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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 301 - 309 (9page)
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Hepatitis B virus x gene product (HBx) is known to be a transactivator of transcriptional elements associated with the growth, diferentiation, survival and the apoptosis of cels. However, the exact mechanism of the activation and inhibition of cellular events by HBx remains uncertain. The present study was designed to measure the effect of HBx, on the signal transduction pathways as-sociated with intracellular Ca2+ mobilization follow-ing HBx transfection in the stable Chang liver cels (CHL-X). Enhanced cell proliferation by HBx in CHL-X was confirmed by MTT asay and by the imunodetection of PCNA. The transactivation of AP-1 by HBx induced in CHL-X was inhibited by cyclosporin A (CsA), a mitochondrial Ca2+ channel blocker and by BAPTA-AM, a cytosolic Ca2+ bloc-ker. Activation of the SAPK/JNK signaling path-way by HBx was evidenced by the increased phos-phorylations of c-Jun (Ser63) and of JNK (Thr183/ Tyr185). Increased phospho-Erk/Erk and phospho- Raf1/Raf in HBx-induced CHL-X indicated that HBx might stimulate the MAPK pathway. PI3K activity and cytosolic free Ca2+levels were elevated in HBx-induced CHL-X. These results imply that HBx duction pathways in association with the mobili-zation of cytosolic Ca2+.
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