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Transforming growth factor beta 1 induces apoptosis through cleavage of BAD in a Smad3-dependent mechanism in FaO hepatoma cells.

Authors
Kim, BC; Mamura, M; Choi, KS; Calabretta, B; Kim, SJ
Citation
Molecular and cellular biology, 22(5):1369-1378, 2002
Journal Title
Molecular and cellular biology
ISSN
0270-73061098-5549
Abstract
Transforming growth factor beta (TGF-beta) induces apoptosis in a variety of cells. We have previously shown that TGF-beta 1 rapidly induces apoptosis in the FaO rat hepatoma cell line. We have now studied the effect of TGF-beta 1 on the expression of different members of the Bcl-2 family in these cells. We observed no detectable changes in the steady-state levels of Bcl-2, Bcl-X(L), and Bax. However, TGF-beta 1 induced caspase-dependent cleavage of BAD at its N terminus to generate a 15-kDa truncated protein. Overexpression of the 15-kDa truncated BAD protein enhanced TGF-beta 1-induced apoptosis, whereas a mutant BAD resistant to caspase 3 cleavage blocked TGF-beta 1-induced apoptosis. Overexpression of Smad3 dramatically enhanced TGF-beta 1-induced cleavage of BAD and apoptosis, whereas antisense Smad3 blocked TGF-beta 1-induced apoptosis and BAD cleavage. These results suggest that TGF-beta 1 induces apoptosis through the cleavage of BAD in a Smad3-dependent mechanism.
MeSH terms
Animals*ApoptosisCarcinoma, Hepatocellular/metabolismCarrier Proteins/genetics/*metabolismDNA-Binding Proteins/*metabolismLiver Neoplasms/metabolismProto-Oncogene Proteins c-bcl-2/genetics/*metabolismRatsSmad3 ProteinTrans-Activators/*metabolismTransforming Growth Factor beta/*pharmacologyTransforming Growth Factor beta1Tumor Cells, Culturedbcl-Associated Death Protein
PMID
11839804
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
최, 경숙
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