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Subcellular distribution of Bcl-2 family proteins and 14-3-3 within the hippocampus during seizure-induced neuronal death in the rat.

Authors: Schindler, CK  Shinoda, S  Simon, RP  Henshall, DC 
Citation: Schindler CK, etal., Neurosci Lett. 2004 Feb 19;356(3):163-6.
Pubmed: (View Article at PubMed) PMID:15036620
DOI: Full-text: DOI:10.1016/j.neulet.2003.11.048

The molecular regulation of seizure-induced neuronal death may involve interactions between proteins of the Bcl-2 and 14-3-3 families. To further examine these pathways we performed subcellular fractionation on hippocampi obtained following a brief period of status epilepticus in the rat. Western blotting determined seizures induced caspase-8 cleavage and increased Bcl-w levels within the cytoplasm. Bax, Bad and Bid were largely present within the cytoplasm before and after seizures, although some Bax and, following seizures, truncated Bid was detected in mitochondria. Levels of 14-3-3 were significantly reduced in the cytoplasm and microsomal fractions. These data establish the expression and distribution profile of key Bcl-2 family proteins and the signaling chaperone 14-3-3 in the rat and provide additional evidence for the activation of programmed cell death pathways by seizures.

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RGD Object Information
RGD ID: 2311439
Created: 2009-07-15
Species: All species
Last Modified: 2009-07-15
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.