Abstract:
:Apoptotic protease activating factor-1 (Apaf-1) is an adaptor molecule essential for caspase-9 activation. Subcellular analysis of Apaf-1 in NIH-3T3 fibroblasts and the immature murine B cell lymphoma WEHI-231 indicates that Apaf-1 is localized in the Golgi apparatus and cytoplasm. Bcl-2 overexpression in WEHI-231 cells disrupts Apaf-1 localization in Golgi, causing a perinuclear Apaf-1 redistribution. Bcl-2 overexpression in NIH-3T3 fibroblasts however does not cause similar Apaf-1 redistribution, suggesting that cell type factors are involved in the redistribution process. The ability of Bcl-2 to modify Apaf-1 subcellular localization is not explained by direct interaction between Apaf-1 and Bcl-2. These data may help to clarify the anti-apoptotic Bcl-2 function.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Ruiz-Vela A,Albar JP,Martínez CAdoi
10.1016/s0014-5793(01)02629-1keywords:
subject
Has Abstractpub_date
2001-07-13 00:00:00pages
79-83issue
1eissn
0014-5793issn
1873-3468pii
S0014579301026291journal_volume
501pub_type
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