关于TNFSF15: Tumor Necrosis Factor Ligand Superfamily Member 15 (TNFSF15) is a new member of the tumor necrosis factor family. TNFSF15 is predominantly an endothelial cell-specific gene, and recombinant TNFSF15 is a potent inhibitor of endothelial cell proliferation, angiogenesis and tumor growth. TNFSF15 exerts two activities on endothelial cells: early G1 arrest of G0/G1-cells responding to growth stimuli and programmed cell death of proliferating cells. These activities are highly specific to endothelial cells. TNFSF15 is also able to regulate the expression of several important genes involved in angiogenesis. These findings are consistent with the view that TNFSF15 functions as an autocrine cytokine to inhibit angiogenesis and stabilize the vasculature.
·重组人羧肽酶M(CPM) 编号:JN1767 英文名称:Recombinant Human Carboxypeptidase M 规格:10μg|50μg|500μg|1mg 本品由我们的哺乳动物细胞表达系统制备而成,目的基因编码的Leu18-His422在C端含有His标签。
CPM质量控制:>95%(还原性SDS-PAGE)
CPM制剂:液体
CPM保存:收到货后请置于-20℃,可保存6个月,避免反复冻融。
关于CPM: Carboxypeptidase M (CPM) specifically removes C-terminal basic residues (Arg or Lys) from peptides and proteins. Carboxypeptidase exert roles in the physiological processes of blood coagulation/fibrinolysis, inflammation, food digestion and pro-hormone and neuropeptide processing. CPM is believed to play important roles in the control of peptide hormone and growth factor activity at the cell surface, and in the membrane-localized degradation of extracellular proteins. It is widely distributed in a variety of tissues and cells. CPM is involved in peptide metabolism on both the cell surface and in extracellular fluids. CPM functions not only as a protease but also as a binding partner in cell-surface protein-protein interactions.
关于CDKN2C: Cyclin-Dependent Kinase 4 Inhibitor C (CDKN2C) is a member of the INK4 family of cyclin dependent kinase inhibitors. CDKN2C contains 4 ANK repeats and interacts with CDK4 or CDK6. Highest levels of CDKN2C can be found in skeletal muscle, pancreas, and heart. CDKN2C inhibits cell growth and proliferation with a correlated dependence on endogenous retinoblastoma protein RB and prevent the activation of the CDK kinases. Studies have been shown the roles of CDKN2C gene in regulating spermatogenesis, as well as in suppressing tumorigenesis.