目录号 | 产品详情 | 靶点 | |
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T38049 | |||
N-Acylated ethanolamines (NAE) are naturally-occurring lipids that have diverse bioactivities. For example, arachidonoyl ethanolamide (AEA) is an endogenous neurotransmitter that evokes cellular responses by activating the cannabinoid receptors, central cannabinoid (CB1) and peripheral cannabinoid (CB2). The different types of NAE are derived from glycerophospho-linked precursors by the activity of glycerophosphodiesterase 1 (GDE1). Glycerophospho-N-palmitoyl ethanolamine (GP-NPEA) is the metabolic precursor of palmitoyl ethanolamide (PEA). PEA is an endogenous cannabinoid found in brain, liver, and other mammalian tissues, that has potent anti-inflammatory activity in vivo. PEA has low affinity for peripheral cannabinoid (CB2) and no appreciable affinity for central cannabinoid (CB1), suggesting that its efficacy is through a different receptor. | |||
T79658 | PI3K | ||
PI3Kδ-IN-14(化合物(S)-29)是一种高选择性PI3Kδ抑制剂,具有出色的靶点亲和力(IC50为0.8 nM,Kd为84.8 nM)。该化合物特异性结合至PI3Kδ激酶的ATP结合位点,并通过抑制PI3K/AKT信号通路发挥抗炎作用。此外,PI3Kδ-IN-14在改善急性肺损伤(ALI)方面显示出潜在效果。 | |||
T79371 | Autophagy | ||
HDAC-IN-62(Compound 5),是一款针对HDAC6/8/11的HDAC抑制剂,IC50分别为0.78、1.0、1.2μM。该化合物通过诱导自噬(Autophagy)来抑制微胶质细胞的激活,进而抑制一氧化氮产生,显示出抗炎和抗抑郁的效果。此外,HDAC-IN-62还能抑制实验小鼠大脑中的微胶质细胞活化。 | |||
T60417 | |||
Fenspiride 是 H1-组胺受体的拮抗剂。 Fenspiride 是一种具有口服活性的非甾体类抗炎药,可用于治疗呼吸道感染和中耳炎。 Fenspiride 抑制磷酸二酯酶 4 和磷酸二酯酶 3 的活性,-logIC50 值分别为 4.16+/-0.09 和 3.44+/-0.12。 磷酸二酯酶 5 活性也受到抑制,-logIC50 值约为 3.8。 | |||
TMIH-0146 | |||
Chloroquine-d5 是 Chloroquine 的氘代化合物。Chloroquine 的 CAS 号为 54-05-7。Chloroquine 是一种自噬和 Toll 样受体抑制剂。 氯喹是一种抗疟疾和抗炎剂,广泛用于治疗疟疾和类风湿性关节炎。它在体外控制 SARS-CoV-2 (COVID-19) 感染方面非常有效,EC50 为 1.13 μM。 | |||
T35946 | |||
Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid.[1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response back to a non-inflamed state.[2] Resolvin D1 is produced physiologically from the sequential oxygenation of DHA by 15- and 5-lipoxygenase.[1] 17(R)-RvD1 is an aspirin-triggered epimer of RvD1 that reduces human polymorphonuclear leukocyte (PMN) transendothelial migration, the earliest event in acute inflammation, with equipotency to RvD1 (EC50 = ~30 nM).[3] 17(R)-RvD1 exhibits a dose-dependent reduction in leukocyte infiltration in a mouse model of peritonitis with maximal inhibition of ~35% at a 100 ng dose.[3] In contrast to RvD1, the aspirin-triggered form resists rapid inactivation by eicosanoid oxidoreductases. Analytical and biological comparisons of synthetic 17(R)-RvD1 with endogenously derived 17(R)-RvD1 have confirmed its identity as matching the natural product.[4] | |||
T36408 | |||
Rhein-13C4 is intended for use as an internal standard for the quantification of rhein by GC- or LC-MS. Rhein is an anti-inflammatory anthraquinone found in rhubarb and is the bioactive derivative of its prodrug diacerein . At 10 μM, rhein inhibits IL-1β signaling, suppressing signaling through NF-κB, and reduces the expression of the matrix metalloproteases MMP-1 and MMP-13.1 It inhibits IKKβ (IC50 = 11.8 μM), decreasing iNOS and IL-6 expression in LPS-stimulated macrophages but paradoxically increasing TNF-α, IL-1β, and HMBG1 expression.2 Rhein shows efficacy against pancreatic fibrosis, chronic pancreatitis, and hyperglycemia-induced pancreatic β-cell apoptosis.3,4 It also inhibits angiogenesis of breast cancer cells under normoxic and hypoxic conditions.5 | |||
T8199 | Apoptosis Antioxidant | ||
(±)-α-Bisabolol (Bisabolol) 是一种从洋甘菊、念珠菌树等植物精油中提取的倍半萜烯醇,是一种天然防腐剂,具有舒缓、抗刺激、抗炎、抗氧化和抗癌活性。(±)-α-Bisabolol 通过诱导细胞周期停滞、线粒体死亡和抑制 PI3K/Akt 信号通路来发挥作用,对 A549 NSC-LC 细胞产生抗癌作用 (IC50 = 15 μM)。(±)-α-Bisabolol 能强效诱导胶质瘤细胞凋亡。 | |||
T61910 | |||
COX-2/5-LOX-IN-2 是苯并噻吩-2-基吡唑羧酸衍生物。COX-2/5-LOX-IN-2 (5b) 对COX-2和5-LOX 均有抑制作用。COX-2/5-LOX-IN-2 抑制 COX-1、COX-2 和 5-LOX 的IC50s 分别为 5.40、0.01 和 1.78 μM。COX-2/5-LOX-IN-2 显示出超过塞来昔布和吲哚美辛的镇痛和抗炎活性。 | |||
T83143 | |||
Alloferon 1 是一种具有抗病毒和抗肿瘤功能的肽。它能激活人外周血淋巴细胞的天然细胞毒性,诱导IFN合成,并在小鼠体内增强其抗病毒和抗肿瘤的防御机制。此外,Alloferon 1 在 λ-角叉菜胶诱导的足水肿模型中展现出抗炎作用。它可从双翅目昆虫丽蝇Calliphora vicina的血液中提取。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-06981 | IL-1 alpha/IL-1A Protein, Human, Recombinant (E. coli) | Human | E. coli | ||
IL-1 alpha is a member of the interleukin 1 cytokine family. Cytokines are proteinaceous signaling compounds that are major mediators of the immune response. They control many different cellular functions including proliferation, differentiation, and cell survival/apoptosis but are also involved in several pathophysiological processes including viral infections and autoimmune diseases. Cytokines are synthesized under various stimuli by a variety of cells of both the innate (monocytes, macrophages, dendritic cells) and adaptive (T- and B-cells) immune systems. Cytokines can be classified into two groups: pro- and anti-inflammatory. Pro-inflammatory cytokines, including IFNgamma, IL-1, IL-6, and TNF-alpha, are predominantly derived from the innate immune cells and Th1 cells. Anti-inflammatory cytokines, including IL-10, IL-4, IL-13, and IL-5, are synthesized from Th2 immune cells. IL-1 alpha is a pleiotropic cytokine involved in various immune responses, inflammatory processes, and hematopoiesis. It is produced by monocytes and macrophages as a proprotein, which is proteolytically processed and released in response to cell injury, and thus induces apoptosis. IL-1 alpha stimulates thymocyte proliferation by inducing IL-2 release, B-cell maturation and proliferation, and fibroblast growth factor activity.
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TMPJ-01467 | Oncostatin M/OSM Protein, Human, Recombinant (E. coli, His) | Human | E. coli | ||
Oncostatin M (OSM) is a glycoprotein belonging to the interleukin-6 family of cytokines that includes leukemia-inhibitory factor, granulocyte colony-stimulating factor, and interleukin 6. OSM encodes a growth regulator, which Inhibits the proliferation of a number of tumor cell lines. It stimulates proliferation of AIDS-KS cells. OSM regulates cytokine production, including IL-6, G-CSF and GM-CSF from endothelial cells. OSM is considered as a pleiotropic cytokine that initiates its biological activities through specific cell surface receptors. The low affinity LIF receptor that shares the similarity of containing protein gp130 has now been identified to be a component of a high- affinity OSM receptor that will transduce OSM signals. OSM has also been shown to play a role in both pro and anti-inflammatory actions. OSM may also be involved in many biometabolism processes including liver development, haematopoeisis, inflammation, bone formation and destruction and possibly CNS development.
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TMPK-00077 | EPO/Erythropoietin Protein, Human, Recombinant | Human | HEK293 Cells | ||
Erythropoietin (EPO) is a circulating hormone conventionally considered to be responsible for erythropoiesis. In addition to facilitating red blood cell production, EPO has pluripotent potential, such as for cognition improvement, neurogenesis, and anti-fibrotic, anti-apoptotic, anti-oxidative, and anti-inflammatory effects.
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TMPK-00768 | ANXA1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Atherosclerosis, characterized by the formation of fat-laden plaques, is a chronic inflammatory disease. ABCA1 promotes cholesterol efflux, reduces cellular cholesterol accumulation, and regulates anti-inflammatory activities in an apoA-I- or ANXA1-dependent manner. The latter activity occurs by mediating the efflux of ANXA1, which plays a critical role in anti-inflammatory effects, cholesterol transport, exosome and microparticle secretion, and apoptotic cell clearance. ANXA1 Protein, Human, Recombinant (His) is expressed in E. coli expression system with C-His tag. The predicted molecular weight is 39.5 kDa and the accession number is P04083.
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TMPK-01291 | ANXA1 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | E. coli | ||
Atherosclerosis, characterized by the formation of fat-laden plaques, is a chronic inflammatory disease. ABCA1 promotes cholesterol efflux, reduces cellular cholesterol accumulation, and regulates anti-inflammatory activities in an apoA-I- or ANXA1-dependent manner. The latter activity occurs by mediating the efflux of ANXA1, which plays a critical role in anti-inflammatory effects, cholesterol transport, exosome and microparticle secretion, and apoptotic cell clearance. ANXA1 Protein, Cynomolgus, Recombinant (His) is expressed in E. coli expression system with C-His tag. The predicted molecular weight is 39.69 kDa and the accession number is A0A2K5W030.
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TMPK-00799 | ANXA1 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Atherosclerosis, characterized by the formation of fat-laden plaques, is a chronic inflammatory disease. ABCA1 promotes cholesterol efflux, reduces cellular cholesterol accumulation, and regulates anti-inflammatory activities in an apoA-I- or ANXA1-dependent manner. The latter activity occurs by mediating the efflux of ANXA1, which plays a critical role in anti-inflammatory effects, cholesterol transport, exosome and microparticle secretion, and apoptotic cell clearance. ANXA1 Protein, Mouse, Recombinant (His) is expressed in E. coli expression system with C-His tag. The predicted molecular weight is 39.6 kDa and the accession number is P10107.
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TMPY-00176 | FNDC4 Protein, Human, Recombinant (mFc) | Human | HEK293 Cells | ||
FNDC4 acts as an anti-inflammatory factor on macrophages and improves mouse model of induced colitis. FNDC4 could suppress osteoclast formation via NF-kappaB pathway and downregulation of CXCL10. Analysis of binding of FNDC4 to different immune cell types reveals strong and specific binding to macrophages and monocytes. FNDC4 treatment of bone marrow-derived macrophages in vitro results in reduced phagocytosis, increased cell survival and reduced proinflammatory chemokine expression. Hence, treatment with FNDC4 results in a state of dampened macrophage activity, while enhancing their survival. That FNDC4 may be a factor with direct therapeutic potential in inflammatory bowel disease and possibly other inflammatory diseases.
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TMPK-01230 | CLEC2D Protein, Human, Recombinant (hFc & Avi) | Human | HEK293 Cells | ||
C-type lectin domain family 2, member D (CLEC2D) is implicated in the immune response. Pre-eclampsia and HIV infection have opposing immune responses. The contrasting expression of CLEC2D in HIV infection and pre-eclampsia is demonstrative of the immunosuppressive and pro-inflammatory roles of the respective pathologies. However, this implication may be confounded by highly active anti-retroviral treatment (HAART).
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TMPY-02128 | Serpin B1 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
SerpinB1 is an endogenous inhibitor of serine proteases recognized for its anti-inflammatory and host-protective properties. Serum SerpinB1 levels are elevated in patients with type 2 diabetes compared with that in healthy subjects and are negatively correlated with serum LDL-C. serpinB1 as an endogenous protein that can potentially be harnessed to enhance functional beta cell mass in patients with diabetes.
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TMPK-00759 | IgG1 Fc Protein, Human, Recombinant | Human | HEK293 Cells | ||
IgG1 is most abundant in serum among the four IgG subclasses (IgG1, 2, 3 and 4) and binds to Fc receptors (FcγR) on phagocytic cells with high affinity. Fc fragment is demonstrated to mediate phagocytosis, trigger inflammation, and target Ig to particular tissues.IgG1 Fc was reported has a novel role as a potential anti-inflammatory drug for treatment of human autoimmune diseases.
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TMPY-00507 | UNC5B Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
The netrin-1 receptor, UNC-5 Homology B, or UNC5B plays vital roles in angiogenesis, inflammation, embryonic development and carcinogenesis. Overexpression of UNC5B human colon epithelial cells suppressed dextran sodium sulfate, or DSS-induced apoptosis and caspase-3 activity. Besides, is a potential anti-neoplastic target in bladder cancer progression and inflammatory arthritis. UNC5B Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 64.8 kDa and the accession number is Q8IZJ1-1.
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TMPY-04133 | UNC5B Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
The netrin-1 receptor, UNC-5 Homology B, or UNC5B plays vital roles in angiogenesis, inflammation, embryonic development and carcinogenesis. Overexpression of UNC5B human colon epithelial cells suppressed dextran sodium sulfate, or DSS-induced apoptosis and caspase-3 activity. Besides, is a potential anti-neoplastic target in bladder cancer progression and inflammatory arthritis. UNC5B Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 39.2 kDa and the accession number is Q8IZJ1-1.
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TMPY-04003 | UNC5B Protein, Rat, Recombinant (hFc) | Rat | HEK293 Cells | ||
The netrin-1 receptor, UNC-5 Homology B, or UNC5B plays vital roles in angiogenesis, inflammation, embryonic development and carcinogenesis. Overexpression of UNC5B human colon epithelial cells suppressed dextran sodium sulfate, or DSS-induced apoptosis and caspase-3 activity. Besides, is a potential anti-neoplastic target in bladder cancer progression and inflammatory arthritis. UNC5B Protein, Rat, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 65.7 kDa and the accession number is O08722.
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TMPK-01137 | FAM3D Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
The physiological homeostasis of gut mucosal barrier is maintained by both genetic and environmental factors and its impairment leads to pathogenesis such as inflammatory bowel disease. A cytokine like molecule, FAM3D (mouse Fam3D), is highly expressed in mouse gastrointestinal tract. Here, we demonstrate that deficiency in Fam3D is associated with impaired integrity of colonic mucosa, increased epithelial hyper-proliferation, reduced anti-microbial peptide production and increased sensitivity to chemically induced colitis associated with high incidence of cancer.
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TMPJ-01252 | CLEC2D Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
C-type lectin domain family 2, member D (CLEC2D) is implicated in the immune response. Sensing tissue damage is an ancient function of immune cells that is central to the regulation of inflammation, tissue repair, and immunity. The C-type lectin receptor Clec2d as a sensor of cell death, which directly detects histones released during necrosis and thus contributes to inflammation and immunopathology. The Clec2d pathway may also be exploited to favor a pro-inflammatory anti-tumor response. And tumor cells can show reduced global levels of histone modification, which may favor Clec2d sensing. The contrasting expression of CLEC2D in HIV infection and pre-eclampsia is demonstrative of the immunosuppressive and pro-inflammatory roles of the respective pathologies.
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TMPK-00057 | IL-10 Protein, Human, Recombinant (His & Avi), Biotinylated | Human | HEK293 Cells | ||
Interleukin 10 (IL10) is a key anti-inflammatory cytokine that can inhibit proinflammatory responses of both innate and adaptive immune cells. An association between IL10 and intestinal mucosal homeostasis became clear with the discovery that IL10 and IL10 receptor (IL10R)-deficient mice develop spontaneous intestinal inflammation. Similarly, patients with deleterious mutations in IL10, IL10RA, or IL10RB present with severe enterocolitis within the first months of life. IL-10 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with N-His-Avi tag. The predicted molecular weight is 21.3 kDa and the accession number is P22301.
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TMPK-00056 | IL-10 Protein, Human, Recombinant (His & Avi) | Human | HEK293 Cells | ||
Interleukin 10 (IL10) is a key anti-inflammatory cytokine that can inhibit proinflammatory responses of both innate and adaptive immune cells. An association between IL10 and intestinal mucosal homeostasis became clear with the discovery that IL10 and IL10 receptor (IL10R)-deficient mice develop spontaneous intestinal inflammation. Similarly, patients with deleterious mutations in IL10, IL10RA, or IL10RB present with severe enterocolitis within the first months of life. IL-10 Protein, Human, Recombinant (His & Avi) is expressed in HEK293 mammalian cells with N-His-Avi tag. The predicted molecular weight is 21.3 kDa and the accession number is P22301.
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TMPH-00672 | Metalloprotease stcE Protein, E. coli O157:H7, Recombinant (His) | E. coli | E. coli | ||
Virulence factor that contributes to intimate adherence of enterohemorrhagic E.coli (EHEC) O157:H7 to host cells. Is able to cleave the secreted human mucin 7 (MUC7) and the glycoprotein 340 (DMBT1/GP340). Also cleaves human C1 inhibitor (SERPING1), a regulator of multiple inflammatory pathways, and binds and localizes it to bacterial and host cell surfaces, protecting them from complement-mediated lysis. Therefore, the current model proposes two roles for StcE during infection: it acts first as a mucinase, allowing passage of EHEC through the oral cavity by cleaving the salivary glycoproteins that are responsible for bacterial aggregation. Similarly, in the colon, StcE cleaves the glycoproteins that protect the intestinal epithelial surface, allowing EHEC to come into close contact with host cell membranes. Secondly, it acts as an anti-inflammatory agent by localizing SERPING1 to cell membranes.
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TMPJ-00766 | ANXA1 Protein, Human, Recombinant | Human | E. coli | ||
Annexin A1 is the first characterized member of the annexin family of proteins and is able to bind to cellular membranes in a calcium-dependent manner, promoting membrane fusion and endocytosis. Annexin A1 has anti-inflammatory properties and inhibits phospholipase A2 activity. Annexin A1 also has roles in many diverse cellular functions, such as membrane aggregation, inflammation, phagocytosis, proliferation, apoptosis, and tumorigenesis and cancer development. ANXA1 is strongly expressed on the cell membrane and occasionally in the cytoplasm of tumor cells in 97% of samples from patients with hairy cell leukemia.
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TMPJ-00931 | Serpin A4 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Serpin Peptidase Inhibitor, Clade A (α-1 Antiproteinase, Antitrypsin), Member 4 (Serpin A4) is a member of the Serpin family. Serpin A4 exists as a monomer and some homodimers. Serpin A4 is expressed by the liver and secreted in plasma. Serpin A4 is a regulator of vascular homeostasis capable of controlling a wide spectrum of biological actions in the cardiovascular and renal systems. It can inhibit intracellular reactive oxygen species formation in cultured cardiac and renal cells. In addition, Serpin A4 has anti-inflammatory effect. Heparin blocks kallistatin's complex formation with tissue kallikrein and abolishes its inhibitory effect on tissue kallikrein's activity.
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TMPK-00650 | HLA-A*02:01 & B2M & MART-1 (ELAGIGILTV) Monomer Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 Cells | ||
Interleukin 10 (IL10) is a key anti-inflammatory cytokine that can inhibit proinflammatory responses of both innate and adaptive immune cells. An association between IL10 and intestinal mucosal homeostasis became clear with the discovery that IL10 and IL10 receptor (IL10R)-deficient mice develop spontaneous intestinal inflammation. Similarly, patients with deleterious mutations in IL10, IL10RA, or IL10RB present with severe enterocolitis within the first months of life. HLA-A*02:01 & B2M & MART-1 (ELAGIGILTV) Monomer Protein, Cynomolgus, Recombinant (His) is expressed in HEK293 mammalian cells with N-His tag. The predicted molecular weight is 19.78 kDa and the accession number is G7NVB0.
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TMPH-01702 | SMAD6 Protein, Human, Recombinant (E. coli, His & Myc) | Human | E. coli | ||
Transforming growth factor-beta superfamily receptors signaling occurs through the Smad family of intracellular mediators. SMAD6 is an inhibitory Smad (i-Smad) that negatively regulates signaling downstream of type I transforming growth factor-beta. Acts as a mediator of TGF-beta and BMP anti-inflammatory activities. Suppresses IL1R-TLR signaling through its direct interaction with PEL1, preventing NF-kappa-B activation, nuclear transport and NF-kappa-B-mediated expression of proinflammatory genes. Blocks the BMP-SMAD1 signaling pathway by competing with SMAD4 for receptor-activated SMAD1-binding. Binds to regulatory elements in target promoter regions.
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TMPJ-01424 | IL-10R alpha/IL-10RA Protein, Macaca mulatta, Recombinant (His) | Macaca Mulatta | HEK293 Cells | ||
Interleukin-10 Receptor alpha (IL-10 R alpha), also known as IL-10 R1, is transmembrane glycoprotein member of the class II cytokine receptor family. Interleukin-10 (IL10) is a key anti-inflammatory cytokine that is produced predominantly by leukocytes including T cells, B cells, monocytes, macrophages, and dendritic cells (DCs), as well as by some epithelial cells. The receptor for IL10 is a heterotetramer complex comprising two IL10Ra (also referred to as IL10R1) molecules and two IL10Rb (also referred to as IL10R2) molecules.IL10Ra is expressed on most hematopoietic cells at a basal level but is upregulated by various cells upon activation, suggesting its importance in inhibitory pathways.
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TMPY-01909 | Elafin Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Elafin, also known as Elastase-specific inhibitor, Peptidase inhibitor 3, Protease inhibitor WAP3, Skin-derived antileukoproteinase, WAP four-disulfide core domain protein 14, PI3, WAP3 and WFDC14, is a secreted protein that contains one WAP domain. Elafin / PI3 consists of two domains: the transglutaminase substrate domain (cementoin moiety) and the elastase inhibitor domain. The transglutaminase substrate domain at the N-terminus serves as an anchor to localize elafin covalently to specific sites on extracellular matrix proteins. The serine anti-protease Elafin / PI3 is expressed by monocytes, alveolar macrophages, neutrophils, and at mucosal surfaces and possesses antimicrobial activity. It is also known to reduce lipopolysaccharide-induced neutrophil influx into murine alveoli as well as to abrogate lipopolysaccharide-induced production of matrix metalloprotease 9, macrophage inhibitory protein 2, and tumor necrosis factor-alpha by as-yet unidentified mechanisms. Elafin / PI3 is a neutrophil serine protease inhibitor expressed in lung and displaying anti-inflammatory and anti-bacterial properties. Elafin / PI3 is a neutrophil and pancreatic elastase-specific inhibitor of skin. It may prevent elastase-mediated tissue proteolysis. Elafin / PI3 will regulate proteolytic enzymes during menstruation and will contribute to the innate defense against uterine infection.
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TMPY-04984 | CXCL17 Protein, Human, Recombinant (His) | Human | P. pastoris (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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TMPY-02891 | PSG6 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
PSG6 is a pregnancy-specific glycoprotein(PSG). PSGs are secreted proteins produced by the rodent and primate placenta and play a critical role in pregnancy success. The levels of PSGs are highest during the third trimester of pregnancy, a time marked by the most profound suppression of MS disease attacks. PSGs regulate T-cell function. The regulation of T-cell function during pregnancy is likely the result of significant hormonal changes and may well involve immunoregulatory proteins derived from the placenta. Pregnancy specific glycoproteins (PSGs) are the most abundant placentally derived glycoproteins in the maternal serum. PSG1, PSG6, PSG6N, and PSG11 induce dose-dependent secretion of anti-inflammatory cytokines by human monocytes. Human and murine PSGs exhibit cross-species activity.
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TMPH-01676 | Meteorin-like/METRNL Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Hormone induced following exercise or cold exposure that promotes energy expenditure. Induced either in the skeletal muscle after exercise or in adipose tissue following cold exposure and is present in the circulation. Able to stimulate energy expenditure associated with the browning of the white fat depots and improves glucose tolerance. Does not promote an increase in a thermogenic gene program via direct action on adipocytes, but acts by stimulating several immune cell subtypes to enter the adipose tissue and activate their prothermogenic actions. Stimulates an eosinophil-dependent increase in IL4 expression and promotes alternative activation of adipose tissue macrophages, which are required for the increased expression of the thermogenic and anti-inflammatory gene programs in fat. Required for some cold-induced thermogenic responses, suggesting a role in metabolic adaptations to cold temperatures.
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TMPY-00410 | EPHX2 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Genetic variation in EPHX2 was significantly associated with risk of incident CHD in Caucasians, implicating EPHX2 as a potential cardiovascular disease-susceptibility gene. Single nucleotide polymorphisms (SNPs) in the human EPHX2 gene had been implicated in susceptibility to cardiovascular disease, including stroke. The human EPHX2 mutations may in part explain the genetic variability in sensitivity to ischemic brain injury and stroke outcome. Epoxide hydrolase is involved in metabolism of vasoactive and anti-inflammatory epoxyeicosatrienoic acids to their corresponding diols. Consequently, epoxide hydrolase 2 (EPHX2) is a candidate cardiovascular disease (CVD) gene. Genetic variation in EPHX2 is associated with forearm vasodilator responses in a bradykinin receptor- and endothelium-independent manner, suggesting an important role for soluble epoxide hydrolase in the regulation of vascular function in humans. EPHX2 variants may mediate EETs levels, and low levels of EETs may be a predictor for END in acute MIS.
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TMPY-06836 | NR3C1 Protein, Human, Recombinant (His) | Human | E. coli | ||
NR3C1 (Nuclear Receptor Subfamily 3 Group C Member 1) is a Protein Coding gene. This gene encodes glucocorticoid receptor, which can function both as a transcription factor that binds to glucocorticoid response elements in the promoters of glucocorticoid responsive genes to activate their transcription, and as a regulator of other transcription factors. NR3C1 is a transcriptional regulator of many drug-metabolizing enzymes and anti-inflammatory molecules. NR3C1 polymorphisms associate with obesity, muscle strength, and cortisol sensitivity. Glucocorticoid receptor gene polymorphism (NR3C1 646 C>G) may play an important role in the development of severe bronchial asthma and resistance to glucocorticoids (GCs). Disturbances in the structure and function of the glucocorticoid receptor (GR) alter the glucocorticoid regulation of the corticotropin-releasing hormone, which leads to nonspecific activation of numerous receptors in the brain and alters the metabolism.
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TMPY-02597 | IL-37 Protein, Human, Recombinant | Human | E. coli | ||
Interleukin 1 family member 7, or interleukin 37 (IL1F7 / IL37 / IL-1H4) is a secretory protein belonging to the Interleukin 1 family. IL-1F7 was localized in human peripheral monocytic cells. It has been localized the expression of IL-1F7b protein in discrete cell populations including plasma cells and tumor cells. These data suggest that IL-1F7 may be involved in immune response, inflammatory diseases, and/or cancer. Through constructing an adenoviral vector that allows high-level expression in murine and human cells, it has been demonstrated that the ability of adenovirus-mediated gene transfer of IL1F7 to induce an IL-12- and Fas ligand-dependent anti-tumor response. Complete inhibition of tumor growth was observed following multiple injections of IL1F7 in most animals. These results suggest that IL1F7 could play a role in both innate and adaptive immune responses, similar to IL-18. Moreover, IL1F7 could be useful for cancer gene therapy.
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TMPY-00186 | GHRH Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
The role of hypothalamic growth hormone-releasing hormone (GHRH) in the release of growth hormone (GH) from the pituitary is well established. Extra-hypothalamic growth hormone-releasing hormone (GHRH) plays an important role in infertility. Growth hormone releasing hormone (GHRH) has recently been shown to increase the level of gamma-aminobutyric acid (GABA) and activate GABA receptors (GABARs) in the cerebral cortex. GABA is an inhibitory neurotransmitter that can inhibit seizures. GHRH may play an important role in inhibiting seizures by activating GABAARs. GHRH is produced by tumor cells, acts in an autocrine/paracrine manner, and requires the presence of GHRH receptor (GHRH-R) on the tumor cells to exert its effects. GHRH activity can be effectively blocked by synthetic antagonists of its receptor and hence, the expression of GHRH-R by tumor cells could serve as a predictor of response to GHRH-R antagonist therapy. The neurovascular protective effect of GHRH analogs during the early stage of diabetic retinopathy through their antioxidant and anti-inflammatory properties. GHRH antagonists can be a therapeutic option for thyroid cancer patients.
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TMPY-05252 | Myeloperoxidase/MPO Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. Myeloperoxidase (MPO) is an important enzyme, which is one of the components of the antibacterial system in neutrophils and monocytes. MPO participates in the inflammatory response in multiple locations in the body, including the mammary glands. Myeloperoxidase (MPO), a specific polymorphonuclear leukocyte enzyme, has been used previously to quantify the number of neutrophils in tissue. MPO activity was found to be linearly related to the number of neutrophil cells. The MPO system plays an important role in the control of infections and the deletion of malignant cells. Nevertheless, alternations in the MPO system can lead to DNA damage and carcinogenesis. Polymorphisms in the MPO gene have been associated with an increased expression of MPO and a higher risk for the development of cancer. Myeloperoxidase (MPO) is one of the major target antigens of antineutrophil cytoplasmic autoantibodies (ANCA) found in patients with small-vessel vasculitis and Pauci-immune necrotizing glomerulonephritis. Myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA) is an autoantibody that is frequently found in patients with vasculitides.
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TMPJ-00751 | IgG4 hFc Protein, Human, Recombinant (aa 99-326) | Human | HEK293 Cells | ||
As a monomeric immunoglobulin that is predominately involved in the secondary antibody response and the only isotype that can pass through the human placenta, Immunoglobulin G (IgG) is synthesized and secreted by plasma B cells, and constitutes 75% of serum immunoglobulins in humans. IgG antibodies protect the body against the pathogens by agglutination and immobilization, complement activation, toxin neutralization, as well as the antibody-dependent cell-mediated cytotoxicity (ADCC). IgG tetramer contains two heavy chains (50 kDa ) and two light chains (25 kDa) linked by disulfide bonds, that is the two identical halves form the Y-like shape. IgG is digested by pepsin proteolysis into Fab fragment (antigen-binding fragment) and Fc fragment ("crystallizable" fragment). IgG1 is most abundant in serum among the four IgG subclasses (IgG1, 2, 3 and 4) and binds to Fc receptors (FcγR ) on phagocytic cells with high affinity. Fc fragment is demonstrated to mediate phagocytosis, trigger inflammation, and target Ig to particular tissues. Protein G or Protein A on the surface of certain Staphylococcal and Streptococcal strains specifically binds with the Fc region of IgGs, and has numerous applications in biotechnology as a reagent for affinity purification. Recombinant IgG Fc Region is suggested to represent a potential anti-inflammatory drug for treatment of human autoimmune diseases.
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TMPY-04550 | JNK2 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of the MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating some transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggests that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance the anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally, the JNK2 protein could be a novel therapeutic target in dry eye disease and may provide a novel target for the prevention of vascular disease and atherosclerosis.
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TMPH-03753 | MYLK Protein, Human, Recombinant (His) | Human | E. coli | ||
Calcium/calmodulin-dependent myosin light chain kinase implicated in smooth muscle contraction via phosphorylation of myosin light chains (MLC). Also regulates actin-myosin interaction through a non-kinase activity. Phosphorylates PTK2B/PYK2 and myosin light-chains. Involved in the inflammatory response (e.g. apoptosis, vascular permeability, leukocyte diapedesis), cell motility and morphology, airway hyperreactivity and other activities relevant to asthma. Required for tonic airway smooth muscle contraction that is necessary for physiological and asthmatic airway resistance. Necessary for gastrointestinal motility. Implicated in the regulation of endothelial as well as vascular permeability, probably via the regulation of cytoskeletal rearrangements. In the nervous system it has been shown to control the growth initiation of astrocytic processes in culture and to participate in transmitter release at synapses formed between cultured sympathetic ganglion cells. Critical participant in signaling sequences that result in fibroblast apoptosis. Plays a role in the regulation of epithelial cell survival. Required for epithelial wound healing, especially during actomyosin ring contraction during purse-string wound closure. Mediates RhoA-dependent membrane blebbing. Triggers TRPC5 channel activity in a calcium-dependent signaling, by inducing its subcellular localization at the plasma membrane. Promotes cell migration (including tumor cells) and tumor metastasis. PTK2B/PYK2 activation by phosphorylation mediates ITGB2 activation and is thus essential to trigger neutrophil transmigration during acute lung injury (ALI). May regulate optic nerve head astrocyte migration. Probably involved in mitotic cytoskeletal regulation. Regulates tight junction probably by modulating ZO-1 exchange in the perijunctional actomyosin ring. Mediates burn-induced microvascular barrier injury; triggers endothelial contraction in the development of microvascular hyperpermeability by phosphorylating MLC. Essential for intestinal barrier dysfunction. Mediates Giardia spp.-mediated reduced epithelial barrier function during giardiasis intestinal infection via reorganization of cytoskeletal F-actin and tight junctional ZO-1. Necessary for hypotonicity-induced Ca(2+) entry and subsequent activation of volume-sensitive organic osmolyte/anion channels (VSOAC) in cervical cancer cells. Responsible for high proliferative ability of breast cancer cells through anti-apoptosis.
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TMPH-01503 | Humanin Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST/GP130, IL27RA/WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2/FPRL1 and FPR3/FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6/APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2/FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A/PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.
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TMPH-01502 | Humanin Protein, Human, Recombinant (GST) | Human | E. coli | ||
Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST/GP130, IL27RA/WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2/FPRL1 and FPR3/FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6/APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2/FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A/PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.
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