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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1999-4-20
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pubmed:abstractText |
Bcl-2-family proteins are key regulators of the apoptotic response. Here, we demonstrate that the pro-survival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-kappaB. We show that bfl-1 gene expression is dependent on NF-kappaB activity and that it can substitute for NF-kappaB to suppress TNFalpha-induced apoptosis. bfl-1 promoter analysis identified an NF-kappaB site responsible for its Rel/NF-kappaB-dependent induction. The expression of bfl-1 in immune tissues supports the protective role of NF-kappaB in the immune system. The activation of Bfl-1 may be the means by which NF-kappaB functions in oncogenesis and promotes cell resistance to anti-cancer therapy.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-1317006,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-1319065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-1381359,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-6312838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-7478596,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-7590249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-7607087,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-7898928,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8035813,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8197184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8345191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8402648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8413269,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8562970,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8605321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8752150,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8864118,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8864119,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8864120,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8887559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8898208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8910286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8950468,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-8995233,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9039262,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9204981,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9285692,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9294162,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9299589,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9343416,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9372964,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9670830,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9695819,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9703517,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9733516,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9735050,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10049353-9846183
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0890-9369
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
13
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
382-7
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10049353-Apoptosis,
pubmed-meshheading:10049353-Cell Line,
pubmed-meshheading:10049353-Gene Expression Regulation,
pubmed-meshheading:10049353-Humans,
pubmed-meshheading:10049353-NF-kappa B,
pubmed-meshheading:10049353-Promoter Regions, Genetic,
pubmed-meshheading:10049353-Proteins,
pubmed-meshheading:10049353-Proto-Oncogene Proteins,
pubmed-meshheading:10049353-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:10049353-Proto-Oncogene Proteins c-rel,
pubmed-meshheading:10049353-RNA, Messenger,
pubmed-meshheading:10049353-Transcription, Genetic,
pubmed-meshheading:10049353-Transcriptional Activation,
pubmed-meshheading:10049353-Tumor Necrosis Factor-alpha
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pubmed:year |
1999
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pubmed:articleTitle |
The prosurvival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-kappaB that blocks TNFalpha-induced apoptosis.
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pubmed:affiliation |
Center for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Jersey 08854-5638 USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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