Source:http://linkedlifedata.com/resource/pubmed/id/11268382
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2001-3-27
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pubmed:abstractText |
Apoptosis is an evolutionarily conserved process for killing unwanted cells. Genetic and biochemical experiments have indicated that three groups of proteins are necessary for activation of the cell-death effector machinery: cysteine proteases, their adaptors, and proapoptotic Bcl-2 family members. Antiapoptotic Bcl-2 family members are needed for cell survival. We have cloned Bim, a proapoptotic Bcl-2 family member that shares with the family only a 9-16 aa region of homology [Bcl-3 homology region(BH3)], but is otherwise unique. Bim requires its BH3 region for binding to Bcl-2 and activation of apoptosis. Analysis of Bim-deficient mice has shown that Bim is essential for the execution of some but not all apoptotic stimuli that can be antagonized by Bcl-2. Bim-deficient mice have increased numbers of lymphocytes, plasma cells, and myeloid cells, and most develop fatal autoimmune glomerulonephritis. In healthy cells, Bim is bound to the microtubule-associated dynein motor complex, and is thereby sequestered from Bcl-2. Certain apoptotic signals unleash Bim and allow it to translocate to intracellular membranes, where it interacts with Bcl-2 or its homologues. These results indicate that BH3-only proteins are essential inducers of apoptosis that can be unleashed by certain death signals. Unleashed BH3-only proteins neutralize the prosurvival function of Bcl-2-like molecules, and this is thought to liberate Apaf-l-like adapters to activate caspase zymogens, which then initiate cell degradation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:issn |
0077-8923
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
917
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
541-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading | |
pubmed:year |
2000
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pubmed:articleTitle |
The role of bim, a proapoptotic BH3-only member of the Bcl-2 family in cell-death control.
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pubmed:affiliation |
Walter and Eliza Hall Institute, Post Office Royal Melbourne Hospital, 3050 Vic., Melbourne, Australia. strasser@wehi.edu.au
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
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