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Titolo:
Killing of sarcoma cells by proapoptotic Bcl-X-S: Role of the BH3 domain and regulation by Bcl-X-L
Autore:
Mitra, RS; Benedict, MA; Qian, DL; Foreman, KE; Ekhterae, D; Nickoloff, BJ; Nunez, G;
Indirizzi:
Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 Dept Pathol, Ann Arbor, MI 48109 USA Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 nternal Med, Ann Arbor, MI 48109 USA Univ Michigan, Sch Med, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 rehens Canc, Ann Arbor, MI 48109 USA Loyola Univ, Med Ctr, Dept Pathol, Chicago, IL 60611 USA Loyola Univ Chicago IL USA 60611 Ctr, Dept Pathol, Chicago, IL 60611 USA Loyola Univ, Med Ctr, Skin Dis Res Labs, Chicago, IL 60611 USA Loyola Univ Chicago IL USA 60611 Skin Dis Res Labs, Chicago, IL 60611 USA
Titolo Testata:
NEOPLASIA
fascicolo: 5, volume: 3, anno: 2001,
pagine: 437 - 445
SICI:
1522-8002(200109/10)3:5<437:KOSCBP>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
KAPOSIS-SARCOMA; INDUCED APOPTOSIS; BCL-X(S); DEATH; PROTEIN; GENE; BAX; MITOCHONDRIA; INHIBITION; SURVIVAL;
Keywords:
apoptosis; Bcl-2; Bcl-X; adenovirus; Kaposi's sarcoma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Nunez, G Univ Michigan, Sch Med, Dept Pathol, 4219 CCGC,1500 E Med Ctr Dr,Ann Arbor, MI 48109 USA Univ Michigan 4219 CCGC,1500 E Med Ctr Dr Ann Arbor MI USA 48109
Citazione:
R.S. Mitra et al., "Killing of sarcoma cells by proapoptotic Bcl-X-S: Role of the BH3 domain and regulation by Bcl-X-L", NEOPLASIA, 3(5), 2001, pp. 437-445

Abstract

Kaposi's sarcoma (KS) is the most common tumor affecting AIDS patients with over 20% of these patients afflicted by this disease. Previous studies have demonstrated that KS tumor cells predominantly express the prosurvival protein Bcl-X-L compared with Bcl-2. In the current study, we have used an adenoviral vector that expresses Bcl-X-S, a functional inhibitor of Bcl-X-L,to study the significance of Bcl-X-L expression in the KS cell line (SLK) or KS primary cultures. The results demonstrate that 75% to 80% of SLK or KS primary cells were killed by the Bcl-X-S containing adenovirus whereas KScells infected with control adenovirus showed no significant cell death orgrowth inhibition. Overexpression of Bcl-XL, but not BcI-2, in SILK cells attenuated apoptosis induced by adenovirus Bcl-X-S. Immunoprecipitation experiments revealed that adenoviral Bcl-X-S associated with Bcl-XL, but not with Bcl-2. Mutational analysis showed that the alpha2 helical region of Bcl-X-S containing the BH3 motif was critical for killing activity and interaction with Bcl-X-L. These results suggest that Bcl-X-S is a direct killer and Bcl-XL may act by interacting with and sequestering Bcl-X-S. These studies also suggest that targeting Bcl-X-L may be of therapeutic benefit for thetreatment of tumors that are characterized by inappropriate expression of Bcl-X-L.

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Documento generato il 29/02/20 alle ore 03:01:10