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BimL involvement in Bax activation during UV irradiation-induced apoptosis

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [1];  [1];  [1]
  1. MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, South China Normal University, Guangzhou 510631 (China)

Bax, a proapoptotic member of the Bcl-2 family, localizes largely in the cytoplasm but translocates to mitochondria and undergoes oligomerization to induce the release of apoptogenic factors in response to apoptotic stimuli. However, the molecular mechanism of Bax activation is not fully understood. We show here the role of BimL in Bax activation during UV irradiation-induced apoptosis. In this study, GFP-BimL plasmid was constructed. The dynamic interaction between BimL and Bax during UV irradiation-induced apoptosis was observed using fluorescence resonance energy transfer (FRET) technique. Our experimental results showed that BimL translocation to mitochondria occurred before Bax translocation, and that BimL activated Bax indirectly. Moreover, inhibition of c-Jun N-terminal protein kinase (JNK) activation blocked BimL translocation, delayed and attenuated Bax translocation and subsequent apoptosis. These results demonstrate that BimL is involved in UV irradiation-induced apoptosis by indirectly activating Bax.

OSTI ID:
20991415
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 2 Vol. 358; ISSN 0006-291X; ISSN BBRCA9
Country of Publication:
United States
Language:
English

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