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- W2062282238 abstract "Cell death/survival following traumatic brain injury (TBI) may be a result of alterations in the intracellular ratio of death and survival factors. Bcl-2 family genes mediate both cell survival and the initiation of cell death. Using lysate RNase protection assays, mRNA expression of the anti-cell death genes Bcl-2 and Bcl-xL, and the pro-cell death gene Bax, was evaluated following experimental brain injuries in adult male Sprague-Dawley rats. Both the lateral fluid-percussion (LFP) and the lateral controlled cortical impact (LCI) models of TBI showed similar patterns of gene expression. Anticell death bcl-2 and bcl-xL mRNAs were attenuated early and tended to remain depressed for at least 3 days after injury in the cortex and hippocampus ipsilateral to injury. Pro-cell death bax mRNA was elevated in these areas, usually following the decrease in anti-cell death genes. These common patterns of gene expression suggest an important role for Bcl-2 genes in cell death and survival in the injured brain. Understanding the regulation of these genes may facilitate the development of new therapeutic strategies for a condition that currently has no proven pharmacologic treatments." @default.
- W2062282238 created "2016-06-24" @default.
- W2062282238 creator A5034507690 @default.
- W2062282238 creator A5049650232 @default.
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- W2062282238 date "2004-01-01" @default.
- W2062282238 modified "2023-09-26" @default.
- W2062282238 title "Common patterns of Bcl-2 family gene expression in two traumatic brain injury models" @default.
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- W2062282238 doi "https://doi.org/10.1007/bf03033444" @default.
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