PMID- 11466612
OWN - NLM
STAT- MEDLINE
DCOM- 20010809
LR  - 20191105
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 20
IP  - 32
DP  - 2001 Jul 19
TI  - Interchangeable binding of Bcl10 to TRAF2 and cIAPs regulates apoptosis 
      signaling.
PG  - 4317-23
AB  - Bcl10 was identified as a candidate gene responsible for low grade B cell 
      lymphomas of mucosa-associated lymphoid tissue. Overexpression of Bcl10 in 
      cultured cells was reported to promote apoptosis, however, the mechanism of 
      regulation of apoptosis mediated by Bcl10 has not been demonstrated. In the 
      present study, we analysed the apoptosis signaling pathway mediated by Bcl10, 
      focusing on phosphorylation of Bcl10 and the dynamic interaction with its binding 
      partners during apoptosis. Previously, we have demonstrated that Bcl10 
      potentially interacts with the other apoptosis regulator, TNF receptor associated 
      factor-2 (TRAF2) and inhibitor of apoptosis proteins (cIAPs). The present results 
      showed that the complex formation of these molecules was regulated by 
      phosphorylation of Bcl10, that is, phosphorylation of Bcl10 resulted in binding 
      of Bcl10 to cIAPs and the dissociation of it from TRAF2. Moreover, 
      hyperphosphorylation of Bcl10 enhanced apoptosis, suggesting that changes in the 
      binding partners of Bcl10 were correlated to the promotion of apoptosis as 
      mediated by Bcl10. Indeed, the mutant which was deleted from the binding site of 
      Bcl10 for cIAPs, could not induce apoptosis. These findings indicate that Bcl10 
      is a mediator of apoptosis signaling, by switching over binding to cIAPs from 
      TRAF2 through the events of Bcl10 phosphorylation.
FAU - Yui, D
AU  - Yui D
AD  - Department of Anatomy and Neuroscience, Graduate School of Medicine, Osaka 
      University. 2-2 Yamadaoka Suita, Osaka 565-0871, Japan. 
      yui@anat2.med.osaka-u.ac.jp
FAU - Yoneda, T
AU  - Yoneda T
FAU - Oono, K
AU  - Oono K
FAU - Katayama, T
AU  - Katayama T
FAU - Imaizumi, K
AU  - Imaizumi K
FAU - Tohyama, M
AU  - Tohyama M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (B-Cell CLL-Lymphoma 10 Protein)
RN  - 0 (BCL10 protein, human)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Inhibitor of Apoptosis Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proteins)
RN  - 0 (TNF Receptor-Associated Factor 2)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - *Apoptosis
MH  - B-Cell CLL-Lymphoma 10 Protein
MH  - Cell Line
MH  - Cells, Cultured
MH  - Enzyme Inhibitors/pharmacology
MH  - Humans
MH  - Inhibitor of Apoptosis Proteins
MH  - Neoplasm Proteins/chemistry/*metabolism
MH  - Phosphorylation
MH  - Protein Structure, Tertiary
MH  - Proteins/*metabolism
MH  - *Signal Transduction
MH  - TNF Receptor-Associated Factor 2
EDAT- 2001/07/24 10:00
MHDA- 2001/08/10 10:01
CRDT- 2001/07/24 10:00
PHST- 2001/01/23 00:00 [received]
PHST- 2001/03/09 00:00 [revised]
PHST- 2001/04/30 00:00 [accepted]
PHST- 2001/07/24 10:00 [pubmed]
PHST- 2001/08/10 10:01 [medline]
PHST- 2001/07/24 10:00 [entrez]
AID - 10.1038/sj.onc.1204576 [doi]
PST - ppublish
SO  - Oncogene. 2001 Jul 19;20(32):4317-23. doi: 10.1038/sj.onc.1204576.