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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제15권 제4호
- 발행연도
- 2005.1
- 수록면
- 756 - 766 (11page)
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초록· 키워드
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The signaling mechanism underlying aburatubolactamC-induced FasL upregulation was investigated in humanJurkat T cells. After treatment with aburatubolactam C, thesrc-family PTKs p56lck and p59fyn, and MAP kinases ERK2and JNK1, were activated prior to FasL upregulation. Bothp56lck and p59fyn were directly activated 2.4- and 2.2-fold,respectively, in vitro by aburatubolactam C. The aburatubolactamC-induced cellular changes, including the activation of ERK2and JNK1, and FasL upregulation, were completely preventedby the PTK inhibitor genistein. The activation of proteinkinase C (PKCδ, ε, and μ) was also induced followingaburatubolactam C treatment. Although the activation of p56lckand tyrosine phosphorylation of the cellular proteins were notblocked by the PKC inhibitor GF109203X, the activation ofERK2 was completely abrogated, along with a detectablyenhanced JNK1 activation, FasL upregulation, and apoptosis.However, the FasL upregulation and apoptosis were significantlyinhibited by the PKC activator PMA, with a remarkableincrease in the ERK2 activation. The cytotoxic effect ofaburatubolactam C was reduced in the presence of the anti-Fas neutralizing antibody ZB-4. Although ectopic expressionof Bcl-2 failed to completely block the cytotoxicity ofaburatubolactam C, it was clearly suppressed. The c-Fos mRNAexpression was upregulated in a biphasic manner, where thesecond phasic expression overlapped with the FasL upregulation.Accordingly, these results demonstrate that aburatubolactamC-induced apoptosis is exerted, at least in part, by FasLupregulation dictated by activation of the PTK (p56lck andp59fyn)/JNK1 pathway, which is negatively affected by theconcurrent activation of the PKC/ERK2 pathway proximal toPTK activation.
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참고문헌 (27)
참고문헌 신청
/ 2002 / Activation ofprotein kinase C for protection of cells against apoptosisinduced by the immunosuppressor prodigiosin 63 : 463 ~ 469
A / 1998 / Effect of age 3 : 1120 ~ 1133
A / 2003 / Tamoxifen inducesapoptosis in Fas+ tumor cells by upregulating the expressionof Fas ligand 51 : 284 ~ 290
Atkinson / 1996 / Aphysical interaction between the cell death protein Fas andthe tyrosine kinase p59fyn 271 : 5968 ~ 5971
Bae / 1996 / a novel inhibitor of superoxideanion generation from a marine microorganism 2 : 315 ~ 318
A / 1998 / Effect of age 3 : 1120 ~ 1133
A / 2003 / Tamoxifen inducesapoptosis in Fas+ tumor cells by upregulating the expressionof Fas ligand 51 : 284 ~ 290
Atkinson / 1996 / Aphysical interaction between the cell death protein Fas andthe tyrosine kinase p59fyn 271 : 5968 ~ 5971
Bae / 1996 / a novel inhibitor of superoxideanion generation from a marine microorganism 2 : 315 ~ 318
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