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Titolo:
PROTOONCOGENE PML CONTROLS GENES DEVOTED TO MHC CLASS-I ANTIGEN PRESENTATION
Autore:
ZHENG P; GUO Y; NIU QT; LEVY DE; DYCK JA; LU SL; SHEIMAN LA; LIU Y;
Indirizzi:
NYU,MED CTR,DEPT PATHOL NEW YORK NY 10016 NYU,MED CTR,DEPT PATHOL NEW YORK NY 10016 NYU,MED CTR,KAPLAN COMPREHENS CANC CTR NEW YORK NY 10016 UNIV CALIF SAN DIEGO,DEPT MED LA JOLLA CA 92093
Titolo Testata:
Nature
fascicolo: 6709, volume: 396, anno: 1998,
pagine: 373 - 376
SICI:
0028-0836(1998)396:6709<373:PPCGDT>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE PROMYELOCYTIC LEUKEMIA; RAR-ALPHA; EXPRESSION; T(15-17); CELLS; TRANSLOCATION; ADENOVIRUS-12; INTERFERON; MOLECULES; PATHWAY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
P. Zheng et al., "PROTOONCOGENE PML CONTROLS GENES DEVOTED TO MHC CLASS-I ANTIGEN PRESENTATION", Nature, 396(6709), 1998, pp. 373-376

Abstract

Fragments of foreign antigens associated with class I molecules of the major histocompatibility complex (MHC) are presented at the cell surface to elicit an immune response. This presentation requires the coordinated expression of several genes contained in the MHC1-5, includingthose encoding the MHC class I heavy chain, the proteins LMP-2 and LMP-7, which are involved in the proteasomal degradation of cytosolic antigens into peptide fragments that are destined for association with MHC class I molecules, and TAP-1 and TAP-2, which transport these fragments across the membrane of the endoplasmic reticulum at the start of their journey to the cell surface. In many virus-transformed cell lines(6,7) and spontaneous tumours(8-10), these genes are simultaneously repressed. However, the key factor(s) that are essential for their expression and repression have not been identified. Here we report that the proto-oncogene product PML induces expression of LMP-2, LMP-7, TAP-1and TAF-2 in an MHC-class I-negative, recurrent tumour, leading to the re-expression of cell-surface MHC in tumours and to rejection of thetumours. PML also regulates MHC expression in untransformed fibroblasts. We conclude that malfunction of PML may enable a tumour to evade the immune defence of its host.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 22:28:11