Cho, Hee Jun Park, Sun-Mi Hwang, Eun Mi Baek, Kyoung Eun Kim, In-Kyu Nam, In-Koo Im, Min-Ju Park, Seung-Ho Bae, Seran Park, Jae-Yong Yoo, Jiyun 2024-01-20T18:34:52Z 2024-01-20T18:34:52Z 2021-09-05 2010-08-13 0021-9258 https://pubs.kist.re.kr/handle/201004/131177 Gadd45b has been known as a positive mediator of apoptosis induced by certain cytokines and oncogenes. Here, we identified Gadd45b as an effector of Fas-induced apoptosis and found that p38-mediated Rb hyperphosphorylation is one of the mechanisms of Fas-induced apoptosis in murine hepatocyte AML12 cells. Gadd45b has been shown to activate p38 through its physical interaction with MTK1 and induce apoptosis. However, in this study, we have showed that the function of Gadd45b during Fas-induced apoptosis in AML12 cells is different from that reported in previous studies. Depletion of Gadd45b expression did not inhibit the phosphorylation of p38, but it suppressed p38-mediated Rb phosphorylation and apoptosis in response to Fas stimulation by reducing the interaction between p38 and Rb. Ectopic expression of Gadd45b was sufficient to enhance this interaction. These findings suggest that Gadd45b mediates p38-induced Rb phosphorylation by enhancing the interaction between p38 and Rb during Fas-induced apoptosis in murine hepatocytes. English AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC SIGNAL-TRANSDUCTION KINASE-ACTIVITY PROTEIN ACTIVATION CELLS MTK1/MEKK4 EXPRESSION GADD45A-DEFICIENT RADIATION PATHWAY Gadd45b Mediates Fas-induced Apoptosis by Enhancing the Interaction between p38 and Retinoblastoma Tumor Suppressor Article 10.1074/jbc.M109.091413 1 JOURNAL OF BIOLOGICAL CHEMISTRY, v.285, no.33, pp.25500 - 25505 JOURNAL OF BIOLOGICAL CHEMISTRY 285 33 25500 25505 scie scopus 000280682400043 2-s2.0-77955499212 Biochemistry & Molecular Biology Biochemistry & Molecular Biology Article SIGNAL-TRANSDUCTION KINASE-ACTIVITY PROTEIN ACTIVATION CELLS MTK1/MEKK4 EXPRESSION GADD45A-DEFICIENT RADIATION PATHWAY