Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Autoamplification of apoptosis following ligation of CD95-L, TRAIL and TNF-alpha
Autore:
Herr, I; Posovszky, C; Di Marzio, L; Cifone, MG; Boehler, T; Debatin, KM;
Indirizzi:
German Canc Res Ctr, Div Pediat Oncol, D-6900 Heidelberg, Germany German Canc Res Ctr Heidelberg Germany D-6900 D-6900 Heidelberg, Germany Univ Aquila, Dept Expt Med, I-67100 Laquila, Italy Univ Aquila Laquila Italy I-67100 Dept Expt Med, I-67100 Laquila, Italy Univ Ulm, Childrens Hosp, Ulm, Germany Univ Ulm Ulm GermanyUniv Ulm, Childrens Hosp, Ulm, Germany
Titolo Testata:
ONCOGENE
fascicolo: 37, volume: 19, anno: 2000,
pagine: 4255 - 4262
SICI:
0950-9232(20000831)19:37<4255:AOAFLO>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; APO-1/FAS LIGAND EXPRESSION; THERAPY-INDUCED APOPTOSIS; HUMAN T-CELLS; FAS LIGAND; SIGNAL-TRANSDUCTION; JNK/SAPK ACTIVITY; ACTIVATION; PROTEIN; STRESS;
Keywords:
FADD; JNK/SAPKs; ATF-2; cJun; APO-1/Fas;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Debatin, KM Univ Kinderklin, Prittwitzstr 43, D-89075 Ulm, Germany Univ Kinderklin Prittwitzstr 43 Ulm Germany D-89075 , Germany
Citazione:
I. Herr et al., "Autoamplification of apoptosis following ligation of CD95-L, TRAIL and TNF-alpha", ONCOGENE, 19(37), 2000, pp. 4255-4262

Abstract

CD95-L, TNP-alpha and TRAIL are death-inducing ligands (DILs) which may signal apoptosis via crosslinking of their cognate receptors, The present study shows that treatment of cells with agonistic mAB alpha APO-1 (CD95), recombinant TRAIL or TNF-alpha leads to enhanced mRNA and protein expression of each DIL with concomitant death in target cells, Immunoprecipitation of CD95-L protein from supernatant as well as neutralizing antibodies suggest DIL proteins to be cooperatively acting mediators of these cytotoxic activity, Antoamplification of the death signal was blocked in cells with a defectin apoptosis signaling either due to a dysfunctional FADD molecule or to the failure to activate JNK/SAPKs, Phosphorylation and enhanced binding of cJun and ATF-2 to DIL promoters suggest JNK/SAPKs as activators of these transcription factors following death receptor triggering, In consequence, autocrine production of DILs allows the spread of death signals to sensitive target cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:56:52