Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Ataxia telangiectasia: new neurons and ATM
Autore:
McKinnon, PJ;
Indirizzi:
St Jude Childrens Res Hosp, Dept Genet, Memphis, TN 38105 USA St Jude Childrens Res Hosp Memphis TN USA 38105 et, Memphis, TN 38105 USA
Titolo Testata:
TRENDS IN MOLECULAR MEDICINE
fascicolo: 6, volume: 7, anno: 2001,
pagine: 233 - 234
SICI:
1471-4914(200106)7:6<233:ATNNAA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
NIJMEGEN BREAKAGE SYNDROME; DNA-DAMAGE RESPONSE; REPAIR; GENE; NEUROGENESIS; DISORDERS; PROTEIN;
Tipo documento:
Editorial Material
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: McKinnon, PJ St Jude Childrens Res Hosp, Dept Genet, 332 N Lauderdale St, Memphis, TN 38105 USA St Jude Childrens Res Hosp 332 N Lauderdale St Memphis TN USA 38105
Citazione:
P.J. McKinnon, "Ataxia telangiectasia: new neurons and ATM", TRENDS MO M, 7(6), 2001, pp. 233-234

Abstract

Despite the rarity of the human autosomal recessive disease ataxia telangiectasia (A-T) (affecting similar to1/40 000-1/100 000). interest in the function of the mutated gene product (ATM) in this syndrome is intense. Mutation of this single gene can lead to a diverse array of features. including cancer, immune defects. infertility end radiosensitivity. However, it is thepronounced and debilitating neurodegeneration that is the hallmark of thisdisease. Thus, from a clinical perspective, it is ATM function in the nervous system that, arguably, is the most important to understand. Although the case for DNA damage as a causative factor for neurodegeneration in A-T iscompelling, new data point to a possible link to defects in neurogenesis. Thus. whereas ATM is important for nervous system development, it could also be important for adult neurogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 00:16:42