目录号 | 产品详情 | 靶点 | |
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TN3539 | ERK IL Receptor IκB/IKK NOS NF-κB Akt | ||
Broussonins A and B, new phytoalexins from diseased paper mulberry. Broussonin A shows estrogenic activity with ligand-binding activity of estrogen receptor, transcriptional activity of estrogen-responsive element-luciferase reporter genes. Broussonin A c | |||
TN3806 | ERK IκB/IKK p38 MAPK TNF NF-κB Akt COX PI3K NADPH DNA/RNA Synthesis Nrf2 JNK Autophagy | ||
Dehydroglyasperin C is a potent NAD(P)H:oxidoquinone reductase (NQO1) and phase 2 enzyme inducer. Dehydroglyasperin C possesses potent antioxidant, cancer chemopreventive, and neuroprotective activities, it has protective effects against chronic diseases | |||
T80653 | Akt | ||
Larixol作为一种fMLP抑制剂,在免疫调节作用上,能够抑制Src激酶、ERK1/2、p38以及AKT的磷酸化信号。它能够通过干扰fMLP受体Gi蛋白的βγ亚基与下游分子之间的作用,抑制fMLP引发的呼吸爆发。此外,Larixol可有效降低由fMLP (0.1 μM) 诱导的超氧阴离子生成(IC50: 1.98 μM)、组织蛋白酶G的释放(IC50: 2.76 μM)及趋化反应,有助于缓解中性粒细胞的过度激活,减少炎症或组织损伤。Larixol衍生物对FSGS相关TRPC6功能突变有显著的抑制效果。 | |||
T36015 | |||
PDMP is a ceramide analog first prepared in a search for inhibitors of glucosylceramide synthase. PDMP has two adjacent chiral centers (C1 and C2) allowing for the formation of four possible isomers. PDMP contains all four of these stereoisomers. PDMP inhibits glucosylceramide synthase by 90% when used at a concentration of 0.8 μM in MDCK cell homogenates, however, the ability to inhibit glucosylceramide synthase has been found to reside in the D-threo (1R,2R) enantiomer. The D-threo PDMP enantiomer is also responsible for inhibition of β-1,4-galactosyltransferase 6 and prevention of lactosylceramide synthesis, which is a promotor of neuroinflammation in mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. PDMP enhances curcumin-induced inhibition of proliferation, JNK activation, and Akt inhibition, as well as induction of apoptosis in WM-115 melanoma cells in vitro. | |||
T83877 | |||
2-(cyclohexylmethyl)-Plumbagin是naphthoquinone plumbagin的衍生物。在模拟胰腺癌肿瘤微环境的营养匮乏条件下,与营养丰富条件下的PANC-1细胞相比,对PANC-1人类胰腺癌细胞表现出选择性的细胞毒性,50%优选细胞毒性值(PC50s)分别为0.11和47.2 µM。1 µM浓度下,还可诱导PANC-1细胞发生凋亡。此外,2-(cyclohexylmethyl)-Plumbagin在营养匮乏条件下,而非营养丰富条件下,选择性降低PANC-1细胞中Akt和哺乳动物雷帕霉素靶蛋白(mTOR)的磷酸化。在以每周五次、每次50和250 µg/动物剂量给药的MiaPaCa-2胰腺癌小鼠异种移植模型中,能减少肿瘤体积和重量。 | |||
T36085 | |||
PKI-179 is an orally bioavailable dual inhibitor of PI3K and mammalian target of rapamycin (mTOR). In an in vitro enzymatic assay, it potently inhibits PI3K (IC50s = 8, 24, 17, and 74 nM for isoforms α, β, δ, and γ, respectively), two common PI3Kα mutants, E545K and H1047R (IC50s = 14 and 11 nM, respectively), and mTOR (IC50 = 0.42 nM). PKI-179 is selective for PI3K and mTOR over a panel of 361 other kinases at IC50 values up to 50 μM, hERG (IC50 > 30 μM), and cytochrome P450 (CYP) isoforms (IC50s > 30 μM), but does have activity for CYP2C8 (IC50 = 3 μM). It inhibits proliferation through the Akt/mTOR signaling pathway in MDA-361 breast and PC3MM2 prostate cancer cell lines in vitro (IC50s = 22 and 29 nM, respectively) and inhibits tumor growth in an MDA-361 mouse xenograft model when used at a dose of 50 mg/kg. | |||
T28157 | |||
Nephrin is a cell surface signaling receptor protein that regulates podocyte function and plays a role in β-cell survival signaling; it is a protein necessary for the proper functioning of the renal filtration barrier. Nephrin belongs to a family of highl | |||
T35897 | |||
ASK120067 is a potent and orally active inhibitor of EGFRT790M (IC50:0.3 nM) with selectivity over EGFRWT (IC50:6.0 nM). ASK120067 is a third-generation EGFR-TKI for the research of non-small cell lung cancer (NSCLC)[1]. In the in vitro kinase assay ASK120067 potently inhibits the EGFR L858R/T790M and EGFR T790M resistant mutants with IC50 values of 0.3 nM and 0.5 nM, respectively, as well as the EGFRexon19del sensitizing mutant (IC50= 0.5 nM). The 50 of ASK120067 against wild-type EGFR (EGFRWT) is 6 nM[1].ASK120067 selectively inhibits the growth of EGFR-mutant cell lines and exhibits potent antiproliferative activity in the mutant EGFR NSCLC cells, with IC50 values of 12 nM, 6 nM and 2 nM against NCI-H1975 (T790M mutation), PC-9, and HCC827 cells (sensitizing mutations), respectively. However, it shows moderate or weak anti-growth activities in A431, LoVo and A549 cells (EGFRWT), with IC50 values ranging from 338 nM to 1541 nM[1].ASK120067 (0.1-100 nM) inhibits the phosphorylation of EGFR at Tyrosine residue 1068 and its downstream signaling proteins AKT and ERK in NCI-H1975 cells (EGFRL858R/T790M) even at low dosage (0.1-1 nM). Additionally, ASK120067 inhibits p-EGFR and p-Akt and p-erk in EGFR WT A431 cell until the concentration reaches 10 to 100 nM[1]. ASK120067 (oral gavage; 5-20 mg/kg; once daily; 21 days) results in significantly regressed tumor growth, with a tumor growth inhibition (TGI) rate of 85.7%, and administration of 10 mg/kg ASK120067 causes dramatic tumor shrinkage with a TGI rate of 99.3%, exhibiting a similar potency with Osimertinib[1]. [1]. Tao Zhang, et al. Discovery of a novel third-generation EGFR inhibitor and identification of a potential combination strategy to overcome resistance. Mol Cancer. 2020 May 13;19(1):90. | |||
T35806 | Phosphatase | ||
N-Stearoylsphingosine (Cer(d18:1/18:0)) 是一种广泛存在真核生物体内的酰胺类化合物,通过干扰PP2A与PP2A抑制剂2的结合来增强蛋白质磷酸酶2A(PP2A)活性,导致Akt去磷酸化。N-Stearoylsphingosine 可用于研究前列腺癌。 | |||
T79311 | |||
CNBCA是一种有效的SHP2酶抑制剂,具有选择性和竞争性,IC50值为0.87 μM。该化合物可结合SHP2全长蛋白并抑制其酶活性,进而阻止Akt和ERK1/2的磷酸化,以及抑制BT474和MDA-MB468乳腺癌细胞的生长。CNBCA主要用于乳腺癌的研究。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04552 | AKT1 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
v-akt murine thymoma viral oncogene homolog 1 (AKT1), or protein kinase B-alpha (PKB-ALPHA) is a serine-threonine protein kinase, belonging to the Protein Kinase Superfamily. AKT1 is a major mediator of the responses to insulin, insulin-like growth factor 1 (IGF1), and glucose. AKT1 also plays a key role in the regulation of both muscle cell hypertrophy and atrophy. AKT1 activity is required for physiologic cardiac growth in response to IGF1 stimulation or exercise training. In contrast, AKT1 activity was found to antagonize pathologic cardiac growth that occurs in response to endothelin 1 stimulation or pressure overload. AKT1 selectively promotes physiological cardiac growth while AKT2 selectively promotes insulin-stimulated cardiac glucose metabolism. AKT1 deletion prevented tumor initiation as well as tumor progression, coincident with decreased Akt signaling in tumor tissues. AKT1 is the primary Akt isoform activated by mutant K-ras in lung tumors, and that AKT3 may oppose AKT1 in lung tumorigenesis and lung tumor progression. A number of separate studies have implicated AKT1 as an inhibitor of breast epithelial cell motility and invasion. AKT1 may have a dual role in tumorigenesis, acting not only pro-oncogenically by suppressing apoptosis but also anti-oncogenically by suppressing invasion and metastasis.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-04387 | AKT2 Protein, Human, Recombinant (His & GST) | Human | Baculovirus Insect Cells | ||
AKT (AK mouse plus Transforming or Thymoma) is a frequent oncogene expressed in most tissues which includes three isoforms AKT1, AKT2, and AKT3. Hyperactivation of AKT signaling is a central key in many human cancer progressions, through modulating angiogenesis, tumor growth, and cell migration, invasion, metastasis, and chemoresistance. Among all three isoforms, AKT2 is most related to cancer cell invasion, metastasis, and survival. Amplification and overexpression of AKT2 have been shown in many cancers. Accumulating evidence shows the potential role of different miRNA involvements in cancer progression by activating or suppressing AKT2 expression. The AKT2/NAB1/SPK1 pathway is a novel regulating factor of macrophage migration and cardiac remodeling after myocardial infarction. The novel mechanism of the AKT2-PKM2-STAT3/NF-kappaB axis in the regulation of ovarian cancer progression, that both AKT2 and PKM2 may be potential targets for the treatment of ovarian cancer. AKT1 and AKT2, the AKT isoforms that are highly expressed in skeletal muscle, have distinct and overlapping functions, with AKT2 more important for insulin-stimulated glucose metabolism. In adipocytes, AKT2 versus AKT1 has greater susceptibility for insulin-mediated redistribution from cytosolic to membrane localization, and insulin also causes subcellular redistribution of AKT Substrate of 160 kDa (AS160), an AKT2 substrate and crucial mediator of insulin-stimulated glucose transport.
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TMPY-04446 | AKT3 Protein, Mouse, Recombinant (aa 106-479) | Mouse | Baculovirus Insect Cells | ||
AKT3 Protein, Mouse, Recombinant (aa 106-479) is expressed in Baculovirus insect cells. The predicted molecular weight is 43.4 kDa and the accession number is Q9WUA6-1.
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TMPY-04574 | AKT3 Protein, Mouse, Recombinant (aa 106-479, His & GST) | Mouse | Baculovirus Insect Cells | ||
AKT3 Protein, Mouse, Recombinant (aa 106-479, His & GST) is expressed in Baculovirus insect cells with His and GST tag. The predicted molecular weight is 71 kDa and the accession number is Q9WUA6-1.
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TMPY-04553 | AKT3 Protein, Human, Recombinant (GST) | Human | Baculovirus Insect Cells | ||
AKT3 Protein, Human, Recombinant (GST) is expressed in Baculovirus insect cells with GST tag. The predicted molecular weight is 81 kDa and the accession number is Q9Y243-1.
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TMPK-00474 | IL-22RA1 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 Cells | ||
IL-22 receptor, also known as IL-22 R alpha 1 and CRF2-9, is an approximately 65 kDa transmembrane glycoprotein in the type II cytokine receptor family (CRF).Component of the receptor for IL20, IL22 and IL24. Component of IL22 receptor formed by IL22RA1 and IL10RB enabling IL22 signaling via JAK/STAT pathways. IL22 also induces activation of MAPK1/MAPK3 and Akt kinases pathways. Component of one of the receptor for IL20 and IL24 formed by IL22RA1 and IL20RB also signaling through STATs activation. Mediates IL24 antiangiogenic activity as well as IL24 inhibitory effect on endothelial cell tube formation and differentiation.
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TMPJ-00059 | IL-7 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Human Interleukin 7 (IL-7) is a potent lymphoid cell growth factor stimulating the proliferation of lymphoid progenitors. IL7 can associate with the hepatocyte growth factor (HGF) to form a hybrid cytokine that functions as a pre-pro-B cell growth-stimulating factor. Human IL7 cDNA encodes a 177 amino acid precursor protein containing a 25 amino acid signal peptide and a 152 amino acid mature protein. Human and mouse IL7 share 65% sequence identity in the mature region and both exhibit cross-species activity. IL-7 signals via IL-7 receptor (IL7R) activating multiple pathways including JaK/STAT and PI3K/AKT, which regulate lymphocyte survival, glucose uptake, proliferation, and differentiation. IL-7 is also associated with cytoplasmic IL2-R gamma for signal transduction.
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TMPY-02518 | TCL1A Protein, Human, Recombinant (His) | Human | E. coli | ||
T-cell leukemia/lymphoma protein 1A (abbreviated for TCL1A) is a member of the TCL1 family. TCL1 protooncogene is expressed in CD3-CD4-CD8-precursor T cells and is extinguished at the CD4+CD8+stage of thymocyte development. In B cells, TCL1 is first expressed in pro-B cells and remains high in naive mantle zone B cells of peripheral lymphoid tissues. The TCL1 protooncogene is overexpressed in many mature B cell lymphomas, especially from AIDS patients. It has been demonstrated that TCL1 is a powerful oncogene that, when overexpressed in both B and T cells, predominantly yields mature B cell lymphomas. All TCL1 isoforms bind to the Akt pleckstrin homology domain. Both in vitro and in vivo TCL1 increases Akt kinase activity and as a consequence enhances substrate phosphorylation. In vivo, TCL1 stabilizes the mitochondrial transmembrane potential and enhances cell proliferation and survival. It has been shown that TCL1 is a novel Akt kinase coactivator, which promotes Akt-induced cell survival and proliferation.
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TMPH-01348 | FSHR Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
G protein-coupled receptor for follitropin, the follicle-stimulating hormone. Through cAMP production activates the downstream PI3K-AKT and ERK1/ERK2 signaling pathways. FSHR Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with N-6xHis tag. The predicted molecular weight is 43.5 kDa and the accession number is P23945.
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TMPH-01347 | FSHR Protein, Human, Recombinant (E. coli, His) | Human | E. coli | ||
G protein-coupled receptor for follitropin, the follicle-stimulating hormone. Through cAMP production activates the downstream PI3K-AKT and ERK1/ERK2 signaling pathways. FSHR Protein, Human, Recombinant (E. coli, His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 44.0 kDa and the accession number is P23945.
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TMPK-01263 | B7-H7 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 Cells | ||
B7-H7, also known as HHLA2 (HERV-H LTR-associating 2), is a member of the B7 family of immune regulatory proteins.Through interaction with TMIGD2, costimulates T-cells in the context of TCR-mediated activation. Enhances T-cell proliferation and cytokine production via an AKT-dependent signaling cascade.
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TMPH-03365 | REG3A Protein, Rat, Recombinant (E.coli, His) | Rat | E. coli | ||
Bactericidal C-type lectin. Regulates keratinocyte proliferation and differentiation after skin injury via activation of EXTL3-PI3K-AKT signaling pathway. REG3A Protein, Rat, Recombinant (E.coli, His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 20.5 kDa and the accession number is P35231.
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TMPK-00136 | ULBP-2 Protein, Human, Recombinant (His & Avi) | Human | HEK293 Cells | ||
ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway, mediating natural killer cell cytotoxicity.
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TMPH-02019 | REG3A Protein, Human, Recombinant (GST) | Human | E. coli | ||
Bactericidal C-type lectin which acts exclusively against Gram-positive bacteria and mediates bacterial killing by binding to surface-exposed carbohydrate moieties of peptidoglycan. Regulates keratinocyte proliferation and differentiation after skin injury via activation of EXTL3-PI3K-AKT signaling pathway. REG3A Protein, Human, Recombinant (GST) is expressed in E. coli expression system with N-GST tag. The predicted molecular weight is 43.6 kDa and the accession number is Q06141.
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TMPK-00723 | RANK/TNFRSF11A Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 Cells | ||
TNFRSF11A, also known as receptor activator of NF-κB (RANK), activates several signaling pathways, such as NF-κB, JNK, ERK, p38α, and Akt/PKB. RANK/TNFRSF11A is a novel and frequent target for de novo methylation in gliomas, which affects apoptotic activity and focus formation thereby contributing to the molecular pathogenesis of gliomas. RANK/TNFRSF11A Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 47.0 kDa and the accession number is O35305.
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TMPH-01231 | DIP2A Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Catalyzes the de novo synthesis of acetyl-CoA in vitro. Promotes acetylation of CTTN, possibly by providing the acetyl donor, ensuring correct dendritic spine morphology and synaptic transmission. Binds to follistatin-related protein FSTL1 and may act as a cell surface receptor for FSTL1, contributing to AKT activation and subsequent FSTL1-induced survival and function of endothelial cells and cardiac myocytes.
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TMPH-01230 | DIP2A Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Catalyzes the de novo synthesis of acetyl-CoA in vitro. Promotes acetylation of CTTN, possibly by providing the acetyl donor, ensuring correct dendritic spine morphology and synaptic transmission. Binds to follistatin-related protein FSTL1 and may act as a cell surface receptor for FSTL1, contributing to AKT activation and subsequent FSTL1-induced survival and function of endothelial cells and cardiac myocytes.
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TMPH-02842 | CD133/PROM1 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
May play a role in cell differentiation, proliferation and apoptosis. Binds cholesterol in cholesterol-containing plasma membrane microdomains and may play a role in the organization of the apical plasma membrane in epithelial cells. During early retinal development acts as a key regulator of disk morphogenesis. Involved in regulation of MAPK and Akt signaling pathways. In neuroblastoma cells suppresses cell differentiation such as neurite outgrowth in a RET-dependent manner.
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TMPK-00732 | WISP1/CCN4 Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
The interplay between glioma stem cells (GSCs) and the tumor microenvironment plays crucial roles in promoting malignant growth of glioblastoma (GBM), the most lethal brain tumor. WISP1 is preferentially expressed and secreted by GSCs. Silencing WISP1 markedly disrupts GSC maintenance, reduces tumor-supportive TAMs (M2), and potently inhibits GBM growth. WISP1 signals through Integrin α6β1-Akt to maintain GSCs by an autocrine mechanism and M2 TAMs through a paracrine manner.
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TMPH-01559 | IL-26 Protein, Human, Recombinant (His) | Human | P. pastoris (Yeast) | ||
May play a role in local mechanisms of mucosal immunity and seems to have a proinflammatory function. May play a role in inflammatory bowel disease. Activates STAT1 and STAT3, MAPK1/3 (ERK1/2), JUN and AKT. Induces expression of SOCS3, TNF-alpha and IL-8, secretion of IL-8 and IL-10 and surface expression of ICAM1. Decreases proliferation of intestinal epithelial cells. Is inhibited by heparin. IL-26 Protein, Human, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 19.6 kDa and the accession number is Q9NPH9.
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TMPK-00925 | Noggin/NOG Protein, Mouse, Recombinant | Mouse | HEK293 Cells | ||
Noggin is an antagonist of bone morphogenetic proteins (BMP), being indispensable for certain developmental events.Noggin expression positively correlated with EGFR expression in both GC cell line models and The Cancer Genome Atlas human GC cohort. Targeting EGFR and its downstream pathways diminished cell proliferation which was promoted by Noggin. Noggin promotes the proliferation of GC cells by upregulating EGFR and enhancing a vicious circle formed by β‑catenin, EGFR, ERK and Akt. Noggin/NOG Protein, Mouse, Recombinant is expressed in HEK293 mammalian cells. The predicted molecular weight is 23.07 kDa and the accession number is P97466.
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TMPK-01034 | SEMA4B Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Semaphorin 4B (SEMA4B) inhibits the invasion of non-small cell lung cancer (NSCLC) through PI3K-dependent suppression of MMP9 activation. SEMA4B may induce FoxO1 nuclear retention through suppressing PI3K/Akt signaling pathway, which subsequently inhibited cell growth through the direct nuclear target of FoxO1, p21. A role of SEMA4B in suppressing NSCLC growth, besides its role in inhibiting cell metastasis, and highlights SEMA4B as a promising therapeutic target for NSCLC.
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TMPH-01560 | IL-26 Protein, Human, Recombinant (His & Trx) | Human | E. coli | ||
May play a role in local mechanisms of mucosal immunity and seems to have a proinflammatory function. May play a role in inflammatory bowel disease. Activates STAT1 and STAT3, MAPK1/3 (ERK1/2), JUN and AKT. Induces expression of SOCS3, TNF-alpha and IL-8, secretion of IL-8 and IL-10 and surface expression of ICAM1. Decreases proliferation of intestinal epithelial cells. Is inhibited by heparin. IL-26 Protein, Human, Recombinant (His & Trx) is expressed in E. coli expression system with N-6xHis-Trx tag. The predicted molecular weight is 35.8 kDa and the accession number is Q9NPH9.
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TMPK-00351 | RANK/TNFRSF11A Protein, Human, Recombinant (aa 30-212, hFc) | Human | HEK293 Cells | ||
TNFRSF11A, also known as receptor activator of NF-κB (RANK), activates several signaling pathways, such as NF-κB, JNK, ERK, p38α, and Akt/PKB. RANK/TNFRSF11A is a novel and frequent target for de novo methylation in gliomas, which affects apoptotic activity and focus formation thereby contributing to the molecular pathogenesis of gliomas. RANK/TNFRSF11A Protein, Human, Recombinant (aa 30-212, hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 46.85 kDa and the accession number is Q9Y6Q6-1.
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TMPK-00926 | Noggin/NOG Protein, Mouse, Recombinant (His & Flag) | Mouse | HEK293 Cells | ||
Noggin is an antagonist of bone morphogenetic proteins (BMP), being indispensable for certain developmental events.Noggin expression positively correlated with EGFR expression in both GC cell line models and The Cancer Genome Atlas human GC cohort. Targeting EGFR and its downstream pathways diminished cell proliferation which was promoted by Noggin. Noggin promotes the proliferation of GC cells by upregulating EGFR and enhancing a vicious circle formed by β‑catenin, EGFR, ERK and Akt. Noggin/NOG Protein, Mouse, Recombinant (His & Flag) is expressed in HEK293 mammalian cells with N-His-Flag tag. The predicted molecular weight is 25.16 kDa and the accession number is P97466.
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TMPH-00001 | CD133/PROM1 Protein-VLP, Human, Recombinant (His) | Human | HEK293 Cells | ||
May play a role in cell differentiation, proliferation and apoptosis. Binds cholesterol in cholesterol-containing plasma membrane microdomains and may play a role in the organization of the apical plasma membrane in epithelial cells. During early retinal development acts as a key regulator of disk morphogenesis. Involved in regulation of MAPK and Akt signaling pathways. In neuroblastoma cells suppresses cell differentiation such as neurite outgrowth in a RET-dependent manner. CD133/PROM1 Protein-VLP, Human, Recombinant (His) is expressed in HEK293 mammalian cells with C-10xHis tag. The predicted molecular weight is 96.7 kDa and the accession number is O43490.
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TMPY-02398 | TLE3 Protein, Human, Recombinant (aa 484-772, GST) | Human | E. coli | ||
The association between high TLE3 expression and a favorable response to taxane-containing chemotherapy regimens was validated in patients with non-serous ovarian cancer. That TLE3 expression may serve as a marker of chemosensitivity in taxane-treated patients with non-serous histologies. Transducin-like enhancer of Split3 (TLE3) serves as a transcriptional corepressor during cell differentiation and shows multiple roles in different kinds of cancers. TLE3 repressed CRC proliferation partly through inhibition of MAPK and AKT signaling pathways, suggesting the possibility of TLE3 as a biomarker for CRC prognosis.
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TMPY-04899 | OGN/Osteoglycin Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
OGN (Osteoglycin) is a Protein Coding gene. This gene encodes a member of the small leucine-rich proteoglycan (SLRP) family of proteins. It belongs to the small leucine-rich proteoglycan (SLRP) family. The encoded protein induces ectopic bone formation in conjunction with transforming growth factor-beta and may regulate osteoblast differentiation. OGN is broadly expressed in the gall bladder, endometrium, and other tissues. OGN reduced Zeb-1 expression via EGFR/Akt leading to inhibition of epithelial-mesenchymal transition. In vitro and in vivo, the OGN expression was demonstrated to reduce cell proliferation, inhibit invasion of colon cancer cells then impede cancer progression. Diseases associated with OGN include Inhibited Male Orgasm and Cornea Plana.
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TMPH-02878 | PTPRS Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Cell surface receptor that binds to glycosaminoglycans, including chondroitin sulfate proteoglycans and heparan sulfate proteoglycans. Binding to chondroitin sulfate and heparan sulfate proteoglycans has opposite effects on PTPRS oligomerization and regulation of neurite outgrowth. Contributes to the inhibition of neurite and axonal outgrowth by chondroitin sulfate proteoglycans, also after nerve transection. Plays a role in stimulating neurite outgrowth in response to the heparan sulfate proteoglycan GPC2. Required for normal brain development, especially for normal development of the pituitary gland and the olfactory bulb. Functions as tyrosine phosphatase. Mediates dephosphorylation of NTRK1, NTRK2 and NTRK3. Plays a role in down-regulation of signaling cascades that lead to the activation of Akt and MAP kinases. Down-regulates TLR9-mediated activation of NF-kappa-B, as well as production of TNF, interferon alpha and interferon beta.
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TMPH-01540 | Intelectin-1/ITLN1 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Lectin that specifically recognizes microbial carbohydrate chains in a calcium-dependent manner. Binds to microbial glycans that contain a terminal acyclic 1,2-diol moiety, including beta-linked D-galactofuranose (beta-Galf), D-phosphoglycerol-modified glycans, D-glycero-D-talo-oct-2-ulosonic acid (KO) and 3-deoxy-D-manno-oct-2-ulosonic acid (KDO). Binds to glycans from Gram-positive and Gram-negative bacteria, including K.pneumoniae, S.pneumoniae, Y.pestis, P.mirabilis and P.vulgaris. Does not bind human glycans. Probably plays a role in the defense system against microorganisms (Probable). May function as adipokine that has no effect on basal glucose uptake but enhances insulin-stimulated glucose uptake in adipocytes. Increases AKT phosphorylation in the absence and presence of insulin. May interact with lactoferrin/LTF and increase its uptake, and may thereby play a role in iron absorption.
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TMPJ-00181 | PD-1 Protein, Human, Recombinant (His & Avi), Biotinylated | Human | HEK293 Cells | ||
Programmed cell death protein 1(PDCD1) is a single-pass type I membrane protein and contains 1 Ig-like V-type domain. PD-1 is a member of the extended CD28/CTLA-4 family of T cell regulators. PDCD1 inhibits the T-cell proliferation and production of related cytokines including IL-1, IL-4, IL-10 and IFN-γ by suppressing the activation and transduction of PI3K/AKT pathway. In addition, coligation of PDCD1 inhibits BCR-mediating signal by dephosphorylating key signal transducer. PDCD1 has been suggested to be involved in lymphocyte clonal selection and peripheral tolerance, and thus contributes to the prevention of autoimmune diseases. As a cell surface molecule, PDCD1 regulates the adaptive immune response. Engagement of PD-1 by its ligands PD-L1 or PD-L2 transduces a signal that inhibits T-cell proliferation, cytokine production, and cytolytic function.
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TMPJ-00978 | PIP4K2A Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Phosphatidylinositol 5-phosphate 4-kinase type-2 alpha (PIP4K2A) is a member of the phosphatidylinositol-4-phosphate 5-kinase family. It contains 1 PIPK domain and is expressed ubiquitously, with high levels in the brain. It catalyzes the phosphorylation of phosphatidylinositol 5-phosphate (PtdIns5P) on the fourth hydroxyl of the myo-inositol ring, to form phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2). It may exert its function by regulating the levels of PtdIns5P, which functions in the cytosol by increasing AKT activity and in the nucleus signals through ING2. It may regulate the pool of cytosolic PtdIns5P in response to the activation of tyrosine phosphorylation, negatively regulate insulin-stimulated glucose uptake by lowering the levels of PtdIns5P. It also involved in thrombopoiesis, and the terminal maturation of megakaryocytes and regulation of their size.
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TMPY-01576 | Artemin Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 Cells | ||
Artemin (ARTN) is a member of glial cell line-derived neurotrophic factor (GDNF) family of ligands, and its signaling is mediated via a multi-component receptor complex including the glycosylphosphatidylinositol-anchored GDNF family receptors a (GFRa1, GFRa3) and RET receptor tyrosine kinase. The major mechanism of ARTN action is via binding to a non-signaling co-receptor. The major function of ARTN is to drive the molecule to induce migration and axonal projection from sympathetic neurons. It also promotes the survival, proliferation and neurite outgrowth of sympathetic neurons in vitro. ARTN triggers oncogenicity and metastasis by the activation of the AKT signaling pathway. Recent studies have reported that the expression of ARTN in hepatocellular carcinoma is associated with increased tumor size, quick relapse and shorter survival. Furthermore, ARTN promotes drug resistance such as antiestrogens, doxorubicin, fulvestrant, paclitaxel, tamoxifen and trastuzumab. Moreover, ARTN also stimulates the radio-therapeutic resistance. Hypoxia has been reported to regulate the cancer stem cell (CSC) population yet the underlying mechanism is poorly characterized. Artemin (ARTN) is a member of the glial cell derived neurotrophic factor family of ligands, is a hypoxia-responsive factor and is essential for hypoxia-induced CSC expansion in hepatocellular carcinoma (HCC). Clinically, elevated expression of ARTN in HCC was associated with larger tumor size, faster relapse and shorter survival. In vitro, HCC cells with forced expression of ARTN exhibited reduced apoptosis, increased proliferation, epithelial-mesenchymal transition (EMT) and enhanced motility. Additionally, ARTN dramatically increased xenograft tumor size and metastasis in vivo. Moreover, ARTN also enhanced tumorsphere formation and the tumor initiating capacity of HCC cells, consequent to expansion of the CD133+ CSC population. ARTN transcription was directly activated by hypoxia-induced factor-1α (HIF-1α) and hypoxia induced ARTN promoted EMT and increased the CSC population via AKT signaling.
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TMPY-05250 | CLEC3A Protein, Mouse, Recombinant (His) | Mouse | Baculovirus Insect Cells | ||
C-type lectin domain family 3 member A (CLEC3A) is a poorly characterized protein belonging to the superfamily of C-type lectins. Elevated CLEC3A expression may correlate with breast IDC metastatic potential and indicated a poor prognosis in breast IDC. CLEC3A knockdown inhibited BC cell growth and metastasis might be through suppressing PI3K/AKT signaling activity. That CLEC3A is a promising therapeutic target for BC in the future. Matrilysin (MMP-7) plays important roles in tumor progression. Previous studies have suggested that MMP-7 binds to tumor cell surface and promotes their metastatic potential. C-type lectin domain family 3 member A (CLEC3A) as a membrane-bound substrate of MMP-7. CLEC3A binds to heparan sulfate proteoglycans on cell surface, leading to the enhancement of cell adhesion to integrin ligands on ECM. It can be speculated that the cleavage of CLEC3A by MMP-7 weakens the stable adhesion of tumor cells to the matrix and promotes their migration in tumor microenvironments.
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TMPJ-00674 | RANK/TNFRSF11A Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Receptor activator of NF-κB(RANK,TNFRSF11A) belongs to one member of tumor necrosis factor receptor family.It is a receptor for TNFSF11/RANKL/TRANCE/OPGL. This gene encodes a type 1 membrane protein with a 30 amino acids (aa) signal peptide, 184 aa extracellular region , a 20 aa transmembrane domain and a 391 aa cytoplasmic region. Human and murine RANK share 81% aa identity in their extracellular domains. RANK is ubiquitous highly expressed in trabecular bone, thymus, small intestine, lung, brain and kidney, but weakly expressed in spleen and bone marrow. After binding its ligand RANKL, RANK can activate signaling pathways such as NF-κB, JNK, ERK, p38, and Akt/PKB, through TRAF protein phosphorylation. RANK/TNFRSF11A signaling is largely considered to be growth promoting and apoptosis reducing such as the effects observed in osteoclasts. RANK/TNFRSF11A was also found to be involved in the regulation of interactions between T-cells and dendritic cells.
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TMPY-03795 | EIF5A2 Protein, Human, Recombinant (His) | Human | E. coli | ||
Eukaryotic translation initiation factor 5A2 (EIF5A2) has been demonstrated to be upregulated in numerous types of human cancer and is associated with cancer progression. Silencing of EIF5A2 in the NSCLC cells resulted in the downregulation of the tumorigenic proteins, apoptosis regulator Bcl-2 and myc proto-oncogene protein, and upregulation of E-cadherin, suggesting that EIF5A2 promotes proliferation and metastasis through these proteins. EIF5A2 may therefore serve as a novel therapeutic target for the treatment of NSCLC. EIF5A2 might be a novel therapeutic target for the inhibition of NPC progress. EIF5A2 overexpression may contribute to cancer progression and poor prognosis, it could be a novel potential prognostic marker for FIGO stage I-II cervical cancer. EIF5A2 upregulation plays an important oncogenic role in gastric cancer. EIF5A2 may represent a new predictor for poor survival and is a potential therapeutic target for gastric cancer. The eukaryotic initiation factor 5A2 (EIF5A2) over-expression enhances HCC cell metastasis. EIF5A2, as a target of PI3K/Akt, promotes melanoma cell invasion and may serve as a promising prognostic marker and a potential therapeutic target for melanoma.
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TMPY-04461 | TRIB3 Protein, Human, Recombinant (GST) | Human | Baculovirus Insect Cells | ||
Tribbles homolog 3, also known as Neuronal cell death-inducible putative kinase, p65-interacting inhibitor of NF-kappa-B, SINK and TRIB3, is a Nucleus protein that belongs to the protein kinase superfamily and CAMK Ser/Thr protein kinase family and Tribbles subfamily. Highest expression Of TRIB3 is in liver, pancreas, peripheral blood leukocytes and bone marrow. It is also highly expressed in a number of primary lung, colon and breast tumors. TRIB3 is expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney. TRIB3 disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. TRIB3 may bind directly to and mask the 'Thr-38' phosphorylation site in AKT1. It binds to ATF4 and inhibits its transcriptional activation activity. TRIB3 interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. It interacts with MAPK kinases and regulates activation of MAP kinases. It may play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. TRIB3 does not display kinase activity.
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TMPY-04484 | ACK1 Protein, Human, Recombinant (GST) | Human | Baculovirus Insect Cells | ||
ACK1 (also known as ACK, TNK2, or activated Cdc42 kinase) is a structurally unique non-receptor tyrosine kinase that is expressed in diverse cell types. This downstream effector of CDC42 mediates CDC42-dependent cell migration via phosphorylation of BCAR1. The ACK1 protein may be involved in a regulatory mechanism that sustains the GTP-bound active form of Cdc42Hs and which is directly linked to a tyrosine phosphorylation signal transduction pathway. ACK1 integrates signals from plethora of ligand-activated receptor tyrosine kinases (RTKs), for example, MERTK, EGFR, HER2 and PDGFR to initiate intracellular signaling cascades. It binds to both poly- and mono-ubiquitin and regulates ligand-induced degradation of EGFR. ACK1 transduces extracellular signals to cytosolic and nuclear effectors such as the protein kinase AKT/PKB and androgen receptor (AR), to promote cell survival and growth. ACK1 participates in tumorigenesis, cell survival, and migration. Gene amplification and overexpression of ACK1 were found in many cancer types such as those of the lung and prostate. Recently, four somatic missense mutations of ACK1, which occur in the N-terminal region, the C-lobe of the kinase domain, and the SH3 domain, were identified in cancer tissue samples.
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TMPY-04562 | GRK2 Protein, Human, Recombinant (His & GST) | Human | Baculovirus Insect Cells | ||
G-protein coupled receptor kinase 2 (GRK2), also referred as Adrenergic, beta, receptor kinase 1 (ADRBK1), is a ubiquitous member of the G protein-coupled receptor kinase (GRK) family that appears to play a central, integrative role in signal transduction cascades. GRK2 can phosphorylate a growing number of non-GPCR substrates and associate with a variety of proteins related to signal transduction, thus suggesting that this kinase could also have diverse 'effector' functions. GRK2 has been reported to interact with a variety of signal transduction proteins related to cell migration such as MEK, Akt, PI3Kgamma or GIT. Interestingly, the levels of expression and activity of this kinase are altered in a number of inflammatory disorders (as rheumatoid arthritis or multiple sclerosis), thus suggesting that GRK2 may play an important role in the onset or development of these pathologies. The important physiological function of GRK2 as a modulator of the efficacy of GPCR signal transduction systems is exemplified by its relevance in cardiovascular physiopathology as well as by its emerging role in the regulation of chemokine receptors. Besides its canonical role in the modulation of the signalling mediated by many G protein-coupled receptors (GPCR), this protein can display a very complex network of functional interactions with a variety of signal transduction partners, in a stimulus, cell type, or context-specific way.
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TMPY-04084 | ANGPTL1 Protein, Canine, Recombinant (hFc) | Canine | HEK293 Cells | ||
Angiopoietin-like protein 1 (ANGPTL1) has been reported to suppress migration and invasion in lung and breast cancer, acting as a novel tumor suppressor candidate. Downregulation of tumor suppressor signaling plays an important role in the pathogenesis of hepatocellular carcinoma (HCC).The downregulation of the angiopoietin-like protein ANGPTL1 is associated with vascular invasion, tumor thrombus, metastasis, and poor prognosis in HCC. Ectopic expression of ANGPTL1 in HCC cells effectively decreased their in vitro and in vivotumorigenicity, cell motility, and angiogenesis. shRNA-mediated depletion of ANGPTL1 exerted opposing effects. ANGPTL1 promoted apoptosis via inhibition of the STAT3/Bcl-2-mediated antiapoptotic pathway and decreased cell migration and invasion via downregulation of transcription factors SNAIL and SLUG. Furthermore, ANGPTL1 inhibited angiogenesis by attenuating ERK and AKT signaling and interacted with integrin α1β1 receptor to suppress the downstream FAK/Src-JAK-STAT3 signaling pathway. Taken together, these results suggest ANGPTL1 as a prognostic biomarker and novel therapeutic agent in HCC. ANGPTL1 expression was down-regulated in CRC tissues and inversely correlated with poor survival. ANGPTL1 repressed migration and invasion of CRC cells, and microRNA-138 was involved in this process. Angiopoietin-like protein 1 (ANGPTL1) has been shown to act as a tumor suppressor by inhibiting angiogenesis, cancer invasion, and metastasis.
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