目录号 | 产品详情 | 靶点 | |
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T35463 | |||
(±)14(15)-EET is a metabolite of arachidonic acid that is formed via epoxidation of arachidonic acid by cytochrome P450.[1],[2] It prevents increases in leukotriene B4, ICAM-1, and chemokine (C-C motif) ligand 1 (CCL2) induced by oxidized LDL in primary rat pulmonary artery endothelial cells (RPAECs) when used at a concentration of 1 μM.[3] (±)14(15)-EET induces dilation of preconstricted isolated canine coronary arterioles (EC50 = 0.2 pM).[4] It reduces myocardial infarct size as a percentage of the area at risk in a canine model of ischemia-reperfusion injury induced by left anterior descending coronary artery (LAD) occlusion when administered at a dose of 0.128 mg/kg prior to occlusion or reperfusion.[5] Reference:[1]. Chacos, N., Falck, J.R., Wixtrom, C., et al. Novel epoxides formed during the liver cytochrome P-450 oxidation of arachidonic acid. Biochem. Biophys. Res. Commun. 104(3), 916-922 (1982).[2]. Oliw, E.H., Guengerich, F.P., and Oates, J.A. Oxygenation of arachidonic acid by hepatic monooxygenases. Isolation and metabolism of four epoxide intermediates. J. Biol. Chem. 257(7), 3771-3781 (1982).[3]. Jiang, J.-X., Zhang, S.-J., Xiong, Y.-K., et al. EETs attenuate ox-LDL-induced LTB4 production and activity by inhibiting p38 MAPK phosphorylation and 5-LO/BLT1 receptor expression in rat pulmonary arterial endothelial cells. PLoS One 10(6), e0128278 (2015).[4]. Oltman, C.L., Weintraub, N.L., VanRollins, M., et al. Epoxyeicosatrienoic acids and dihydroxyeicosatrienoic acids are potent vasodilators in the canine coronary microcirculation. Circ. Res. 83(9), 932-939 (1998).[5]. Nithipatikom, K., Moore, J.M., Isbell, M.A., et al. Epoxyeicosatrienoic acids in cardioprotection: Ischemic versus reperfusion injury. Am. J. Physiol. Heart Circ. Physiol. 291(2), H537-H542 (2006). | |||
T83727 | |||
Tat-NTS肽是一种能穿透细胞的肽,由HIV-1 Tat蛋白的转导域与对应于脂联素A1重复III域残基228-237的10个氨基酸肽链接而成,扮演核转运信号(NTS)的角色。它通过阻断脂联素A1与进口素β之间的蛋白质-蛋白质相互作用,阻止脂联素A1在初级鼠海马神经元中的核内转运。Tat-NTS抑制初级鼠海马神经元在葡萄糖-氧剥夺及再灌注诱导的细胞凋亡。在体内,Tat-NTS(10 mg/kg)有效减少了由中脑动脉闭塞(MCAO)引起的缺血-再灌注损伤模型小鼠的梗塞体积和神经元凋亡,并缩短了在Morris水迷宫测试中达到平台的时间。 | |||
T36851 | |||
Connexin43 mimetic peptide. Reduces swelling, astrogliosis, neuroinflammation and neuronal cell death following spinal cord injury ex vivo and in vivo. Exhibits analgesic effects in models of neuropathic pain. O'Carroll et al (2008) Connexin 43 mimetic peptides reduce swelling, astrogliosis and neuronal cell death after spinal cord injury. Cell.Commun.Adhes. 15 27 PMID:18649176 |Mao et al (2017) Characterisation of Peptide5 systemic administration for treating traumatic spinal cord injured rats. Exp.Brain.Res. 235 3033 PMID:28725925 |Kim et al (2017) Characterising the mode of action of extracellular Connexin43 channel mimetic peptides in an in vitro ischemia injury model. Biochem.Biophys.Acta. 1861 68 PMID:27816754 |Tonkin et al (2017) Attenuation of mechanical pain hypersensitivity by treatment with Peptide5, a connexin-43 mimetic peptide, involves inhibition of NLRP3 inflammasome in nerve-injured mice. Exp.Neurol. 300 1 PMID:29055716 | |||
T83770 | |||
Klotho衍生肽1(KP1)(56-87)是从人类Klotho蛋白质中衍生的肽,具有扰乱TGF-β信号传导的作用。它与TGF-β受体类型1(TGFBR2)和TGF-β受体类型2(TGFBR2;Kds分别为1.41和14.6µM)结合。KP1(10 µg/ml)的预孵育抑制TGF-β在NRK-49F大鼠成纤维细胞中诱导的纤维连接蛋白和α-平滑肌肌动蛋白(α-SMA)水平的增加。在体内,KP1(每天1 mg/kg)选择性地定位于受损的肾脏,并减少血清肌酐和血尿素氮水平,这些是肾功能的标志物,同时也减少了小鼠单侧输尿管阻塞(UUO)和单侧缺血-再灌注损伤诱导的肾脏纤维化模型中的肾纤维化。 | |||
T83731 | |||
Tat-CBD3是一种抑制N型电压门控钙通道Cav2.2与collapsin response mediator protein 2 (CRMP2)之间的蛋白质-蛋白质相互作用的抑制剂。它还能抑制CRMP2与NMDA受体NR2B亚单位之间的蛋白质-蛋白质相互作用。在无细胞实验中,Tat-CBD3 (10 µM)能将Cav2.2-CRMP2相互作用抑制43%,并在免疫共沉淀实验中抑制NMDA受体NR2B亚单位-CRMP2相互作用。它能在初级大鼠背根神经节 (DRG) 神经元中减少约60%的电压诱导钙电流,并在初级大鼠海马神经元中减少谷氨酸诱导的胞内钙水平增加。Tat-CBD3 (20 mg/kg)在大鼠中脑动脉闭塞 (MCAO) 引发的脑缺血模型中减少梗死体积。鞘内给药Tat-CBD3 (20 µg/5 µl)可防止大鼠卡拉胶诱导的热敏感性。 | |||
T83682 | |||
Tat-Gap 19是一种针对连接蛋白43 (Cx43) 半通道的肽抑制剂,由HIV-1 Tat蛋白传导域与对应于Cx43第128-136残基的九氨基酸肽连接而成。Tat-Gap 19 (10 µM) 能够抑制初级大鼠肝细胞中由谷氨酸引发的ATP释放,这是Cx43半通道活性的标志。在通过中脑动脉堵塞(MCAO)诱导的小鼠脑缺血再灌注损伤模型中,以25 mg/kg的剂量进行给药,可减少梗死体积。腹腔内注射Tat-Gap 19 (1 mg/kg 每天) 能够减少硫代乙酰胺引起的小鼠肝损伤模型中的纤维化病灶面积及表达α-平滑肌肌动蛋白 (α-SMA) 的肝星状细胞(成纤维细胞的前体)面积,并提高同种小鼠分离的肝细胞中超氧化物歧化酶 (SOD) 活性。 | |||
T36673 | |||
High affinity JNK inhibitor (Ki values are 25-50 nM). Inhibits JNK via competitive binding of the ATP-binding site of active, phosphorylated JNK. Exhibits > 40-fold selectivity for JNK over p38, ERK, IKK2, protein kinase C, Lck and ZAP70. Hepatoprotective. Also inhibits HCMV replication. Uehara et al (2004) c-Jun N-terminal kinase mediates hepatic injury after rat liver transplantation. Transplantation. 78 324 PMID:15316358 |Uehara et al (2005) JNK mediates hepatic ischemia reperfusion injury. J.Hepatol. 42 850 PMID:15885356 |Ma et al (2007) A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J.Am.Soc.Nephrol. 18 472 PMID:17202416 |Ma et al (2009) Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab.Invest. 89 470 PMID:19188913 |Zhang et al (2015) The c-Jun N-terminal kinase inhibitor SP600125 inhibits human cytomegalovirus replication. J.Med.Virol. 87 2135 PMID:26058558 |Vasilevskaya et al (2015) Inhibition of JNK sensitizes hypoxic colon cancer cells to DNA-damaging agents. Clin.Cancer.Res. 21 4143 PMID:26023085 | |||
T83768 | |||
Zofenoprilat是一种血管紧张素转换酶(ACE; IC50 = 8 nM for the rabbit lung enzyme)的抑制剂,同时也是前体药zofenopril的活性代谢产物。它能够抑制分离的豚鼠小肠中由血管紧张素I或缓激肽诱导的收缩(EC50s = 3 and 1 nM, respectively)。在人类脐静脉内皮细胞(HUVECs)中,Zofenoprilat (10 nM)降低基础内皮素-1分泌和一氧化氮(NO)生成,并阻止TNF-α诱导的活性氧种(ROS)增加以及谷胱甘肽(GSH)水平降低。Zofenoprilat (10 µM)保护初级人类心脏微血管内皮细胞免受多柔比星诱导的细胞毒性。此外,Zofenoprilat (10 µM)还能增加HUVECs中的硫化氢(H2S)生成,以及细胞的黏着、迁移和增殖。在以400 µM浓度使用时,它可以减少Langendorff分离的大鼠心脏灌流缺血再灌注损伤模型中的舒张末压和乳酸脱氢酶(LDH)释放。 | |||
T37297 | |||
Ru360, an oxygen-bridged dinuclear ruthenium amine complex, is a selective mitochondrial calcium uptake inhibitor. Ru360 potently inhibits Ca2+ uptake into mitochondria with an IC50 of 0.184 nM. Ru360 binds to mitochondria with high affinity (Kd of 0.34 nM). Ru360 has antiarrhythmic and cardioprotective effects[1][2]. Ru360 permeates slowly into the cell, and specifically inhibits mitochondrial calcium uptake in intact cardiomyocytes and in isolated heart. 1 μm Ru360 is taken up by myocardial cells and accumulated in the cytosol in a biphasic manner[1]. During pelleting hypoxia, Ru360 (10 µM) significantly improves cell viability in wild type cardiomyocytes[3]. Ru360 (15-50 nmol/kg) treatment abolishes the incidence of arrhythmias and haemodynamic dysfunction elicited by reperfusion in a whole rat model. Ru360 administration partially inhibits calcium uptake, preventing mitochondria from depolarization by the opening of the mitochondrial permeability transition pore (mPTP)[1]. [1]. G de J García-Rivas, et al. Ru360, a Specific Mitochondrial Calcium Uptake Inhibitor, Improves Cardiac Post-Ischaemic Functional Recovery in Rats in Vivo. Br J Pharmacol. 2006 Dec;149(7):829-37. [2]. M A Matlib, et al. Oxygen-bridged Dinuclear Ruthenium Amine Complex Specifically Inhibits Ca2+ Uptake Into Mitochondria in Vitro and in Situ in Single Cardiac Myocytes. J Biol Chem. 1998 Apr 24;273(17):10223-31. [3]. Lukas J Motloch, et al. UCP2 Modulates Cardioprotective Effects of Ru360 in Isolated Cardiomyocytes During Ischemia. Pharmaceuticals (Basel). 2015 Aug 4;8(3):474-82. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-00639 | EPO/Erythropoietin Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Erythropoietin is a member of the EPO / TPO family. It is a secreted, glycosylated cytokine composed of four alpha helical bundles. Erythropoietin can be found in the plasma and regulates red cell production by promoting erythroid differentiation and initiating hemoglobin synthesis. It also has neuroprotective activity against a variety of potential brain injuries and antiapoptotic functions in several tissue types. Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is produced by kidney or liver of adult mammals and by liver of fetal or neonatal mammals. Genetic variation in erythropoietin is associated with susceptbility to microvascular complications of diabetes type 2. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. It has a longer circulating half-life in vivo. Erythropoietin is being much misused as a performance-enhancing drug in endurance athletes.
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TMPY-00443 | EPO/Erythropoietin Protein, Mouse, Recombinant | Mouse | HEK293 | ||
Erythropoietin is a member of the EPO / TPO family. It is a secreted, glycosylated cytokine composed of four alpha helical bundles. Erythropoietin can be found in the plasma and regulates red cell production by promoting erythroid differentiation and initiating hemoglobin synthesis. It also has neuroprotective activity against a variety of potential brain injuries and antiapoptotic functions in several tissue types. Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is produced by kidney or liver of adult mammals and by liver of fetal or neonatal mammals. Genetic variation in erythropoietin is associated with susceptbility to microvascular complications of diabetes type 2. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. It has a longer circulating half-life in vivo. Erythropoietin is being much misused as a performance-enhancing drug in endurance athletes.
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TMPY-00853 | IL-1RA Protein, Human, Recombinant | Human | E. coli | ||
Interleukin-1 receptor antagonist (IL-1RA) also known as IL1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A), and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses. A polymorphism of this protein-encoding gene is reported to be associated with an increased risk of osteoporotic fractures and gastric cancer. IL-1RA/IL1RN may inhibit the activity of IL-1 by binding to its receptor and it has no IL-1 like activity. Genetic variation in IL-1RA/IL1RN is associated with susceptibility to microvascular complications of diabetes type 4 (MVCD4). These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. Defects in IL-1RA/IL1RN are the cause of interleukin 1 receptor antagonist deficiency (DIRA) which is also known as deficiency of interleukin 1 receptor antagonist. Autoinflammatory diseases manifest inflammation without evidence of infection, high-titer autoantibodies, or autoreactive T-cells. DIRA is a rare, autosomal recessive, genetic autoinflammatory disease that results in sterile multifocal osteomyelitis, and pustulosis from birth.
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TMPY-05053 | ANGPTL2 Protein, Human, Recombinant (His) | Human | HEK293 | ||
The angiopoietin-like protein (ANGPTL) family is homologous to angiopoietins but does not bind to the Tie2 receptor. The function of ANGPTLs has been elucidated largely in the context of angiogenesis and lipid metabolism. Morinaga et al. demonstrated that genetic depletion of Angptl2 confers amelioration of the mouse kidney fibrosis induced by a unilateral ureteral obstruction, implicating that ANGPTL2, predominantly in the renal tubular compartments, activates the transforming growth factor-β signaling and vice versa through miR-221. Angiopoietin-like protein 2 (ANGPTL2) maintains tissue homeostasis by inducing inflammation and angiogenesis. It is produced in infiltrating immune cells or resident cells, such as adipocytes, vascular endothelial cells, and tumor cells. The classic sequential cascade of P. gingivalis LPS → inflammatory cytokine induction is well established. However, in the current study, we reveal a novel cascade comprising sequential P. gingivalis LPS → ANGPTL2 → integrin α5β1 → inflammatory cytokine induction, which might be responsible for inducing potent periodontal disorganization activity in gingival epithelial cells. Via this pathway, ANGPTL2 functions in the pathogenesis of periodontitis and contributes to prolonging chronic inflammation in patients with systemic disease. That MAC-3-positive immune cells, including infiltrating bone marrow-derived macrophages and activated microglia, express abundant angiopoietin-like protein (ANGPTL) 2 in ischemic mouse brain in a transient middle cerebral artery occlusion (MCAO) model. Both neurological deficits and infarct volume decreased in transient MCAO model mice established in Angptl2 knockout (KO) relative to wild-type mice. Acute brain inflammation after ischemia-reperfusion, as estimated by expression levels of pro-inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor alpha (TNF)-α, was significantly suppressed in Angptl2 KO compared to control mice.
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TMPY-04424 | MST3 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
Aberrant STK24 expression was an independent prognostic indicator in lung adenocarcinoma patients. Its dysregulation was associated with its DNA copy number alteration and methylation. STK24/CCM3-regulated exocytosis plays an important role in the protection of kidneys from ischemia-reperfusion injury.
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TMPK-00481 | PDGF R beta/CD140b Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
Platelet-derived growth factor receptor (PDGFR) signaling is involved in proliferation and survival in a wide array of cell types.PDGFR-β signalling, via TGF-β signalling, may be crucial for restoration of BBB integrity after cerebral ischemia and therefore represents a novel potential therapeutic target.
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TMPJ-01051 | Pleiotrophin/PTN Protein, Mouse, Recombinant (His) | Mouse | Human Cells | ||
Pleiotrophin (PTN) is a secreted, strongly heparinbinding, developmentally regulated cytokine. PTN is a highly conserved protein,Human, mouse, rat, canine, porcine, equine and bovine PTN share 98% aa sequence identity or greater. PTN and midkine share 50% amino acid (aa) sequence identity, share some functions, and constitute a family. During development, PTN is involved in development of brain, bone, and organs undergoing branching morphogenesis. PTN causes PTPRB dimerization and inactivates its phosphatase activity, which allows increased tyrosine phosphorylation of its substrates. Increased expression of PTN is correlated with neuronal development or stresses such as brain ischemia and Parkinson’s disease.
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TMPK-01168 | LOX-1 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
LOX-1 is a transmembrane glycoprotein that binds to and internalizes ox-LDL.LOX-1 gene deletion in mice and anti-LOX-1 therapy has been shown to decrease inflammation, oxidative stress and atherosclerosis. LOX-1 deletion also results in damage from ischemia, making LOX-1 a promising target of therapy for atherosclerosis and related disorders. In this article we focus on the different mechanisms for regulation, signaling and the various effects of LOX-1 in contributing to atherosclerosis.
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TMPJ-01074 | PKCE Protein, Human, Recombinant (His) | Human | E. coli | ||
Protein Kinase C Epsilon type is a member of the serine- and threonine-specific protein kinase family that can be activated by calcium and the second messenger diacylglycerol. Protein Kinase C Epsilon contains these domains: one AGC-kinase C-terminal domain, one C2 domain, one protein kinase domain and two phorbol-ester/DAG-type zinc fingers. Protein Kinase C Epsilon phosphorylate a variety of protein targets and has been identified to participate in diverse cellular signaling pathways. It has many different cellular functions, such as neuron channel activation, apoptosis, cardioprotection from ischemia, heat shock response, as well as insulin exocytosis. Protein Kinase C Epsilon also serves as the receptor for phorbol esters, a class of tumor promoters.
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TMPJ-01022 | SUMO3 Protein, Human, Recombinant (HEK293, His) | Human | Human Cells | ||
Small ubiquitin-like modifier (SUMO), also known as SUMO homologue and SMT3, is a member of the superfamily of ubiquitin-like polypeptides that become covalently attached to various intracellular target proteins as a way to alter their function, location, and/or half-life. Small ubiquitin-like modifiers include SUMO1, SUMO2, SUMO3, and SUMO4. Except for SUMO4, all other SUMOs are ubiquitously expressed, including in the brain. In human, SUMO2 and SUMO3 are two highly homologous proteins, collectively called SUMO2/3. Several studies suggest that SUMO3 are associated with pathogenesis in several neurological diseases, including Alzheimer's disease, Parkinson's disease, and cerebral ischemia/stroke.
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TMPJ-00082 | NGAL/Lipocalin-2 Protein, Mouse, Recombinant (hFc) | Mouse | Human Cells | ||
Lipocalin-2, also known as Neutrophil Gelatinase-Associated Lipocalin (NGAL), is a secretory protein of the lipocalin superfamily. Lipocalin-2 contains a signal peptide that enables it to be secreted and form complexes with matrix metalloproteinase-9 (MMP-9) through disulfide bonds. Similar to other lipocalin family members, Lipocalin-2 is involved in diverse cellular processes, including the transport of small hydrophobic molecules, protection of MMP-9 from proteolytic degradation, and cell signaling. Furthermore, Lipocalin-2 can tightly bind to bacterial siderophore through a cell surface receptor, possibly serving as a potent bacteriostatic agent by sequestering iron, regulating innate immunity and protecting kidney epithelial cells from ischemia–reperfusion injury. This protein is mainly expressed in neutrophils and in lower levels in the kidney, prostate, and epithelia of the respiratory and alimentary tracts.Recent evidence also suggests its role as a biomarker for renal injury and inflammation.
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TMPY-00462 | EPO/Erythropoietin Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
Erythropoietin is a member of the EPO / TPO family. It is a secreted, glycosylated cytokine composed of four alpha helical bundles. Erythropoietin can be found in the plasma and regulates red cell production by promoting erythroid differentiation and initiating hemoglobin synthesis. It also has neuroprotective activity against a variety of potential brain injuries and antiapoptotic functions in several tissue types. Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is produced by kidney or liver of adult mammals and by liver of fetal or neonatal mammals. Genetic variation in erythropoietin is associated with susceptbility to microvascular complications of diabetes type 2. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. It has a longer circulating half-life in vivo. Erythropoietin is being much misused as a performance-enhancing drug in endurance athletes.
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TMPY-02073 | EPO/Erythropoietin Protein, Rat, Recombinant (His) | Rat | Baculovirus-Insect Cells | ||
Erythropoietin is a member of the EPO / TPO family. It is a secreted, glycosylated cytokine composed of four alpha helical bundles. Erythropoietin can be found in the plasma and regulates red cell production by promoting erythroid differentiation and initiating hemoglobin synthesis. It also has neuroprotective activity against a variety of potential brain injuries and antiapoptotic functions in several tissue types. Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is produced by kidney or liver of adult mammals and by liver of fetal or neonatal mammals. Genetic variation in erythropoietin is associated with susceptbility to microvascular complications of diabetes type 2. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. It has a longer circulating half-life in vivo. Erythropoietin is being much misused as a performance-enhancing drug in endurance athletes.
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TMPY-02043 | PARK7/DJ-1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Parkinson's disease locus DJ-1 (PARK7) is a differentially expressed transcript. DJ-1 plays a physiologic role in protection of erythroid cells from oxidant damage, a function unmasked in the context of oxidative stress. PARK7 belongs to the peptidase C56 family of proteins. It acts as a positive regulator of androgen receptor-dependent transcription. It may also function as a redox-sensitive chaperone, as a sensor for oxidative stress, and it apparently protects neurons against oxidative stress and cell death. Mutations in the DJ-1 gene are associated with rare forms of autosomal recessive early-onset Parkinson's disease (PD). DJ-1/p53 interactions contribute to apoptosis resistance in clonal myeloid cells and may serve as a prognostic marker in patients with myelodysplastic syndromes (MDS). DJ-1 regulates redox signaling kinase pathways and acts as a transcriptional regulator of antioxidative gene batteries. Therefore, DJ-1 is an important redox-reactive signaling intermediate controlling oxidative stress after ischemia, upon neuroinflammation, and during age-related neurodegenerative processes. Augmenting DJ-1 activity might provide novel approaches to treating chronic neurodegenerative illnesses such as Parkinson's disease and acute damage such as stroke.
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TMPY-02986 | EPO/Erythropoietin Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Erythropoietin is a member of the EPO / TPO family. It is a secreted, glycosylated cytokine composed of four alpha helical bundles. Erythropoietin can be found in the plasma and regulates red cell production by promoting erythroid differentiation and initiating hemoglobin synthesis. It also has neuroprotective activity against a variety of potential brain injuries and antiapoptotic functions in several tissue types. Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is produced by kidney or liver of adult mammals and by liver of fetal or neonatal mammals. Genetic variation in erythropoietin is associated with susceptbility to microvascular complications of diabetes type 2. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. It has a longer circulating half-life in vivo. Erythropoietin is being much misused as a performance-enhancing drug in endurance athletes.
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TMPY-05837 | IL-1RA Protein, Rat, Recombinant (His) | Rat | E. coli | ||
Interleukin-1 receptor antagonist (IL-1RA) also known as IL1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A), and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses. A polymorphism of this protein-encoding gene is reported to be associated with an increased risk of osteoporotic fractures and gastric cancer. IL-1RA/IL1RN may inhibit the activity of IL-1 by binding to its receptor and it has no IL-1 like activity. Genetic variation in IL-1RA/IL1RN is associated with susceptibility to microvascular complications of diabetes type 4 (MVCD4). These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. Defects in IL-1RA/IL1RN are the cause of interleukin 1 receptor antagonist deficiency (DIRA) which is also known as deficiency of interleukin 1 receptor antagonist. Autoinflammatory diseases manifest inflammation without evidence of infection, high-titer autoantibodies, or autoreactive T-cells. DIRA is a rare, autosomal recessive, genetic autoinflammatory disease that results in sterile multifocal osteomyelitis, and pustulosis from birth.
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TMPY-03081 | IL-1RA Protein, Rat, Recombinant (hFc) | Rat | HEK293 | ||
Interleukin-1 receptor antagonist (IL-1RA) also known as IL1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A), and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses. A polymorphism of this protein-encoding gene is reported to be associated with an increased risk of osteoporotic fractures and gastric cancer. IL-1RA/IL1RN may inhibit the activity of IL-1 by binding to its receptor and it has no IL-1 like activity. Genetic variation in IL-1RA/IL1RN is associated with susceptibility to microvascular complications of diabetes type 4 (MVCD4). These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. Defects in IL-1RA/IL1RN are the cause of interleukin 1 receptor antagonist deficiency (DIRA) which is also known as deficiency of interleukin 1 receptor antagonist. Autoinflammatory diseases manifest inflammation without evidence of infection, high-titer autoantibodies, or autoreactive T-cells. DIRA is a rare, autosomal recessive, genetic autoinflammatory disease that results in sterile multifocal osteomyelitis, and pustulosis from birth.
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TMPY-00913 | S100B Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
S100B is a member of the S100 family of proteins containing two EF-hand-type calcium-binding motifs. S100B exerts both intracellular and extracellular functions. Intracellular S100B acts as a stimulator of cell proliferation and migration and an inhibitor of apoptosis and differentiation, which might have important implications during brain, cartilage and skeletal muscle development and repair, activation of astrocytes in the course of brain damage and neurodegenerative processes, and of cardiomyocyte remodeling after infarction, as well as in melanomagenesis and gliomagenesis. As an extracellular factor, S100B engages RAGE (receptor for advanced glycation end products) in a variety of cell types with different outcomes (i.e. beneficial or detrimental, pro-proliferative or pro-differentiative) depending on the concentration attained by the protein, the cell type and the microenvironment. This calcium binding astrocyte-specific cytokine, presents a marker of astrocytic activation and reflects CNS injury. The excellent sensitivity of S100B has enabled it to confirm the existence of subtle brain injury in patients with mild head trauma, strokes, and after successful resuscitation from cardiopulmonary arrest. Recent findings provide evidence, that S100B may decrease neuronal injury and/or contribute to repair following traumatic brain injury (TBI). Hence, S100B, far from being a negative determinant of outcome, as suggested previously in the human TBI and ischemia literature, is of potential therapeutic value that could improve outcome in patients who sustain various forms of acute brain damage.
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TMPY-03020 | S100B Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
S100B is a member of the S100 family of proteins containing two EF-hand-type calcium-binding motifs. S100B exerts both intracellular and extracellular functions. Intracellular S100B acts as a stimulator of cell proliferation and migration and an inhibitor of apoptosis and differentiation, which might have important implications during brain, cartilage and skeletal muscle development and repair, activation of astrocytes in the course of brain damage and neurodegenerative processes, and of cardiomyocyte remodeling after infarction, as well as in melanomagenesis and gliomagenesis. As an extracellular factor, S100B engages RAGE (receptor for advanced glycation end products) in a variety of cell types with different outcomes (i.e. beneficial or detrimental, pro-proliferative or pro-differentiative) depending on the concentration attained by the protein, the cell type and the microenvironment. This calcium binding astrocyte-specific cytokine, presents a marker of astrocytic activation and reflects CNS injury. The excellent sensitivity of S100B has enabled it to confirm the existence of subtle brain injury in patients with mild head trauma, strokes, and after successful resuscitation from cardiopulmonary arrest. Recent findings provide evidence, that S100B may decrease neuronal injury and/or contribute to repair following traumatic brain injury (TBI). Hence, S100B, far from being a negative determinant of outcome, as suggested previously in the human TBI and ischemia literature, is of potential therapeutic value that could improve outcome in patients who sustain various forms of acute brain damage.
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TMPY-01000 | BVES Protein, Human, Recombinant (GST) | Human | E. coli | ||
Blood vessel epicardial substance (BVES), or POPDC1, is a tight junction-associated transmembrane protein that modulates epithelial-to-mesenchymal transition (EMT) via junctional signaling pathways. BVES plays a protective role both in ulcerative and infectious colitis and identify BVES as a critical protector of colonic mucosal integrity. The Popeye domain containing1, also called Bves (Popdc1/Bves), is a transmembrane protein that functions in muscle regeneration, heart rate regulation, hypoxia tolerance, and ischemia preconditioning. The expression of Popdc1/Bves is elevated in cardiomyocytes maintained in serum free defined medium. Popdc1/Bves plays a role in the preservation of cardiomyocyte viability under serum deficiency through the alteration of Rac1 activity and the regulation of Bnip3 expression by FoxO3 and NFκB transcription factors pointing to Popdc1/Bves as a potential target to enhance heart protection. Blood vessel epicardial substance (BVES) is a tight junction-associated protein that regulates epithelial-mesenchymal states and is underexpressed in epithelial malignancy. Loss of BVES promotes inflammatory tumourigenesis through dysregulation of Wnt signalling and the oncogene c-Myc. BVES promoter methylation status may serve as a CAC biomarker. Blood vessel epicardial substance (BVES/Popdc1) is a junctional-associated transmembrane protein that is underexpressed in a number of malignancies and regulates epithelial-to-mesenchymal transition. BVES is a key regulator of intestinal stem cell programs and mucosal homeostasis.
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TMPY-00852 | IL-1RA Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Interleukin-1 receptor antagonist (IL-1RA) also known as IL1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A), and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses. A polymorphism of this protein-encoding gene is reported to be associated with an increased risk of osteoporotic fractures and gastric cancer. IL-1RA/IL1RN may inhibit the activity of IL-1 by binding to its receptor and it has no IL-1 like activity. Genetic variation in IL-1RA/IL1RN is associated with susceptibility to microvascular complications of diabetes type 4 (MVCD4). These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. Defects in IL-1RA/IL1RN are the cause of interleukin 1 receptor antagonist deficiency (DIRA) which is also known as deficiency of interleukin 1 receptor antagonist. Autoinflammatory diseases manifest inflammation without evidence of infection, high-titer autoantibodies, or autoreactive T-cells. DIRA is a rare, autosomal recessive, genetic autoinflammatory disease that results in sterile multifocal osteomyelitis, and pustulosis from birth.
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TMPY-02531 | S100B Protein, Human, Recombinant (His) | Human | E. coli | ||
S100B is a member of the S100 family of proteins containing two EF-hand-type calcium-binding motifs. S100B exerts both intracellular and extracellular functions. Intracellular S100B acts as a stimulator of cell proliferation and migration and an inhibitor of apoptosis and differentiation, which might have important implications during brain, cartilage and skeletal muscle development and repair, activation of astrocytes in the course of brain damage and neurodegenerative processes, and of cardiomyocyte remodeling after infarction, as well as in melanomagenesis and gliomagenesis. As an extracellular factor, S100B engages RAGE (receptor for advanced glycation end products) in a variety of cell types with different outcomes (i.e. beneficial or detrimental, pro-proliferative or pro-differentiative) depending on the concentration attained by the protein, the cell type and the microenvironment. This calcium binding astrocyte-specific cytokine, presents a marker of astrocytic activation and reflects CNS injury. The excellent sensitivity of S100B has enabled it to confirm the existence of subtle brain injury in patients with mild head trauma, strokes, and after successful resuscitation from cardiopulmonary arrest. Recent findings provide evidence, that S100B may decrease neuronal injury and/or contribute to repair following traumatic brain injury (TBI). Hence, S100B, far from being a negative determinant of outcome, as suggested previously in the human TBI and ischemia literature, is of potential therapeutic value that could improve outcome in patients who sustain various forms of acute brain damage.
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TMPY-05845 | IL-1RA Protein, Cynomolgus, Recombinant (His) | Cynomolgus | E. coli | ||
Interleukin-1 receptor antagonist (IL-1RA) also known as IL1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A), and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses. A polymorphism of this protein-encoding gene is reported to be associated with an increased risk of osteoporotic fractures and gastric cancer. IL-1RA/IL1RN may inhibit the activity of IL-1 by binding to its receptor and it has no IL-1 like activity. Genetic variation in IL-1RA/IL1RN is associated with susceptibility to microvascular complications of diabetes type 4 (MVCD4). These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. Defects in IL-1RA/IL1RN are the cause of interleukin 1 receptor antagonist deficiency (DIRA) which is also known as deficiency of interleukin 1 receptor antagonist. Autoinflammatory diseases manifest inflammation without evidence of infection, high-titer autoantibodies, or autoreactive T-cells. DIRA is a rare, autosomal recessive, genetic autoinflammatory disease that results in sterile multifocal osteomyelitis, and pustulosis from birth.
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TMPY-03998 | ANGPTL2 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
The angiopoietin-like protein (ANGPTL) family is homologous to angiopoietins but does not bind to the Tie2 receptor. The function of ANGPTLs has been elucidated largely in the context of angiogenesis and lipid metabolism. Morinaga et al. demonstrated that genetic depletion of Angptl2 confers amelioration of the mouse kidney fibrosis induced by a unilateral ureteral obstruction, implicating that ANGPTL2, predominantly in the renal tubular compartments, activates the transforming growth factor-β signaling and vice versa through miR-221. Angiopoietin-like protein 2 (ANGPTL2) maintains tissue homeostasis by inducing inflammation and angiogenesis. It is produced in infiltrating immune cells or resident cells, such as adipocytes, vascular endothelial cells, and tumor cells. The classic sequential cascade of P. gingivalis LPS → inflammatory cytokine induction is well established. However, in the current study, we reveal a novel cascade comprising sequential P. gingivalis LPS → ANGPTL2 → integrin α5β1 → inflammatory cytokine induction, which might be responsible for inducing potent periodontal disorganization activity in gingival epithelial cells. Via this pathway, ANGPTL2 functions in the pathogenesis of periodontitis and contributes to prolonging chronic inflammation in patients with systemic disease. That MAC-3-positive immune cells, including infiltrating bone marrow-derived macrophages and activated microglia, express abundant angiopoietin-like protein (ANGPTL) 2 in ischemic mouse brain in a transient middle cerebral artery occlusion (MCAO) model. Both neurological deficits and infarct volume decreased in transient MCAO model mice established in Angptl2 knockout (KO) relative to wild-type mice. Acute brain inflammation after ischemia-reperfusion, as estimated by expression levels of pro-inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor alpha (TNF)-α, was significantly suppressed in Angptl2 KO compared to control mice.
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TMPY-04408 | CAMKII beta/CAMK2B Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
Calcium/calmodulin-dependent protein kinase II beta (CAMK2B) is a member of the serine/threonine protein kinase family and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. CaMKII is an important player in prostate cancer cells ability to escape apoptosis under androgen ablation and facilitate the progression of prostate cancer cells to an androgen independent state. As a multifunctional protein kinase, the loss of activity may play a critical role in initiating the changes leading to ischemia-induced cell death. CaMKII are found to be important for the functions of immune cells. CaMKII can be activated by TLR ligands, and in turn promotes both myeloid differentiating factor 88 and Toll/IL-1 receptor domain-containing adaptor protein-inducing IFN-beta-dependent inflammatory responses by directly activating TAK1 and IRF3. CAMKII has four subunit isoforms (alpha, beta, gamma, delta). It is possible that distinct isoforms of this chain have different cellular localizations and interact differently with calmodulin. The alpha- and beta-isoforms have narrow distributions restricted mainly to neuronal tissues, but the gamma- and delta-isoforms are ubiquitously expressed within neuronal and non-neuronal tissues. CAMK2B is important for controlling the direction of plasticity at the parallel fiber-Purkinje cell synapse. CaMK2 is involved in neuronal survival through the reorganization of the neuroarchitecture and that the regulation of this role is controlled at the level of gene expression. Because CaMK2B influences the expression of many neuroreceptors and influences neural outgrowth and pruning, its altered expression in the cerebral cortex in schizophrenia or depression may contribute to schizophrenia and depression.
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TMPH-01045 | CEACAM1 Protein, Human, Recombinant | Human | E. coli | ||
Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Plays a role as coinhibitory receptor in immune response, insulin action and functions also as an activator during angiogenesis. Its coinhibitory receptor function is phosphorylation- and PTPN6 -dependent, which in turn, suppress signal transduction of associated receptors by dephosphorylation of their downstream effectors. Plays a role in immune response, of T cells, natural killer (NK) and neutrophils. Upon TCR/CD3 complex stimulation, inhibits TCR-mediated cytotoxicity by blocking granule exocytosis by mediating homophilic binding to adjacent cells, allowing interaction with and phosphorylation by LCK and interaction with the TCR/CD3 complex which recruits PTPN6 resulting in dephosphorylation of CD247 and ZAP70. Also inhibits T cell proliferation and cytokine production through inhibition of JNK cascade and plays a crucial role in regulating autoimmunity and anti-tumor immunity by inhibiting T cell through its interaction with HAVCR2. Upon natural killer (NK) cells activation, inhibit KLRK1-mediated cytolysis of CEACAM1-bearing tumor cells by trans-homophilic interactions with CEACAM1 on the target cell and lead to cis-interaction between CEACAM1 and KLRK1, allowing PTPN6 recruitment and then VAV1 dephosphorylation. Upon neutrophils activation negatively regulates IL1B production by recruiting PTPN6 to a SYK-TLR4-CEACAM1 complex, that dephosphorylates SYK, reducing the production of reactive oxygen species (ROS) and lysosome disruption, which in turn, reduces the activity of the inflammasome. Downregulates neutrophil production by acting as a coinhibitory receptor for CSF3R by downregulating the CSF3R-STAT3 pathway through recruitment of PTPN6 that dephosphorylates CSF3R. Also regulates insulin action by promoting INS clearance and regulating lipogenesis in liver through regulating insulin signaling. Upon INS stimulation, undergoes phosphorylation by INSR leading to INS clearance by increasing receptor-mediated insulin endocytosis. This inernalization promotes interaction with FASN leading to receptor-mediated insulin degradation and to reduction of FASN activity leading to negative regulation of fatty acid synthesis. INSR-mediated phosphorylation also provokes a down-regulation of cell proliferation through SHC1 interaction resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 and phosphatidylinositol 3-kinase pathways. Functions as activator in angiogenesis by promoting blood vessel remodeling through endothelial cell differentiation and migration and in arteriogenesis by increasing the number of collateral arteries and collateral vessel calibers after ischemia. Also regulates vascular permeability through the VEGFR2 signaling pathway resulting in control of nitric oxide production. Downregulates cell growth in response to EGF through its interaction with SHC1 that mediates interaction with EGFR resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 pathway. Negatively regulates platelet aggregation by decreasing platelet adhesion on type I collagen through the GPVI-FcRgamma complex. Inhibits cell migration and cell scattering through interaction with FLNA; interfers with the interaction of FLNA with RALA. Mediates bile acid transport activity in a phosphorylation dependent manner. Negatively regulates osteoclastogenesis.; Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Promotes populations of T cells regulating IgA production and secretion associated with control of the commensal microbiota and resistance to enteropathogens.
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TMPH-01044 | CEACAM1 Protein, Human, Recombinant (His & Myc & SUMO) | Human | E. coli | ||
Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Plays a role as coinhibitory receptor in immune response, insulin action and functions also as an activator during angiogenesis. Its coinhibitory receptor function is phosphorylation- and PTPN6 -dependent, which in turn, suppress signal transduction of associated receptors by dephosphorylation of their downstream effectors. Plays a role in immune response, of T cells, natural killer (NK) and neutrophils. Upon TCR/CD3 complex stimulation, inhibits TCR-mediated cytotoxicity by blocking granule exocytosis by mediating homophilic binding to adjacent cells, allowing interaction with and phosphorylation by LCK and interaction with the TCR/CD3 complex which recruits PTPN6 resulting in dephosphorylation of CD247 and ZAP70. Also inhibits T cell proliferation and cytokine production through inhibition of JNK cascade and plays a crucial role in regulating autoimmunity and anti-tumor immunity by inhibiting T cell through its interaction with HAVCR2. Upon natural killer (NK) cells activation, inhibit KLRK1-mediated cytolysis of CEACAM1-bearing tumor cells by trans-homophilic interactions with CEACAM1 on the target cell and lead to cis-interaction between CEACAM1 and KLRK1, allowing PTPN6 recruitment and then VAV1 dephosphorylation. Upon neutrophils activation negatively regulates IL1B production by recruiting PTPN6 to a SYK-TLR4-CEACAM1 complex, that dephosphorylates SYK, reducing the production of reactive oxygen species (ROS) and lysosome disruption, which in turn, reduces the activity of the inflammasome. Downregulates neutrophil production by acting as a coinhibitory receptor for CSF3R by downregulating the CSF3R-STAT3 pathway through recruitment of PTPN6 that dephosphorylates CSF3R. Also regulates insulin action by promoting INS clearance and regulating lipogenesis in liver through regulating insulin signaling. Upon INS stimulation, undergoes phosphorylation by INSR leading to INS clearance by increasing receptor-mediated insulin endocytosis. This inernalization promotes interaction with FASN leading to receptor-mediated insulin degradation and to reduction of FASN activity leading to negative regulation of fatty acid synthesis. INSR-mediated phosphorylation also provokes a down-regulation of cell proliferation through SHC1 interaction resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 and phosphatidylinositol 3-kinase pathways. Functions as activator in angiogenesis by promoting blood vessel remodeling through endothelial cell differentiation and migration and in arteriogenesis by increasing the number of collateral arteries and collateral vessel calibers after ischemia. Also regulates vascular permeability through the VEGFR2 signaling pathway resulting in control of nitric oxide production. Downregulates cell growth in response to EGF through its interaction with SHC1 that mediates interaction with EGFR resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 pathway. Negatively regulates platelet aggregation by decreasing platelet adhesion on type I collagen through the GPVI-FcRgamma complex. Inhibits cell migration and cell scattering through interaction with FLNA; interfers with the interaction of FLNA with RALA. Mediates bile acid transport activity in a phosphorylation dependent manner. Negatively regulates osteoclastogenesis.; Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Promotes populations of T cells regulating IgA production and secretion associated with control of the commensal microbiota and resistance to enteropathogens.
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