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Titolo:
Presenilins - Structural aspects and posttranslational events
Autore:
Checler, F;
Indirizzi:
Inst Pharmacol Mol & Cellulaire, UPR 411 CNRS, F-06560 Valbonne, France Inst Pharmacol Mol & Cellulaire Valbonne France F-06560 Valbonne, France
Titolo Testata:
MOLECULAR NEUROBIOLOGY
fascicolo: 3, volume: 19, anno: 1999,
pagine: 255 - 265
SICI:
0893-7648(199906)19:3<255:P-SAAP>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL ALZHEIMERS-DISEASE; ENDOPLASMIC-RETICULUM; BETA-CATENIN; MOUSE-BRAIN; IN-VIVO; IMMUNOHISTOCHEMICAL ANALYSIS; CAENORHABDITIS-ELEGANS; NEURONAL EXPRESSION; MISSENSE MUTATIONS; CULTURED-CELLS;
Keywords:
Alzheimer's disease; presenilins; beta APP processing; A beta peptide; mutations; embryogenesis; development; apoptosis; maturation; caspases;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
90
Recensione:
Indirizzi per estratti:
Indirizzo: Checler, F Inst Pharmacol Mol & Cellulaire, UPR 411 CNRS, 660 Route des Lucioles, F-06560 Valbonne, France Inst Pharmacol Mol & Cellulaire 660 Route des Lucioles Valbonne France F-06560
Citazione:
F. Checler, "Presenilins - Structural aspects and posttranslational events", MOL NEUROB, 19(3), 1999, pp. 255-265

Abstract

Most of early-onset forms of Alzheimer's disease (AD) are caused by inherited mutations located on chromosomes 14 and 1, the gene products of which have been recently identified and referred to as presenilins 1 (PS1) and 2 (PS2), respectively. The first phenotypic alterations triggered by mutated PS were reported to be an increased production of the amyloid peptide (A beta) and, more precisely, its 42 amino-acids long counterpart A beta 42. Thisoverproduction is thought to be responsible for the genesis of the senile plaques that invade the cortical and subcortical areas of these AD-affectedbrains. The discovery of PSs has triggered numerous studies aimed at better understanding their normal physiology and the dysfunctions brought by themutations that could explain, at least in part, the neurodegenerative process taking place in this syndrome. In this review, I will focus on the structural aspects of PS and on the various posttranscriptional events they undergo. I will also briefly discuss that current hypotheses concerning their normal functions and the influence of FAD-linked mutations.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:47:00