Transforming growth factor-β1 suppresses serum deprivation-induced apop-tosis via activation of ERK1/ERK2 and the inhibition of p38 activity and ceramide production  

作　　者：HEHUACHEN SHENGZHAO 等 

机构地区：[1]LaboratoryofMolecularCellBiology,InstituteofBiochemistryandCellBiology,ShanghaiInstitutesforBiologicalSciences,ChineseAcademyofSciences,320,Yue－YangRoad,Shanghai200031,China [2]LaboratoryofMolecularCellB

出　　处：《Cell Research》2002年第3期298-298,共1页细胞研究（英文版）

摘　　要：In this report we studied the effects and mechanism of transforming growth factor-β1 (TGF-β1) on serum deprivation-induced cell apoptosis. Serum deprivation induces apoptosis, which is associated with an increase in intracellular ceramide level and with the activation of p38 mitogen-activated protein (MAP) kinase. Inhibition of p38 MAP kinase by SB203580 significantly reduced apoptosis induced by serum-deprivation. Treatment of cells with TGF-β1 stimulated cell proliferation and suppressed the serum deprivation-induced apoptotic response. The anti-apoptotic effect of TGF-β1 is correlated with its ability to inhibit the serum deprivation-induced activation of p38 MAP kinase and the increase in intracellular ceramide level.

关 键 词：转化生长因子-β1 失血清诱发凋亡 抑制作用 ERK1/ERK2 活化 p38活性抑制 神经酰胺生成量 

分 类 号：Q25[生物学—细胞生物学] Q266