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Titolo:
Syk is required for the activation of Akt survival pathway in B cells exposed to oxidative stress
Autore:
Ding, JY; Takano, T; Gao, SY; Han, WH; Noda, C; Yanagi, S; Yamamura, H;
Indirizzi:
Kobe Univ, Sch Med, Dept Biochem, Kobe, Hyogo 6500017, Japan Kobe Univ Kobe Hyogo Japan 6500017 pt Biochem, Kobe, Hyogo 6500017, Japan Hyogo Coll, Kakogawa 6750101, Japan Hyogo Coll Kakogawa Japan 6750101Hyogo Coll, Kakogawa 6750101, Japan
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 40, volume: 275, anno: 2000,
pagine: 30873 - 30877
SICI:
0021-9258(20001006)275:40<30873:SIRFTA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-B; NF-KAPPA-B; P56/P53(LYN) TYROSINE KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; HYDROGEN-PEROXIDE; HEAT-SHOCK; PHOSPHOINOSITIDE 3-KINASE; SIGNAL-TRANSDUCTION; INDUCED APOPTOSIS; LYMPHOMA-CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Yamamura, H 7-5-1 Kusunokicho,Chuo Ku, Kobe, Hyogo 6500017, Japan 7-5-1 Kusunokicho,Chuo Ku Kobe Hyogo Japan 6500017 017, Japan
Citazione:
J.Y. Ding et al., "Syk is required for the activation of Akt survival pathway in B cells exposed to oxidative stress", J BIOL CHEM, 275(40), 2000, pp. 30873-30877

Abstract

Syk has been demonstrated to play a crucial role in oxidative stress signaling in B cells. Here we report that Syk is required for the activation of the phosphatidylinositol (PI) 3-kinase-Akt survival pathway in B cells exposed to oxidative stress. Phosphorylation and activation of the serine-threonine kinase Akt were markedly increased in B cells treated with H2O2. In Syk-deficient DT40 cells treated with low doses of H2O2 (10-100 mu M), Akt activation was considerably reduced. Pretreatment with wortmannin, a PI 3-kinase-specific inhibitor, completely blocked the Syk-dependent Akt activation. Following stimulation by low doses of H2O2, a significant increase in PI 3-kinase activity was found in wild-type but not in Syk-deficient cells. These findings suggest that PI 3-kinase mediates Syk-dependent Akt activationpathway, Furthermore, viability of Syk-deficient cells, after exposure to H2O2, was dramatically decreased and caspase-9 activity was greatly increased compared with that of the wild-type cells. These results suggest that Syk is essential for the Akt survival pathway in B cells and enhances cellular resistance to oxidative stress-induced apoptosis.

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Documento generato il 13/07/20 alle ore 14:59:31