NM23-H2 involves in negative regulation of Diva and Bcl2L10 in apoptosis signaling
- Authors
- Kang, Yeongsup; Lee, Deug-Chan; Han, Jiyou; Yoon, Seongmin; Won, Miae; Yeom, Ji-Hyun; Seong, Maeng-Je; Ko, Jeong-Jae; Lee, Kyung-Ah; Lee, Kangseok; Bae, Jeehyeon
- Issue Date
- Jul-2007
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Diva; Bcl2L10; Boo; Bcl-B; NM23-H2; NME; apoptosis
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.359, no.1, pp 76 - 82
- Pages
- 7
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 359
- Number
- 1
- Start Page
- 76
- End Page
- 82
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/24031
- DOI
- 10.1016/j.bbrc.2007.05.090
- ISSN
- 0006-291X
1090-2104
- Abstract
- The Bcl-2 family members are evolutionally conserved and crucial regulators of apoptosis. Diva (Boo), an ortholog of Bcl2L10 or Bcl-B, is a member of the Bcl-2 family that has contradictory functions in apoptosis. To understand the signaling mechanisms of Diva, we searched for proteins that interact with Diva using the yeast two-hybrid system. We identified a nucleoside diphosphate kinase isoform, NM23-H2. Here, we show that Diva bound to NM23-H2 in cells in which the transmembrane domain of Diva was required, and both proteins were colocalized in cytoplasm. Of interest, Diva protein level was significantly down-regulated by NM23-H2 as knock down of NM23-H2 restored Diva expression. Overexpression of NM23-H2 induced apoptosis, and the depletion of NM23-H2 led to the increase of Diva's apoptotic activity. Thus, these results indicate the existence of a previously undiscovered mechanism by which NM23-H2 involves in the regulation of Diva-mediated apoptosis. (C) 2007 Elsevier Inc. All rights reserved.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
- College of Natural Sciences > Department of Physics > 1. Journal Articles
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