Source:http://linkedlifedata.com/resource/pubmed/id/16737462
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2006-6-1
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pubmed:abstractText |
Prenatal alcohol exposure produces anatomical and behavioral abnormalities associated with fetal alcohol syndrome (FAS). Animal FAS models have demonstrated temporal windows of vulnerability in the developing cerebellum, with substantial ethanol (EtOH)-mediated apoptotic activation during these periods. In rodents, the cerebellum is most sensitive to EtOH on postnatal days 4 to 6 (P4 to P6). At slightly later ages (P7 and later), this region is less vulnerable to EtOH. The present study investigated EtOH effects on mechanisms related to activities of Bad, a proapoptotic member of the Bcl-2 gene family, to further characterize processes underlying these disparate EtOH sensitivities. In healthy cells, Bad is retained in the cytosol by association with 14-3-3, a primarily cytosolic protein. Bad promotes apoptosis by disassociating from 14-3-3 and sequestering Bcl-xL through heterodimerization. This dimerization prevents the neutralizing association of Bcl-xL with Bax, freeing Bax to perform in a prodeath manner. Caspase-dependent cleavage of Bad to a 15-kDa fragment increases its proapoptogenic capacity.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/14-3-3 Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Bad protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Bcl2l1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Ethanol,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-Associated Death Protein,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0145-6008
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1031-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16737462-14-3-3 Proteins,
pubmed-meshheading:16737462-Aging,
pubmed-meshheading:16737462-Animals,
pubmed-meshheading:16737462-Animals, Newborn,
pubmed-meshheading:16737462-Blotting, Western,
pubmed-meshheading:16737462-Cell Fractionation,
pubmed-meshheading:16737462-Cerebellum,
pubmed-meshheading:16737462-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:16737462-Ethanol,
pubmed-meshheading:16737462-Female,
pubmed-meshheading:16737462-Male,
pubmed-meshheading:16737462-Mitochondria,
pubmed-meshheading:16737462-Peptide Fragments,
pubmed-meshheading:16737462-Rats,
pubmed-meshheading:16737462-Rats, Long-Evans,
pubmed-meshheading:16737462-bcl-Associated Death Protein,
pubmed-meshheading:16737462-bcl-X Protein
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pubmed:year |
2006
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pubmed:articleTitle |
Effects of acute ethanol exposure on regulatory mechanisms of Bcl-2-associated apoptosis promoter, bad, in neonatal rat cerebellum: differential effects during vulnerable and resistant developmental periods.
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pubmed:affiliation |
Department of Neuroscience, Center for Alcohol Research, McKnight Brain Institute, University of Florida, Gainesville, Florida 32611, USA. kendra@ufl.edu
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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