目录号 | 产品详情 | 靶点 | |
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T7677 | JNK | ||
JNK Inhibitor VIII (TCS JNK 6o) 是一种 c-Jun N-末端激酶(JNK-1, -2, -3)抑制剂,对 JNK-1、JNK-2 的IC50值分别是 45 nM 和 160 nM,对JNK-1、JNK-2、JNK-3 的Ki 分别为 2 nM、4 nM、52 nM。 | |||
T3598 | JNK | ||
JNK-IN-7 (JNK inhibitor) 是 JNK 抑制剂,抑制 JNK1、JNK2和 JNK3,IC50分别为 1.5、2 和 0.7 nM。 | |||
T2668 | JNK c-Kit | ||
JNK-IN-8 (JNK Inhibitor XVI) 是一种有效的JNK 抑制剂,抑制JNK1、JNK2和JNK3,IC50分别为 4.7、18.7 和 1 nM。 | |||
T2234 | Apoptosis JNK | ||
TCS JNK 5a (SC202671) 是一种 JNK2和 JNK3的有效抑制剂,pIC50分别为 6.5和 6.7。 | |||
T60534 | |||
JNK-IN-11 (compound 1) 是一种有效的 JNK 抑制剂,具有用于阿尔茨海默病和帕金森病研究的潜力。JNK-IN-11对 JNK1、JNK2、JNK3 的IC50值分别为 1.8、21.4、2.2 μM 。 | |||
T38260 | |||
SP 600125, negative control 是 SP 600125 的甲基化类似物,可用作SP 600125的阴性对照,对 DTP3和GADD45β/MKK7(生长停滞和 DNA 损伤诱导型 β/介原活化蛋白激酶激酶 7)具有抑制作用,能够恢复活化。SP 600125, negative control 对 JNK2 和 JNK3 的 IC50s 分别为 18 和 24 μM。 | |||
TQ0089 | Apoptosis JNK Autophagy | ||
Juglanin 是来自金鸡脚的一种黄酮类天然产物,是一种 JNK 的激活剂,能诱导人乳腺癌细胞的凋亡和自噬,具有炎症和抗肿瘤活性。 | |||
T3109 | Apoptosis Ferroptosis Trk receptor JNK Aurora Kinase Autophagy | ||
SP600125 (JNK Inhibitor II) 是一种 JNK 抑制剂,抑制 JNK1、JNK2 和 JNK3 (IC50=40/40/90 nM),具有口服有效性、可逆性和 ATP 竞争性。SP600125 可以抑制自噬,诱导凋亡。 | |||
T5S2283 | p38 MAPK Caspase JNK | ||
Sesaminol 是从Justicia orbiculata 中分离得到的一种天然产物,抑制脂质过氧化,具有神经保护作用和抗氧化活性。它通过抑制JNK、p38 MAPKs 和caspase-3磷酸化,抑制MAPK 的级联反应。 | |||
T40248 | |||
JNK3 inhibitor-1 is a highly potent and selective compound that specifically inhibits JNK3 with an impressive IC50 value of 0.005 μM. In addition to its remarkable inhibitory effects, JNK3 inhibitor-1 possesses excellent oral bioavailability and the ability to efficiently penetrate the brain. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04554 | JNK1 Protein, Human, Recombinant (GST) | Human | Baculovirus-Insect Cells | ||
Mitogen-activated protein kinase 8 (MAPK8), also known as JNK1, is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation, and development. The protein kinases JNK1 has been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. It is critically involved in the promotion of diet-induced obesity, metabolic inflammation, and beta-cell dysfunction. The selective deficiency of JNK1 in the murine nervous system is sufficient to suppress diet-induced obesity. Genetic analysis indicates that the effects of JNK1 can be separated from the effects of JNK1 on obesity. JNK1 is a potential pharmacological target for the development of drugs that might be useful for the treatment of metabolic syndrome, and type 2 diabetes. Furthermore, JNK1 plays a major role in hypoxic cellular damage. JNK1 protein might be an attractive target for anti-hypoxic therapy in increasing resistance to many pathological conditions and diseases, leading to the oxygen deficit.
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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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TMPK-01204 | TNFRSF19 Protein, Human, Recombinant (His) | Human | HEK293 | ||
A novel susceptibility gene TNFRSF19, which encodes an orphan member of the TNF receptor superfamily known to be associated with nasopharyngeal carcinoma (NPC) and lung cancer risk. TNFRSF19, a susceptibility gene for nasopharyngeal carcinoma and other cancers, functions as a potent inhibitor of the TGFβ signaling pathway.
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TMPK-01203 | TNFRSF19 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
A novel susceptibility gene TNFRSF19, which encodes an orphan member of the TNF receptor superfamily known to be associated with nasopharyngeal carcinoma (NPC) and lung cancer risk. TNFRSF19, a susceptibility gene for nasopharyngeal carcinoma and other cancers, functions as a potent inhibitor of the TGFβ signaling pathway.
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TMPY-03102 | IL-18R beta/IL-18RAP Protein, Rhesus, Recombinant (hFc) | Rhesus | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-01446 | IL-18R beta/IL-18RAP Protein, Human, Recombinant (His) | Human | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-04572 | MKK4 Protein, Mouse, Recombinant (His & GST) | Mouse | Baculovirus-Insect Cells | ||
Dual specificity mitogen-activated protein kinase kinase 4, also known as MAP kinase kinase 4, MAPKK4, JNK-activating kinase 1, MAPK/ERK kinase 4, SAPK/ERK kinase 1, c-Jun N-terminal kinase kinase 1, JNKK, and MAP2K4, is a protein that belongs to the protein kinase superfamily, STE Ser/Thr protein kinase family and MAP kinase kinase subfamily. MAP2K4 / JNKK1 is a protein kinase that is a direct activator of MAP kinases in response to various environmental stresses or mitogenic stimuli. MAP2K4 / JNKK1 has been shown to activate MAPK8 / JNK1, MAPK9 / JNK2, and MAPK14 / p38, but not MAPK1 / ERK2 or MAPK3 / ERK1. MAP2K4 / JNKK1 is phosphorylated, and thus activated by MAP3K1 / MEKK. The stress-activated protein kinase (SAPK) pathways represent phosphorylation cascades that convey pro-apoptotic signals. The mitogen-activated protein kinase kinase (MAPKK) homolog MAP2K4 ( MKK4, SEK, JNKK1 ) is a centrally-placed mediator of the SAPK pathways.
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TMPY-02115 | R-Spondin 3/RSPO3 Protein, Human, Recombinant (aa 1-146, His) | Human | HEK293 | ||
R-spondin 3 (RSPO3) is a member of the R-Spondin (RSPO) family in vertebrates that activate Wnt/beta-catenin signaling, plays a key role in these processes. The RSPO family of secreted Wnt modulators is involved in development and disease and holds therapeutic promise as stem cell growth factors. The four members have high structural homology. RSPO2 and RSPO3 are more potent than RSPO1, whereas RSPO4 is relatively inactive. All RSPO members require Wnt ligands and LRP6 for activity and amplify signaling of Wnt3A, Wnt1, and Wnt7A, suggesting that RSPO proteins are general regulators of canonical Wnt signaling. RSPO3/PCP signaling during gastrulation requires Wnt5a and is transduced via Fz7, Dvl, and JNK. RSPO3 functions by inducing Sdc4-dependent, clathrin-mediated endocytosis. RSPO3 is a novel, evolutionarily conserved angiogenic factor in embryogenesis. RSPO3 has a key role in the interaction between chorion and allantois in labyrinthine development.
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TMPY-04142 | RANK/TNFRSF11A Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
TNFRSF11A is a member of the TNF-receptor superfamily. In mouse, it is also known as CD265. TNFRSF11A contains 4 TNFR-Cys repeats and is widely expressed with high levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland. It is an essential mediator for osteoclast and lymph node development. TNFRSF11A and its ligand are important regulators of the interaction between T cells and dendritic cells. It can interact with various TRAF family proteins, through which this receptor induces the activation of NF-kappa B and MAPK8/JNK. Defects in TNFRSF11A can cause familial expansile osteolysis (FEO). FEO is a rare autosomal dominant bone disorder characterized by focal areas of increased bone remodeling. Defects in TNFRSF11A also can cause Paget disease of bone type 2 (PDB2). PDB2 is a bone-remodeling disorder with clinical similarities to FEO. Defects in TNFRSF11A are the cause of osteopetrosis autosomal recessive type 7 which characterized by abnormally dense bone, due to defective resorption of immature bone.
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TMPY-05319 | BCMA/TNFRSF17 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-03213 | BCMA/TNFRSF17 Protein, Rhesus, Recombinant (hFc) | Rhesus | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05568 | BCMA/TNFRSF17 Protein, Human (His & hFc), PE conjugated | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-02028 | RON/CD136 Protein, Human, Recombinant (His) | Human | HEK293 | ||
The tyrosine kinase receptor, macrophage-stimulating 1 receptor (MST1R), a c-met-related tyrosine kinase, also known as the Ron receptor or CD136, controls cell survival and motility programs related to invasive growth. As the tyrosine kinase receptor is comprised of an extracellular domain, MST1R protein contains the ligand-binding pocket and an intracellular region where the kinase domain is located. MST1R signaling may be involved in the regulation of macrophage and T-lymphocyte activation in vivo during injury. This assessment of gene expression indicates the importance of genetic factors in contributing to lung injury and points to strategies for intervention in the progression of inflammatory diseases. It had been shown that MST1R/CD136 plays a critical role in Ni-induced lung injury in mice. The overexpression of MSP, MT-SP1, and MST1R was a strong independent indicator of both metastasis and death in human breast cancer patients and significantly increased the accuracy of an existing gene expression signature for poor prognosis. Stimulation of MST1R leads to its transphosphorylation and the ultimate activation of numerous intracellular signaling pathways, such as the classical mitogen-activated protein kinase pathway, the phosphatidylinositol (PI)3-kinase pathway, and the JNK pathway.
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TMPY-04493 | BCMA/TNFRSF17 Protein, Human, Recombinant (rFc) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPK-00723 | RANK/TNFRSF11A Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
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.
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TMPH-01251 | DUSP26 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Inactivates MAPK1 and MAPK3 which leads to dephosphorylation of heat shock factor protein 4 and a reduction in its DNA-binding activity. Inhibits MAP kinase p38 by dephosphorylating it and inhibits p38-mediated apoptosis in anaplastic thyroid cancer cells. Can also induce activation of MAP kinase p38 and c-Jun N-terminal kinase (JNK).
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TMPH-02209 | TRAF5 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Adapter protein and signal transducer that links members of the tumor necrosis factor receptor family to different signaling pathways by association with the receptor cytoplasmic domain and kinases. Mediates activation of NF-kappa-B and probably JNK. Seems to be involved in apoptosis. Plays a role in mediating activation of NF-kappa-B by EIF2AK2/PKR.
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TMPY-03655 | GADD45G Protein, Human, Recombinant | Human | E. coli | ||
GADD45G, also known as CR6, is part of the nuclear proteins to interact with various proteins whose transcript levels are raised after stressful growth arrest conditions and treatment with DNA-damaging agents. GADD45G reacts to environmental stresses by mediating activation of the p38/JNK pathway which is mediated through their protein binding and activating MTK1/MEKK4 kinase, which is an upstream activator of both p38 and JNK MAPKs. GADD45G acts as a new-age tumor suppressor however is being frequently inactivated epigenetically in multiple tumors. GADD45G mRNA expression is down-regulated in hepatocellular carcinoma. GADD45G causes cell cycle arrest at G2/M transition when transfected into Hep-G2 cells. GADD45G induction by androgens involves new protein synthesis. Overexpression of GADD45G inhibits cell growth and causes morphological modifications in prostate cell lines thus GADD45G takes part in differentiation induction by androgens.
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TMPK-00351 | RANK/TNFRSF11A Protein, Human, Recombinant (aa 30-212, hFc) | Human | HEK293 | ||
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.
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TMPH-01015 | BMP-3 Protein, Human, Recombinant (His) | Human | E. coli | ||
Growth factor of the TGF-beta superfamily that plays an essential role in developmental process by inducing and patterning early skeletal formation and by negatively regulating bone density. Antagonizes the ability of certain osteogenic BMPs to induce osteoprogenitor differentitation and ossification. Initiates signaling cascades by associating with type II receptor ACVR2B to activate SMAD2-dependent and SMAD-independent signaling cascades including TAK1 and JNK pathways.
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TMPJ-00344 | IL-18RAP Protein, Human, Recombinant (hFc & His) | Human | Human Cells | ||
IL-18RAP is a single-pass type I membrane protein and contains two Ig-like C2-type domains and one TIR domain, IL18RAP can be induced by IFN-alpha and IL12 in nature killer cells and T-cells. The coexpression of IL18R1 and IL18RAP is required for the activation of NF-kappa B and JNK in response to IL-18.Defects in IL18RAP are associated with Coeliac disease.
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TMPY-03103 | IL-18R beta/IL-18RAP Protein, Rhesus, Recombinant (His) | Rhesus | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-04399 | TAOK3 Protein, Human, Recombinant (aa 1-411, His & GST) | Human | Baculovirus-Insect Cells | ||
Serine/threonine-protein kinase TAO3, also known as cutaneous T-cell lymphoma-associated antigen HD-CL-9, CTCL-associated antigen HD-CL-9, Dendritic cell-derived protein kinase, JNK / SAPK-inhibitory kinase, Jun kinase-inhibitory kinase, Kinase from chicken homolog A, Thousand and one amino acid protein 3, JIK, TAOK3 and MAP3K18, is cytoplasm and peripheral membrane protein which belongs to the protein kinase superfamily, STE Ser/Thr protein kinase family and STE2 subfamily. Protein kinases are pivotal regulators of cell signaling that modulate each other's functions and activities through site-specific phosphorylation events. TAOK3 / JIK contains one protein kinase domain. TAOK3 / JIK is ubiquitously expressed at a low level, and highly expressed in peripheral blood leukocytes (PBLs), thymus, spleen, kidney, skeletal muscle, heart and liver. TAOK3 / JIK inhibits the basal activity of Jun kinase. It is negatively regulated by epidermal growth factor (EGF). When overexpressed, TAOK3 / JIK may activate ERK1 / ERK2 and JNK / SAPK.
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TMPY-03571 | TROY Protein, Human, Recombinant (His) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 19 (TNFRSF19), also known as TAJ-alpha or TROY, is a member of the TNF-receptor superfamily. TNFRSF19/TROY expression is detected in the pulmonary epithelium and the ductal epithelium of the prostate and parotid glands. TNFRSF19/TROY expression is detected in some adenocarcinoma cell lines that arise from this tissue. It has been shown to interact with TRAF family members, and to activate JNK signaling pathway when overexpressed in cells. TNFRSF19/TROY is capable of inducing apoptosis by a caspase-independent mechanism, and it is thought to play an essential role in embryonic development. TNFRSF19/TROY was negatively regulated by adipogenic transcription factor CCAAT/enhancer-binding proteins (C/EBP). TNFRSF19 signals activation of the Jnk pathway and induces cell death. Overexpression of TNFRSF19 also signals NFB activation, comparable and similar to that by p75NGFR. TNFRSF19/TROY is capable of activating key signaling pathways of the TNF receptor family, and its predominant expression patterns suggest that it plays a role in the growth and regulation of epithelial tissues.
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TMPY-06316 | IL-18R beta/IL-18RAP Protein, Human, Recombinant (hFc & Avi), Biotinylated | Human | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-00609 | IL-18R beta/IL-18RAP Protein, Mouse, Recombinant (His) | Mouse | Baculovirus-Insect Cells | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPJ-01353 | MBIPP Protein, Human, Recombinant (His) | Human | E. coli | ||
MAP3K12-binding inhibitory protein 1 (MBIP) is a 39kD protein high expression in the heart and lung. It is a component of the ADA2A-containing complex (ATAC) complex, a complex with histone acetyltransferase activity on histones H3 and H4, and composed of CSRP2BP, KAT2A, TADA2L, TADA3L, ZZ3, MBIP, WDR5, YEATS2, CCDC101 and DR1. In the complex, it probably interacts directly with KAT2A, CSRP2BP and WDR5. It’s function to inhibit the MAP3K12 activity to induce the activation of the JNK/SAPK pathway.
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TMPY-06750 | IL-18R beta/IL-18RAP Protein, Rabbit, Recombinant (His) | Rabbit | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-06761 | IL-18R beta/IL-18RAP Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-03194 | TROY Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 19 (TNFRSF19), also known as TAJ-alpha or TROY, is a member of the TNF-receptor superfamily. TNFRSF19/TROY expression is detected in the pulmonary epithelium and the ductal epithelium of the prostate and parotid glands. TNFRSF19/TROY expression is detected in some adenocarcinoma cell lines that arise from this tissue. It has been shown to interact with TRAF family members, and to activate JNK signaling pathway when overexpressed in cells. TNFRSF19/TROY is capable of inducing apoptosis by a caspase-independent mechanism, and it is thought to play an essential role in embryonic development. TNFRSF19/TROY was negatively regulated by adipogenic transcription factor CCAAT/enhancer-binding proteins (C/EBP). TNFRSF19 signals activation of the Jnk pathway and induces cell death. Overexpression of TNFRSF19 also signals NFB activation, comparable and similar to that by p75NGFR. TNFRSF19/TROY is capable of activating key signaling pathways of the TNF receptor family, and its predominant expression patterns suggest that it plays a role in the growth and regulation of epithelial tissues.
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TMPJ-00700 | GADD45B Protein, Human, Recombinant (His) | Human | E. coli | ||
Growth Arrest and DNA Damage-Inducible Protein GADD45 β (GADD45B) is a member of the GADD45 family. GADD45B has been shown to interact with MAP3K4, ASK1, MAP2K7, and GADD45GIP1. GADD45B is involved in the regulation of growth and apoptosis. GADD45B reacts to environmental stresses by mediating activation of stress-responsive MTK1/MEKK4 kinase, which is an upstream activator of both p38 and JNK MAPKs. In addition, GADD45B participates in the down-regulation of hepatocellular carcinoma (HCC). It may serve as a possible therapeutic target.
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TMPY-01388 | TROY Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 19 (TNFRSF19), also known as TAJ-alpha or TROY, is a member of the TNF-receptor superfamily. TNFRSF19/TROY expression is detected in the pulmonary epithelium and the ductal epithelium of the prostate and parotid glands. TNFRSF19/TROY expression is detected in some adenocarcinoma cell lines that arise from this tissue. It has been shown to interact with TRAF family members, and to activate JNK signaling pathway when overexpressed in cells. TNFRSF19/TROY is capable of inducing apoptosis by a caspase-independent mechanism, and it is thought to play an essential role in embryonic development. TNFRSF19/TROY was negatively regulated by adipogenic transcription factor CCAAT/enhancer-binding proteins (C/EBP). TNFRSF19 signals activation of the Jnk pathway and induces cell death. Overexpression of TNFRSF19 also signals NFB activation, comparable and similar to that by p75NGFR. TNFRSF19/TROY is capable of activating key signaling pathways of the TNF receptor family, and its predominant expression patterns suggest that it plays a role in the growth and regulation of epithelial tissues.
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TMPY-06312 | IL-18R beta/IL-18RAP Protein, Human, Recombinant (His & Avi), Biotinylated | Human | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-01200 | IL-18R beta/IL-18RAP Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
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TMPY-05792 | TROY Protein, Mouse, Recombinant (mFc) | Mouse | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 19 (TNFRSF19), also known as TAJ-alpha or TROY, is a member of the TNF-receptor superfamily. TNFRSF19/TROY expression is detected in the pulmonary epithelium and the ductal epithelium of the prostate and parotid glands. TNFRSF19/TROY expression is detected in some adenocarcinoma cell lines that arise from this tissue. It has been shown to interact with TRAF family members, and to activate JNK signaling pathway when overexpressed in cells. TNFRSF19/TROY is capable of inducing apoptosis by a caspase-independent mechanism, and it is thought to play an essential role in embryonic development. TNFRSF19/TROY was negatively regulated by adipogenic transcription factor CCAAT/enhancer-binding proteins (C/EBP). TNFRSF19 signals activation of the Jnk pathway and induces cell death. Overexpression of TNFRSF19 also signals NFB activation, comparable and similar to that by p75NGFR. TNFRSF19/TROY is capable of activating key signaling pathways of the TNF receptor family, and its predominant expression patterns suggest that it plays a role in the growth and regulation of epithelial tissues.
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TMPY-04906 | RGMB Protein, Human, Recombinant (His) | Human | HEK293 | ||
RGMB was knocked down in breast cancer cells by way of an anti-RGMB ribozyme transgene. Knockdown of RGMB resulted in enhanced capacities of proliferation, adhesion, and migration in breast cancer cells. Further investigations demonstrated RGMB knockdown resulted in a reduced expression and activity of Caspase-3, accompanied with better survival in RGMB knockdown cells under serum starvation, which might be induced by its repression on MAPK JNK pathway. That RGMB may act as a negative regulator in breast cancer through BMP signaling.
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TMPY-04916 | RGMB Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
RGMB was knocked down in breast cancer cells by way of an anti-RGMB ribozyme transgene. Knockdown of RGMB resulted in enhanced capacities of proliferation, adhesion, and migration in breast cancer cells. Further investigations demonstrated RGMB knockdown resulted in a reduced expression and activity of Caspase-3, accompanied with better survival in RGMB knockdown cells under serum starvation, which might be induced by its repression on MAPK JNK pathway. That RGMB may act as a negative regulator in breast cancer through BMP signaling.
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TMPJ-00711 | GADD45G Protein, Human, Recombinant (His) | Human | E. coli | ||
Growth Arrest and DNA Damage-Inducible Protein GADD45 Υ (GADD45G) is a nuclear protein which belongs to the GADD45 family. GADD45G is highly expressed in placenta. GADD45G interacts with various proteins whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. GADD45G responds to environmental stresses by mediating activation of the p38/JNK pathway via MTK1/MEKK4 kinase. GADD45G is also involved in the regulation of growth and apoptosis. GADD45G inhibits cell growth and differentiation by androgens. The mRNA expression is down-regulated in hepatocellular carcinoma.
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TMPJ-00358 | DR6 Protein, Mouse, Recombinant (hFc & His) | Mouse | Human Cells | ||
Tumor necrosis factor receptor superfamily member 21(DR6) is a single-pass type I membrane protein and contains 1 death domain and 4 TNFR-Cys repeats. The protein may activate NF-kappa-B and promote apoptosis and it may activate JNK and be involved in T-cell differentiation.It is required for both normal cell body death and axonal pruning. Trophic-factor deprivation triggers the cleavage of surface APP by beta-secretase to release sAPP-beta which is further cleaved to release an N-terminal fragment of APP (N-APP). N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).
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TMPY-02191 | BLNK Protein, Human, Recombinant (His) | Human | HEK293 | ||
B-cell linker protein, also known as B-cell adapter containing a SH2 domain protein, B-cell adapter containing a Src homology 2 domain protein, Cytoplasmic adapter protein, Src homology 2 domain-containing leukocyte protein of 65 kDa, SLP-65 and BLNK, is a cytoplasm and cell membrane protein which contains oneSH2 domain. BLNK is expressed in B-cell lineage and fibroblast cell lines. Highest levels of expression is in the spleen, with lower levels in the liver, kidney, pancreas, small intestines and colon. BLNK functions as a central linker protein that bridges kinases associated with the B-cell receptor (BCR) with a multitude of signaling pathways, regulating biological outcomes of B-cell function and development. BLNK plays a role in the activation of ERK / EPHB2, MAP kinase p38 and JNK. BLNK modulates AP1 activation. It is important for the activation of NF-kappa-B and NFAT. BLNK plays an important role in BCR-mediated PLCG1 and PLCG2 activation and Ca2+mobilization and is required for trafficking of the BCR to late endosomes. BLNK may be required for the RAC1-JNK pathway. It plays a critical role in orchestrating the pro-B cell to pre-B cell transition. BLNK also plays an important role in BCR-induced B-cell apoptosis.Defects in BLNK are the cause of agammaglobulinemia type 4 (AGM4) which is a primary immunodeficiency characterized by profoundly low or absent serum antibodies and low or absent circulating B cells due to an early block of B-cell development.
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TMPJ-00376 | IL-17RD Protein, Human, Recombinant (hFc) | Human | Human Cells | ||
Interleukin-17 receptor D (IL-17 RD), also known as SEF (similar expression to FGFs), is a type I transmembrane protein that is found in both the cytoplasm and plasma membrane. IL-17RD functions as a feedback inhibitor of fibroblast growth factor mediated Ras-MAPK signaling and ERK activation. It may inhibit FGF-induced FGFR1 tyrosine phosphorylation, regulate the nuclear ERK signaling pathway by spatially blocking nuclear translocation of activated ERK By similarity, and mediate JNK activation and may be involved in apoptosis. IL-17RD interacts with the IL-17R downstream molecule TRAF6. It has been proposed that the IL-17RD intracellular domain interacts with IL-17R and TRAF6 to deliver the downstream signal.
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TMPH-02194 | TAB2 Protein, Human, Recombinant (His & Myc) | Human | Baculovirus | ||
Adapter required to activate the JNK and NF-kappa-B signaling pathways through the specific recognition of 'Lys-63'-linked polyubiquitin chains by its RanBP2-type zinc finger (NZF). Acts as an adapter linking MAP3K7/TAK1 and TRAF6 to 'Lys-63'-linked polyubiquitin chains. The RanBP2-type zinc finger (NZF) specifically recognizes Lys-63'-linked polyubiquitin chains unanchored or anchored to the substrate proteins such as RIPK1/RIP1: this acts as a scaffold to organize a large signaling complex to promote autophosphorylation of MAP3K7/TAK1, and subsequent activation of I-kappa-B-kinase (IKK) core complex by MAP3K7/TAK1. Regulates the IL1-mediated translocation of NCOR1 out of the nucleus. Involved in heart development.
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TMPY-02567 | PPM1A Protein, Human, Recombinant (His) | Human | E. coli | ||
Protein phosphatase 1A (PPM1A / PP2CA) is an enzyme belonging to the PP2C family of Ser / Thr protein phosphatases. Members of PP2C family are negative regulators of cell stress response pathways and the MAP kinases and MAP kinase kinases. It has also been demonstrated to inhibit the activation of p38 and JNK kinase cascades. PPM1A dephosphorylates and promotes nuclear export of TGFβ-activated Smad2/3. Ectopic expression of PPM1A abolishes TGFβ-induced antiproliferative and transcriptional responses, whereas depletion of PPM1A enhances TGFβ signaling in mammalian cells. It has been demonstrated that PPM1A / PP2CA, through dephosphorylation of Smad2/3, plays a critical role in terminating TGFβ signaling. Overexpression of PPM1A is reported to activate the expression of the tumor suppressor gene TP53 / p53, which leads to cell apoptosis.
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TMPY-02444 | ATF2 Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
Activating transcription factor 2, also known as ATF2, is a member of the leucine zipper family of DNA-binding proteins that binds to the cAMP response element. Its activity is enhanced after phosphorylation by stress-activated protein kinases such as c-Jun N-terminal kinase and p38. ATF2 has been found to be a target of the JNK signal transduction pathway and mediate adenovirus E1A-inducible transcriptional activation. ATF2 is also been reported playing roles in TGF-β signaling pathway. It has been shown that the transcription factor ATF2 is bound by a hetero-oligomer of Smad3 and Smad4 upon TGF-β stimulation. Studies indicate that ATF-2 plays a central role in TGF-β signaling by acting as a common nuclear target of both Smad and TAK1 pathways.
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TMPJ-00397 | IL-17RA Protein, Human, Recombinant (His & Avi), Biotinylated | Human | Human Cells | ||
CD217, also known as Interleukin-17 receptor A, is a T cell expressed pleotropic cytokine with 866 amino acids in length. CD217 functions as receptors for IL17A and IL17F, it binds to IL17A with higher affinity than to IL17F and binds IL17A and IL17F homodimers as part of a heterodimeric complex with IL17RC. It also binds heterodimers formed by IL17A and IL17F as part of a heterodimeric complex with IL17RC. The activation of IL17RA would lead to induction of expression of inflammatory chemokines and cytokines such as CXCL1, CXCL8/IL8 and IL6. The signaling events of IL 17 includes activation of NF kappa B and JNK, and require TNF receptor associated factors 6 (TRAF6) in the signaling pathway.
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TMPY-02774 | Galectin-7 Protein, Human, Recombinant (GST) | Human | E. coli | ||
LGALS7, also known as Galectin-7, is a member of the galectins family. The galectins are a family of beta-galactoside-binding proteins. There are at least 14 identified members of this family. Galectins share similarities in the CRD (the carbohydrate recognition domain). They are synthesized as cytosolic proteins. Though localized principally in the cytoplasm and lacking a classical signal peptide, galectins can also be stimulated to secretion by non-classical pathways or targeted to the nucleus. Galectins are implicated in modulating cell-cell and cell-matrix interactions. LGALS7 contains 1 galectin domain and is mainly expressed in stratified squamous epithelium. Galectin-7 could be involved in cell-cell and/or cell-matrix interactions necessary for normal growth control. LGALS7 is a pro-apoptotic protein that functions intracellularly upstream of JNK activation and cytochrome c release.
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TMPY-04109 | Galectin-7 Protein, Human, Recombinant (His) | Human | E. coli | ||
LGALS7, also known as Galectin-7, is a member of the galectins family. The galectins are a family of beta-galactoside-binding proteins. There are at least 14 identified members of this family. Galectins share similarities in the CRD (the carbohydrate recognition domain). They are synthesized as cytosolic proteins. Though localized principally in the cytoplasm and lacking a classical signal peptide, galectins can also be stimulated to secretion by non-classical pathways or targeted to the nucleus. Galectins are implicated in modulating cell-cell and cell-matrix interactions. LGALS7 contains 1 galectin domain and is mainly expressed in stratified squamous epithelium. Galectin-7 could be involved in cell-cell and/or cell-matrix interactions necessary for normal growth control. LGALS7 is a pro-apoptotic protein that functions intracellularly upstream of JNK activation and cytochrome c release.
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TMPJ-00616 | CD27/TNFRSF7 Protein, Rhesus macaque, Recombinant (His) | Rhesus macaque | Human Cells | ||
CD27 antigen, also known as CD27L receptor, T-cell activation antigen CD27, T14, S152, Tp55, TNFRSF7 and Tumor necrosis factor receptor for superfamily member 7,belongs to the TNF-receptor superfamily. CD27 is a single-pass type I membrane protein and exists as a homodimer form, containing three TNFR-Cys repeats. CD27 transduces signals that lead to the activation of NF-KappaB and MAPK8/JNK. CD27 is involved in regulating B-cell activation and immunoglobulin synthesis, binding to the ligand CD70. TRAF2 and TRAF5 have been shown to mediate the signaling process of CD27. CD27-binding protein (SIVA), which is a proapoptotic protein, can bind to CD27 and is thought to play a key role in the apoptosis. CD27 is required for generation and long-term maintenance of T cell immunity.
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TMPY-02907 | FGF-19 Protein, Human, Recombinant | Human | E. coli | ||
FGF19, also known as FGF-19, is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. FGF19 interacts with FGFR1, FGFR2, FGFR3 and FGFR4. Affinity between fibroblast growth factors (FGFs) and their receptors is increased by KL, KLB and heparan sulfate glycosaminoglycans that function as coreceptors. It interacts with KL and KLB directly. However, it interacts with FGFR4 in the presence of heparin, KL or KLB. FGF19 is involved in the suppression of bile acid biosynthesis through down-regulation of CYP7A1 expression, following positive regulation of the JNK and ERK1/2 cascades. It also stimulates glucose uptake in adipocytes.
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TMPY-01663 | PPM1A Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Protein phosphatase 1A (PPM1A / PP2CA) is an enzyme belonging to the PP2C family of Ser / Thr protein phosphatases. Members of PP2C family are negative regulators of cell stress response pathways and the MAP kinases and MAP kinase kinases. It has also been demonstrated to inhibit the activation of p38 and JNK kinase cascades. PPM1A dephosphorylates and promotes nuclear export of TGFβ-activated Smad2/3. Ectopic expression of PPM1A abolishes TGFβ-induced antiproliferative and transcriptional responses, whereas depletion of PPM1A enhances TGFβ signaling in mammalian cells. It has been demonstrated that PPM1A / PP2CA, through dephosphorylation of Smad2/3, plays a critical role in terminating TGFβ signaling. Overexpression of PPM1A is reported to activate the expression of the tumor suppressor gene TP53 / p53, which leads to cell apoptosis.
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