目录号 | 产品详情 | 靶点 | |
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T5S1632 | VEGFR TNF NF-κB Akt Caspase | ||
Barlerin (8-O-Acetylshanzhiside methyl ester) 是一种环孢菌素葡萄糖苷,从中国西藏民间药用植物中分离得到,能够抑制NF-κB 活性。 | |||
T2S0500 | Others | ||
Ilexsaponin A (Ilexsaponin A1)1 是分离自冬凌草的根中,利用抗凋亡途径减轻缺血再灌注引起的心肌损伤。它能够减少心肌梗塞的大小,减少 LDH,AST 和 CK-MB 的血清水平,促进细胞活力并抑制缺氧/复氧心肌细胞的凋亡。 | |||
T3597 | Sigma receptor | ||
Cutamesine dihydrochloride (SA4503 dihydrochloride) 是一种选择性 σ1 受体激动剂,IC50值为 17.4 nM。 | |||
T0988 | Autophagy Fatty Acid Synthase | ||
Trimetazidine dihydrochloride (Vastarel F) 是细胞保护性抗缺血剂,也用作缺血性心脏病或心绞痛的血管扩张剂,具有抗氧化,抗炎,抗伤害和胃保护作用。它可通过抑制脂肪酸代谢提高心肌葡萄糖利用率。 | |||
TP2279L | GHSR | ||
Obestatin (rat) acetate 是 G 蛋白偶联受体 39 (GPR39) 的内源性配体。它具有抗炎、抗心肌梗塞和抗氧化特性。 它抑制食物摄入,抑制空肠收缩,并减少体重增加。 | |||
T9180 | Adenosine Receptor | ||
LUF6096 (CF-602) 是一种有效的腺苷 A3 受体 (adenosine A3 receptor) 变构增强剂。LUF6096 对任何腺苷受体显示出低正构亲和力。LUF6096 在心肌缺血/再灌注损伤中显示出保护作用。 | |||
T3920 | Others Endogenous Metabolite | ||
Pseudoginsenoside F11 (Ginsenoside A1) 从人参根和叶中分离得到。PF11在一系列心血管和中枢神经系统疾病中具有广泛的保护作用。 | |||
T5S2178 | Adrenergic Receptor | ||
Fargesin ((+/-)-Fargesin) 是一种活性新木脂素,从木兰植物中分离得到,具有抗高血压和抗炎活性。 | |||
T20563 | MMP | ||
PD-166793是一种具有口服活性、有效性和选择性的 MMP 抑制剂,对 MMP-2,MMP-3 和 MMP-13 具有抑制作用。PD-166793 在大鼠心力衰竭模型中改善心肌缺血和再灌注损伤。 | |||
T6633 | Calcium Channel Sodium Channel | ||
Ranolazine (RS 43285-003) 具有抗心绞痛和抗缺血的功效,通过抑制内向钠电流的后期作用 (对INa 和IKr 的IC50值分别为 6 μM 和 12 μM) 发挥作用,而不会影响心率或血压。Ranolazine 还是脂肪酸氧化 (FAO) 的部分抑制剂。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-05004 | FGF-4 Protein, Human, Recombinant | Human | E. coli | ||
FGF (fibroblast growth factor) signalling is known to be required for many aspects of mesoderm formation and patterning during Xenopus development and has been implicated in regulating genes required for the specification of both blood and skeletal muscle lineages. Fibroblast growth factor 4 (FGF4) signaling induces differentiation from embryonic stem cells (ESCs) via the phosphorylation of downstream molecules such as mitogen-activated protein kinase/extracellular signal-related kinase (MEK) and extracellular signal-related kinase 1/2 (ERK1/2). Fibroblast Growth Factor 4 (FGF-4) could not only increase the proliferation of bone marrow mesenchymal stem cells (BMSCs), but also induce BMSCs into hepatocyte-like cells in vitro. FGF4 transduced BMSCs contributed to liver regeneration might by the transplanted microenvironment. The FGF4-bFGF BMSCs thus can enhance the survival of the transplanted cells, diminish myocardial fibrosis, promote myocardial angiogenesis, and improve cardiac functions.
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TMPY-00545 | Dermcidin Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Hepatocellular carcinoma (HCC) is a major contributor to cancer-related deaths due to its often late stage diagnosis, and dermcidin (DCD) may have the potential to be used as a serum biomarker for HCC for more timely diagnoses. Human dermcidin (DCD) is an antimicrobial peptide secreted constitutively by sweat glands. And the role of DCD in ischemic heart disease has drawn increasing attention in particular its relationship with insulin secretion and glycemic control, nitric oxide (NO) synthesis and hypertension, platelet aggregation and acute myocardial infarction (AMI).
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TMPY-00369 | LY6D Protein, Human, Recombinant (mFc) | Human | HEK293 Cells | ||
LY6D (Lymphocyte Antigen 6 Family Member D) is a Protein Coding gene. It may act as a specification marker at the earliest stage specification of lymphocytes between B- and T-cell development. Marks the earliest stage of B-cell specification. The expression of LY6D is induced in MCF10A cells by X-ray irradiation. The induction of LY6D expression is triggered through a pathway regulated by ATM, CHK2, and p53. This method is a new Ab-directed proteomic strategy for the analysis of membrane proteins and applies to various biological phenomena in situations in which both target molecule-expressing cells and nonexpressing cells are available. Diseases associated with LY6D include Alzheimer's Disease 16 and Inferior Myocardial Infarction.
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TMPK-01229 | IL-19 Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Interleukin-19 (IL-19) has been shown to be involved in coronary artery diseases and atherosclerosis, while its expression in myocardial infarction is poorly understood. In this study, the dynamic increase in circulating IL-19 in acute ST-segment elevation myocardial infarction (STEMI) patients was detected.IL-19 is correlated with the severity of acute myocardial infarction, which may be a new idea for the clinical treatment of myocardial infarction.
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TMPH-01595 | KMO Protein, Human, Recombinant (His) | Human | E. coli | ||
Catalyzes the hydroxylation of L-kynurenine (L-Kyn) to form 3-hydroxy-L-kynurenine (L-3OHKyn). Required for synthesis of quinolinic acid, a neurotoxic NMDA receptor antagonist and potential endogenous inhibitor of NMDA receptor signaling in axonal targeting, synaptogenesis and apoptosis during brain development. Quinolinic acid may also affect NMDA receptor signaling in pancreatic beta cells, osteoblasts, myocardial cells, and the gastrointestinal tract (Probable).
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TMPY-01481 | FLAP Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Arachidonate 5-Lipoxygenase-Activating Protein (ALOX5AP), also known as FLAP, belongs to the MAPEG family. ALOX5AP/FLAP is an essential partner of 5-LO for this process. The FLAP (ALOX5AP) gene has been linked to risk for myocardial infarction, stroke and restenosis, reigniting pharmaceutical interest in this target. It had been found that ALOX5AP/FLAP is a key enzyme in leukotriene formation, in both human pulmonary microvascular endothelial cells and a transformed human brain endothelial cell line. In addition, the protein FLAP has recently been identified as an emerging target in metabolic disease. In fact, FLAP is overexpressed in the adipose tissue of patients and experimental animals with obesity.
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TMPJ-00091 | G-CSF Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Granulocyte colony-stimulating factor (G-CSF) is a growth factor and an essential cytokine which belongs to the IL-6 superfamily. Granulocyte/macrophage colony-stimulating factors are cytokines that act in hematopoiesis by controlling the production, differentiation, and function of 2 related white cell populations of the blood, the granulocytes and the monocytes-macrophages. G-CSF binding to its receptor G-CSF-R which belongs to the cytokine receptor type I family depends on the interaction of alpha-helical motifs of the former and two fibronectin type III as well as an immunoglobulin-like domain of the latter. G-CSF is a cytokine that have been demonstrated to improve cardiac function and perfusion in myocardial infarction. And it was initially evaluated as a stem cell mobilizer and erythropoietin as a cytoprotective agent.
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TMPJ-00402 | CD117 Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
C-Kit/SCF R is a type 3 transmembrane receptor for MGF (mast cell growth factor, also known as stem cell factor). c-Kit contains 5 Ig-like C2-type (immunoglobulin-like) domains and 1 protein kinase domain. It belongs to the protein kinase superfamily and CSF-1/PDGF receptor subfamily. SCF R expression on mast cells enables them to infiltrate SCF-secreting tumors where they promote tumor growth and induce local immune suppression. SCF R is up-regulated on dendritic cells by Th2-orTh17-biasing stimuli, and it is required for subsequent dendritic cell induction of Th2 and Th17 responses. SCF R protects vascular smooth muscle cells from apoptosis and assists in the recovery of cardiac function following myocardial infarction.
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TMPJ-00362 | MMP-2 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
72 kDa type IV collagenase also known as matrix metalloproteinase-2 (MMP-2) and gelatinase A is an enzyme that in humans is encoded by the MMP2 gene.It belongs to the matrix metalloproteinase (MMP) family. Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade components of the extracellular matrix (ECM) and play essential roles in various physiological processes such as morphogenesis, differentiation, angiogenesis and tissue remodeling, as well as pathological processes including inflammation, arthritis, cardiovascular diseases, pulmonary diseases and tumor invasion. MMP-2 is ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, atherosclerotic plaque rupture, as well as degrading extracellular matrix proteins. MMP-2 can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. MMP-2 cleaves KISS at a Gly-|-Leu bond and appears to have a role in myocardial cell death pathways.
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TMPJ-00785 | FABP3 Protein, Human, Recombinant (His) | Human | E. coli | ||
Fatty Acid Binding Protein 3 (FABP3) is a small cytoplasmic protein (15 kDa) that is released from cardiac myocytes following an ischemic episode. Like the nine other distinct FABPs that have been identified, FABP3 is involved in active fatty acid metabolism where it transports fatty acids from the cell membrane to mitochondria for oxidation. FABPs are divided into at least three distinct types, namely the hepatic-, intestinal- and cardiac-types. They form 14-15 kDa proteins and are thought to participate in the uptake, intracellular metabolism and/or transport of long-chain fatty acids. They may also be responsible in the modulation of cell growth and proliferation. The FABP3 gene contains four exons and its function is to arrest growth of mammary epithelial cells. This gene is also a candidate tumor suppressor gene for human breast cancer. FABP3 is a sensitive biomarker for myocardial infarction and can be detected in the blood within one to three hours of onset of pain.
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TMPY-04387 | AKT2 Protein, Human, Recombinant (His & GST) | Human | Baculovirus Insect Cells | ||
AKT (AK mouse plus Transforming or Thymoma) is a frequent oncogene expressed in most tissues which includes three isoforms AKT1, AKT2, and AKT3. Hyperactivation of AKT signaling is a central key in many human cancer progressions, through modulating angiogenesis, tumor growth, and cell migration, invasion, metastasis, and chemoresistance. Among all three isoforms, AKT2 is most related to cancer cell invasion, metastasis, and survival. Amplification and overexpression of AKT2 have been shown in many cancers. Accumulating evidence shows the potential role of different miRNA involvements in cancer progression by activating or suppressing AKT2 expression. The AKT2/NAB1/SPK1 pathway is a novel regulating factor of macrophage migration and cardiac remodeling after myocardial infarction. The novel mechanism of the AKT2-PKM2-STAT3/NF-kappaB axis in the regulation of ovarian cancer progression, that both AKT2 and PKM2 may be potential targets for the treatment of ovarian cancer. AKT1 and AKT2, the AKT isoforms that are highly expressed in skeletal muscle, have distinct and overlapping functions, with AKT2 more important for insulin-stimulated glucose metabolism. In adipocytes, AKT2 versus AKT1 has greater susceptibility for insulin-mediated redistribution from cytosolic to membrane localization, and insulin also causes subcellular redistribution of AKT Substrate of 160 kDa (AS160), an AKT2 substrate and crucial mediator of insulin-stimulated glucose transport.
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TMPJ-00952 | CXCL12 Protein, Mouse, Recombinant | Mouse | E. coli | ||
Mouse Cxcl12 is a secreted and highly conserved protein which belongs to the intercrine alpha (chemokine CxC) family.CXCL12 is widely expressed in various organs including brain, kidney, skeletal muscle, heart, liver, and lymphoid organs. Cxcl12 activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis. It also binds to atypical chemokine receptor ACKR3 which activates the beta-arrestin pathway and acts as a scavenger receptor for SDF-1. Cxcl12 has several critical functions during embryonic development such as B-cell lymphopoiesis, myelopoiesis in bone marrow and heart ventricular septum formation. Cxcl12 plays an important role in acting as a positive regulator of monocyte migration and a negative regulator of monocyte adhesion via the LYN kinase. It stimulates migration of monocytes and T-lymphocytes through its receptors, CXCR4 and ACKR3, and decreases monocyte adherence to surfaces coated with ICAM-1, a ligand for beta-2 integrins. SDF1A/CXCR4 signaling axis inhibits beta-2 integrin LFA-1 mediated adhesion of monocytes to ICAM-1 through LYN kinase. It also plays a protective role after myocardial infarction, induces down-regulation and internalization of ACKR3 expressed in various cells and stimulates the proliferation of bone marrow-derived b progenitor cells in the presence of IL-7 as well as growth of the stromal cell-dependent B-cell clone DW34 cells.
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TMPY-00681 | BMP-5 Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Bone Morphogenetic Protein 5 (BMP-5) is a member of the structurally and functionally related bone morphogenetic proteins (BMPs) which constitute a novel subfamily of the transforming growth factor β (TGF-β) superfamily. In agreement with a possible role in the control of cell death, BMP-5 exhibited a regulated pattern of expression in the interdigital tissue. Transcripts of BMP-5 and BMP-5 protein were abundant within the cytoplasm of the fragmenting apoptotic interdigital cells in a way suggesting that delivery of BMPs into the tissue is potentiated during apoptosis. Gain-of-function experiments demonstrated that BMP-5 has the same effect as other interdigital BMPs inducing apoptosis in the undifferentiated mesoderm and growth in the prechondrogenic mesenchyme. BMP-5 is a member of the 60A subgroup of BMPs, other members of which have been shown to stimulate dendritic growth in central and peripheral neurons. The signaling pathway that mediates the dendrite-promoting activity of BMP-5 may involve binding to BMPR-IA and activation of Smad-1, and relative levels of BMP antagonists such as noggin and follistatin may modulate BMP-5 signaling. Since BMP-5 is expressed at relatively high levels not only in the developing but also the adult nervous system, these findings suggest the possibility that BMP-5 regulates dendritic morphology not only in the developing but also the adult nervous system. BMP-5 may play important roles not only in myocardial differentiation but also in the formation and maintenance of endocardial cushion tissue. Additionally, a high expression level of BMP-5 has been detected in certain tumors of mesenchymal origin.
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