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Titolo:
Transcriptional regulation of the BCL-X gene by NF-kappa B is an element of hypoxic responses in the rat brain
Autore:
Glasgow, JN; Qiu, JX; Rassin, D; Grafe, M; Wood, T; Perez-Polo, JR;
Indirizzi:
Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 l Chem & Genet, Galveston, TX 77555 USA
Titolo Testata:
NEUROCHEMICAL RESEARCH
fascicolo: 6, volume: 26, anno: 2001,
pagine: 647 - 659
SICI:
0364-3190(200106)26:6<647:TROTBG>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; TRANSIENT FOREBRAIN ISCHEMIA; CYTOCHROME-C RELEASE; PERMEABILITY TRANSITION PORE; CEREBRAL-ARTERY OCCLUSION; GLOBAL-ISCHEMIA; IN-VIVO; DNA-BINDING; HIPPOCAMPAL-NEURONS; ALZHEIMERS-DISEASE;
Keywords:
hypoxia; NF-kappa B; bcl-x; c-Rel; p50; apoptosis;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
211
Recensione:
Indirizzi per estratti:
Indirizzo: Perez-Polo, JR Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 Galveston, TX 77555 USA
Citazione:
J.N. Glasgow et al., "Transcriptional regulation of the BCL-X gene by NF-kappa B is an element of hypoxic responses in the rat brain", NEUROCHEM R, 26(6), 2001, pp. 647-659

Abstract

Signal transduction pathways that mediate neuronal commitment to apoptosisinvolve the nuclear factor kappa B (NF-kappaB) transcription factor. The bcl-x gene is a member of the bcl-2 family of genes that regulate apoptosis,and gives rise to two proteins, Bcl-X-L and Bcl-X-S, via alternative mRNA splicing. Bcl-X-L protein, like Bcl-2, is a dominant inhibitor of apoptoticcell death, whereas Bcl-X-S promotes apoptosis. While there is high expression of Bcl-X-L in the developing and adult brain, few transcriptional control elements have been identified in the bcl-x promoter. There are two functional nuclear factor-kappa B (NF-kappaB) DNA binding sites clustered upstream of the brain-specific transcription start site in the upstream promoterregion of murine bcl-x. Recombinant NF-kappaB proteins bind to these sites. Also NF-kappaB overexpression, coupled with bcl-x promoter/reporter assays using a series of murine bcl-x promoter and deletion mutants, has identified the downstream 1.1kb of the bcl-x promoter as necessary for basal promoter activity and induction by NF-kappaB in support of the hypothesis that NF-kappaB can act to enhance Bcl-X-L expression via highly selective interactions with the bcl-x promoter, where NF-kappaB binding and promoter activation are dependent on specific DNA binding site sequences and NF-kappaB protein dinner composition. Hypoxia induces apoptosis in the hippocampus where the NF-kappaB dimers c-Rel/p50 and p50/p50 bind to the bcl-x promoter NF-kappaB site.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 06:20:02