synthase kinase subfamily. It Contains 1 protein kinase domain, and is expressed in the testis, thymus, prostate, and ovary and weakly expressed in the lung, brain, and kidney. GSK3B is involved in energy metabolism, neuronal cell development, and body pattern formation. Polymorphisms in the GSK3B gene have been implicated in modifying the risk of Parkinson's disease, and studies in mice show that overexpression of this gene may be relevant to the pathogenesis of Alzheimer's disease. GSK3B participates in the Wnt signaling pathway. It is implicated in the hormonal control of several regulatory proteins including glycogen synthase, MYB, and the transcription factor JUN. Phosphorylates JUN at sites proximal to its DNA-binding domain, thereby reducing its affinity for DNA. Phosphorylates MUC1 in breast cancer cells, and decreases the interaction of MUC1 with CTNNB1/beta-catenin. GSK3B also plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex. It prevents the phosphorylation of APC and CLASP2, allowing its association with the cell membrane. In turn, membrane-bound APC allows the localization of MACF1 to the cell membrane, which is required for microtubule capture and stabilization. GSK3B phosphorylates MACF1 and this phosphorylation inhibits the binding of MACF1 to microtubules which are critical for its role in bulge stem cell migration and skin wound repair. It may be required for early embryo development and neuron differentiation.
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TMPH-01576 | KRT16 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Epidermis-specific type I keratin that plays a key role in skin. Acts as a regulator of innate immunity in response to skin barrier breach: required for some inflammatory checkpoint for the skin barrier maintenance.
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TMPH-03551 | Exfoliative toxin A Protein, S. aureus, Recombinant (His) | Staphylococcus aureus | E. coli | ||
Has serine protease-like properties and binds to the skin protein profilaggrin. Cleaves substrates after acidic residues. Exfoliative toxins cause impetigous diseases commonly referred as staphylococcal scalded skin syndrome (SSSS).
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TMPK-01057 | CLEC9A Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
CLEC9A expression was significantly higher in psoriatic skin compared with healthy donor. In psoriatic skin and PsA ST, CLEC9A() cells were in close proximity to TUNEL() cells. SF CLEC9A levels were significantly lower compared with paired PsA serum. Adalimumab treatment did not affect CLEC9A serum level and skin expression. The downregulation of synovial CLEC9A might be associated with a novel mechanism by which anti-TNF therapy might reduce CD8-mediated inflammation in PsA patients.
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TMPH-03552 | Exfoliative toxin B Protein, S. aureus, Recombinant (His & Myc) | Staphylococcus aureus | E. coli | ||
Has serine protease-like properties and binds to the skin protein profilaggrin. Cleaves substrates after acidic residues. Exfoliative toxins cause impetigous diseases commonly referred as staphylococcal scalded skin syndrome (SSSS).
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TMPY-03779 | CCL27 Protein, Human, Recombinant (His) | Human | E. coli | ||
CCL27, also known as CTACK, is a small cytokine belonging to the CC chemokine family. Members of this family are proteins characterized by two adjacent cysteines. CCL27 is chemotactic for skin-associated memory T lymphocytes. CCL27 may also play a role in mediating homing of lymphocytes to cutaneous sites. CCL27 plays a pivotal role in establishing the inflammatory infiltrate characteristic for common inflammatory skin diseases. Through binding to the chemokine receptor 1 (CCR1), CCL27 mediates inflammation by promoting lymphocyte migration into the skin.
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TMPY-03476 | IL-20 Protein, Rat, Recombinant | Rat | E. coli | ||
IL20/Interleukin-20 belongs to the IL-10 family. It is a cytokine structurally related to interleukin 10. IL20/Interleukin-20 can be detected in skin, trachea, and other tissues. It is produced by activated keratinocytes and monocytes and transmits an intracellular signal through two distinct cell-surface receptor complexes on keratinocytes and other epithelial cells. It has been shown that interleukin-20 transduces its signal through signal transducer and activator of transcription 3 (STAT3) in keratinocytes. It may be involved in epidermal function and psoriasis. It also regulates the proliferation and differentiation of keratinocytes during inflammation, particularly inflammation associated with the skin. Also, IL20/Interleukin-20 also causes cell expansion of multipotential hematopoietic progenitor cells. A specific receptor for this cytokine is found to be expressed in skin and upregulated dramatically in psoriatic skin, suggesting a role for this protein in epidermal function and psoriasis.
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TMPJ-01409 | CCL27 Protein, Human, Recombinant | Human | E. coli | ||
Human Chemokine (C-C Motif) Ligand 27 (CCL27) is a small cytokine that is a member of the CC chemokine family; it is expressed in numerous tissues, including gonads, thymus, placenta and skin. CCL27 elicits its chemotactic effects by binding to the chemokine receptor CCR10. Predominantly expressed in the skin, CCL27 is associated with T cell-mediated inflammation of the skin. Human and Mouse CCL27 share 84% sequence identity in the mature form.
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TMPK-01158 | Kallikrein 5/KLK5 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
The inhibition of kallikrein 5 (KLK5) has been identified as a potential strategy for treatment of the genetic skin disorder Netherton syndrome, in which loss-of-function mutations in the SPINK5 gene lead to down-regulation of the endogenous inhibitor LEKTI-1 and profound skin-barrier defects with severe allergic manifestations. To aid in the development of a medicine for this target, an X-ray crystallographic system was developed to facilitate fragment-guided chemistry and knowledge-based drug-discovery approaches.
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TMPJ-00030 | IL-1F10 Protein, Human, Recombinant | Human | E. coli | ||
Human Interleukin 1 Family Member 10 (IL-1F10) is thought to participate in a network of Interleukin 1 cytokine family members to regulate adapted and innate immune responses. IL-1F10 was expressed in fetal skin, spleen and tonsil, mostly in the basal epithelia of skin and in proliferating B-cells of the tonsil. IL-1F10 binds soluble IL-1 receptor type 1 and may be implicated in regulating adapted and innate immune responses. Two alternatively spliced transcript variants encoding the same protein have been reported.
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TMPJ-01145 | ABCB5 Protein, Human, Recombinant (Trx) | Human | E. coli | ||
ATP-binding cassette sub-family B member 5(ABCB5) is a plasma membrane-spanning protein. ABCB5 is principally expressed in physiological skin and human malignant melanoma. ABCB5 has been suggested to regulate skin progenitor cell fusion and mediate chemotherapeutic drug resistance in stem-like tumor cell subpopulations in human malignant melanoma. It is commonly over-expressed on circulating melanoma tumour cells. Furthermore, the ABCB5+ melanoma- initiating cells were demonstrated to express FLT1 (VEGFR1) receptor tyrosine kinase which was functionally required for efficient xenograft tumor formation, as demonstrated by shRNA knockdown experiments.
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TMPY-01346 | Psoriasin/S100A7 Protein, Human, Recombinant | Human | E. coli | ||
Protein S100-A7, also known as S100 calcium-binding protein A7, Psoriasin, S100A7, and PSOR1, is a secreted protein which belongs to theS-100 family. S100A7 was first isolated from skin involved by psoriasis, which can be induced in cultured squamous epithelial cells. S100A7 is expressed by both normal cultured and malignant keratinocytes and malignant breast epithelial cells within ductal carcinoma in situ, suggesting an association with abnormal pathways of differentiation. S100A7 plays a role in the pathogenesis of inflammatory skin disease, as a chemotactic factor for hematopoietic cells. It also plays a role in early stages of breast tumor progression in association with the development of the invasive phenotype.
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TMPY-01824 | Caspase-14 Protein, Human, Recombinant (His) | Human | E. coli | ||
Caspase 14 is a member of the caspase family. Caspases are a kind of cysteine proteinase consisting of a prodomain plus large and small catalytic subunits, that play a central role in cell apoptosis. Caspase 14 possesses an unusually short prodomain and is highly expressed in embryonic tissues but absent from most of the adult tissues except for the skin, which suggests a role in ontogenesis and skin physiology. Unlike the other short prodomain caspases(caspase-3, caspase-6, and caspase-7), Caspase 14 was not processed by multiple death stimuli including activation of members of the tumor necrosis factor receptor family and expression of proapaptotic members of the bcl-2 family. Caspase 14 has been described to be processed and activated by anti-Fas agonist antibody or TNF-related apoptosis inducing ligand in vivo. The expression and processing of this caspase may take part in keratinocyte terminal differentiation, which is essential for the skin barrier.
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TMPY-03017 | Kallikrein 7/KLK7 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Kallikrein-7, also known as kallikrein-related peptidase 7, Stratum corneum chymotryptic enzyme, Serine protease 6, KLK7, and PRSS6, is a secreted protein that belongs to the peptidase S1 family and Kallikrein subfamily. Members of the Kallikrein family are involved in various malignancies such as prostate (PSA, KLK2, KLK15), ovarian (KLK4, KLK5, KLK6, KLK8, KLK1), and breast cancer (KLK1, KLK13, KLK14). Kallikrein-7 / KLK7 appears to be increased in ovarian cancer and higher KLK7 expression in ovarian cancer tissue is associated with poorer prognosis of ovarian cancer patients. Kallikrein-7 / KLK7 is abundantly expressed in the skin and is expressed by keratinocytes in the epidermis. Kallikrein-7 / KLK7 is up-regulated in ovarian carcinoma, especially late-stage serous carcinoma, compared with normal ovaries and benign adenomas (at the protein level). It was significantly associated with shorter overall survival (OS) and disease-free survival (DFS). Kallikrein-7 / KLK7 may catalyze the degradation of intercellular cohesive structures in the cornified layer of the skin in the continuous shedding of cells from the skin surface. KLK7 also plays a role in the activation of precursors to inflammatory cytokines.
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TMPJ-01292 | Chemerin/RARRES2 Protein, Human, Recombinant (His) | Human | Human Cells | ||
Retinoic acid receptor responder protein 2(RARRES2) is a secreted protein that in humans is encoded by the RARRES2 gene. It is highly expressed in skin, also found in pancreas, liver, spleen, prostate, ovary, small intestine and colon. It is a chemoattractant protein that acts as a ligand for the G protein-coupled receptor CMKLR1. RARRES2 is secreted in an inactive form as prochemerin and is activated through cleavage of the C-terminus by inflammatory and coagulation serine proteases. It is thought to act as a cell surface receptor, found to stimulate chemotaxis of dendritic cells and macrophages to the site of inflammation. RARRES2 is inhibited in psoriatic lesions,it is activated by tazarotene in skin rafts and in the epidermis of psoriatic lesions.
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TMPJ-00544 | Kallikrein 7/KLK7 Protein, Human, Recombinant (aa 23-252, His) | Human | Human Cells | ||
Human Kallikrein 7 is a member of the tissue kallikrein family of extracellular serine proteases that is made up of 15 members. It is predominantly expressed in the skin. A major physiological function of Kallikrein 7 is to regulate the desquamation process (the shedding of corneocytes from the outer layer of the epidermis) through proteolysis of the intercellular adhesive structures between corneocytes. Dysregulation of Kallikrein 7 has been linked to several inflammatory skin diseases including atopic dermatitis, psoriasis, and Netherton syndrome. Studies have shown that Kallikrein 5 is a potential physiological activator for Kallikrein 7. The proform of Kallikrein 7 can be activated by thermolysin.
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TMPY-04984 | CXCL17 Protein, Human, Recombinant (His) | Human | Yeast | ||
Chemokine (C-X-C motif) ligand 17 (CXCL17) is the latest member of the chemokine family. CXCL17 is a potential oncogene and promising therapeutic target, is an independent biomarker of poor prognosis in patients with breast cancer, and can promote proliferation and migration of breast cancer cells in vitro and in vivo. CXCL17 is expressed in a variety of cancers and promotes tumor progression by recruiting myeloid-derived suppressor cells (MDSCs). CXCL17 attenuates IMQ-induced psoriasis-like skin inflammation by recruiting MDSCs and Tregs, which may be important for regulating excessive inflammation in psoriasis skin. CXCL17 production correlated with adverse immune infiltration and might be an important target for anti-HCC therapies. CXCL17 is a major regulator of mucosal inflammatory responses.
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TMPK-00127 | CLEC4A Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Clec4a has been reported to be an immune suppressor of dendritic cells (DCs), but its potential role in cancer therapy remains to be elucidated. silencing of Clec4a2 expression via skin delivery of shRNA produces an effective antitumor response and that Clec4a2 shRNA may have therapeutic potential as an adjuvant for cancer immunotherapy.
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TMPY-01417 | Kallikrein 7/KLK7 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Kallikrein-7, also known as kallikrein-related peptidase 7, Stratum corneum chymotryptic enzyme, Serine protease 6, KLK7, and PRSS6, is a secreted protein that belongs to the peptidase S1 family and Kallikrein subfamily. Members of the Kallikrein family are involved in various malignancies such as prostate (PSA, KLK2, KLK15), ovarian (KLK4, KLK5, KLK6, KLK8, KLK1), and breast cancer (KLK1, KLK13, KLK14). Kallikrein-7 / KLK7 appears to be increased in ovarian cancer and higher KLK7 expression in ovarian cancer tissue is associated with poorer prognosis of ovarian cancer patients. Kallikrein-7 / KLK7 is abundantly expressed in the skin and is expressed by keratinocytes in the epidermis. Kallikrein-7 / KLK7 is up-regulated in ovarian carcinoma, especially late-stage serous carcinoma, compared with normal ovaries and benign adenomas (at the protein level). It was significantly associated with shorter overall survival (OS) and disease-free survival (DFS). Kallikrein-7 / KLK7 may catalyze the degradation of intercellular cohesive structures in the cornified layer of the skin in the continuous shedding of cells from the skin surface. KLK7 also plays a role in the activation of precursors to inflammatory cytokines.
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TMPH-01607 | LCE3A Protein, Human, Recombinant (His) | Human | E. coli | ||
A structural component of the cornified envelope of the stratum corneum involved in innate cutaneous host defense (Probable). Possesses defensin-like antimicrobial activity against a broad spectrum of Gram-positive and Gram-negative bacteria, both aerobic and anaerobic species. Upon inflammation, may regulate skin barrier repair by shaping cutaneous microbiota composition and immune response to bacterial antigens.
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TMPY-04286 | IL-22RA1 Protein, Rat, Recombinant (hFc) | Rat | HEK293 | ||
IL-22R belongs to the type II cytokine receptor family. It contains 2 fibronectin type-III domains and is expressed in the colon, liver, lung, pancreas, and kidney. IL-22R also can be expressed in keratinocytes of normal skin as well as in psoriatic skin lesions. Overexpression of IL-22R can be detected in synovial fluid cells from rheumatoid arthritis and spondyloarthropathy patients. IL-22R is a component of the receptor for IL20, IL22, and IL24. The component of IL-22R formed by IL22RA1 and IL10RB enables IL22 signaling via JAK/STAT pathways. IL22 also induces activation of MAPK1/MAPK3 and Akt kinases pathways. Component of one of the receptors for IL20 and IL24 formed by IL22RA1 and IL20RB also signaling through STATs activation. IL-22R mediates IL24 antiangiogenic activity as well as IL24 inhibitory effect on endothelial cell tube formation and differentiation.
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TMPY-00320 | APOA1BP Protein, Human, Recombinant (His) | Human | HEK293 | ||
APOA1BP, now renamed NAXE, encodes an epimerase essential in the cellular metabolite repair for NADHX and NADPHX. The enzyme catalyzes the epimerization of NAD(P)HX, thereby avoiding the accumulation of toxic metabolites.Pathogenic biallelic mutations in NAXE in children from four families with (sub-) acute-onset ataxia, cerebellar edema, spinal myelopathy, and skin lesions.
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TMPK-00126 | CLEC4A Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Clec4a has been reported to be an immune suppressor of dendritic cells (DCs), but its potential role in cancer therapy remains to be elucidated. silencing of Clec4a2 expression via skin delivery of shRNA produces an effective antitumor response and that Clec4a2 shRNA may have therapeutic potential as an adjuvant for cancer immunotherapy.
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TMPH-02430 | SNCG Protein, Cynomolgus, Recombinant | Cynomolgus | E. coli | ||
Plays a role in neurofilament network integrity. May be involved in modulating axonal architecture during development and in the adult. In vitro, increases the susceptibility of neurofilament-H to calcium-dependent proteases. May also function in modulating the keratin network in skin. Activates the MAPK and Elk-1 signal transduction pathway.
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TMPH-01370 | SNCG Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Plays a role in neurofilament network integrity. May be involved in modulating axonal architecture during development and in the adult. In vitro, increases the susceptibility of neurofilament-H to calcium-dependent proteases. May also function in modulating the keratin network in skin. Activates the MAPK and Elk-1 signal transduction pathway.
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TMPY-02497 | S100A15 Protein, Mouse, Recombinant (His & MBP) | Mouse | E. coli | ||
Koebnerisin is also known as protein S100-A7A (S100A7A), S100 calcium-binding protein A7-like 1 (S100A7L1) or S100 calcium-binding protein A15 (S100A15). Human S100A7A / S100A15 is a novel member of the S100 family of EF-hand calcium-binding proteins and was recently identified in psoriasis, where it is significantly upregulated in lesional skin. S100A7 is expressed by both normal cultured and malignant keratinocytes and malignant breast epithelial cells within ductal carcinoma in situ, suggesting an association with abnormal pathways of differentiation. S100A7 plays a role in the pathogenesis of inflammatory skin disease, as a chemotactic factor for hematopoietic cells. It also plays a role in early stages of breast tumor progression in association with the development of the invasive phenotype. The association of the 11.2 kDa S100A7A / S100A15 with psoriasis suggests that it contributes to the pathogenesis of the disease and could provide a molecular target for therapy.
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