| pubmed-article:11494146 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11494146 | lifeskim:mentions | umls-concept:C0205169 | lld:lifeskim |
| pubmed-article:11494146 | lifeskim:mentions | umls-concept:C1517342 | lld:lifeskim |
| pubmed-article:11494146 | lifeskim:mentions | umls-concept:C1366450 | lld:lifeskim |
| pubmed-article:11494146 | lifeskim:mentions | umls-concept:C1512424 | lld:lifeskim |
| pubmed-article:11494146 | lifeskim:mentions | umls-concept:C0741847 | lld:lifeskim |
| pubmed-article:11494146 | lifeskim:mentions | umls-concept:C0181586 | lld:lifeskim |
| pubmed-article:11494146 | pubmed:issue | 33 | lld:pubmed |
| pubmed-article:11494146 | pubmed:dateCreated | 2001-8-8 | lld:pubmed |
| pubmed-article:11494146 | pubmed:abstractText | The pro-apoptotic molecule BAD binds BCL-[X(L)] or BCL2 and inactivates their survival function. In addition to their anti-apoptotic function, BCL2 and BCL-[X(L)] also delay cell cycle entry from quiescence. We found that the BH3-only molecule BAD also exerted a cell cycle effect. BAD expression resulted in failure to cell cycle block in growth arrest conditions. In low serum and in confluence, fibroblasts constitutively or inducibly expressing BAD persisted in S phase, continued to incorporate BrdU, and exhibited sustained cyclin E/cdk2 activity. Mutation analysis indicated that the cell cycle effect of BAD was not dependent on its phosphorylation status or subcellular localization, but strictly co-segregated with BCL-[X(L)] binding. bclx(-/-) MEFs expressing BAD and bad(-/-) MEFs both arrested in G0/G1 in low serum similar to wild-type controls, suggesting that the ability to overcome the G0/G1 checkpoint resulted from the presence of BAD/BCL-x(L) heterodimers, rather than the absence of BCL-[X(L)] or BAD. These data provide evidence that in addition to regulating apoptosis, the BAD/BCL-[X(L)] heterodimer has a novel cell cycle function. | lld:pubmed |
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| pubmed-article:11494146 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11494146 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11494146 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11494146 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:11494146 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:11494146 | pubmed:author | pubmed-author:YanoMM | lld:pubmed |
| pubmed-article:11494146 | pubmed:author | pubmed-author:Chattopadhyay... | lld:pubmed |
| pubmed-article:11494146 | pubmed:author | pubmed-author:ChiangC WCW | lld:pubmed |
| pubmed-article:11494146 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11494146 | pubmed:day | 27 | lld:pubmed |
| pubmed-article:11494146 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:11494146 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11494146 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11494146 | pubmed:pagination | 4507-18 | lld:pubmed |
| pubmed-article:11494146 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11494146 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11494146 | pubmed:articleTitle | BAD/BCL-[X(L)] heterodimerization leads to bypass of G0/G1 arrest. | lld:pubmed |
| pubmed-article:11494146 | pubmed:affiliation | Department of Pediatrics, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. | lld:pubmed |
| pubmed-article:11494146 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11494146 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11494146 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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