TY - JOUR
T1 - JAB1/CSN5
T2 - A new player in cell cycle control and cancer
AU - Shackleford, Terry J.
AU - Claret, Francois X.
N1 - Funding Information:
We thank Drs Q. Zhang, L. Tian and A. Korapati for providing helpful comments on the manuscript. T.J.S. is a recipient of fellowships from Susan G. Komen for the Cure and the Department of Defense US Army Breast Cancer Research Program. This work was supported by grants from the National Cancer Institute (CA90853-01A1), U.S. Department of Defense, and the Susan G. Komen for the Cure to F.X.C.
PY - 2010/10/18
Y1 - 2010/10/18
N2 - c-Jun activation domain-binding protein-1 (Jab1) acts as a modulator of intracellular signaling and affects cellular proliferation and apoptosis, through its existence as a monomer or as the fifth component of the constitutive photomorphogenic-9 signalosome (CSN5). Jab1/CSN5 is involved in transcription factor specificity, deneddylation of NEDD8, and nuclear-to-cytoplasmic shuttling of key molecules. Jab1/CSN5 activities positively and negatively affect a number of pathways, including integrin signaling, cell cycle control, and apoptosis. Also, more recent studies have demonstrated the intriguing roles of Jab1/CSN5 in regulating genomic instability and DNA repair. The effects of Jab1/CSN5's multiple protein interactions are generally oncogenic in nature, and overexpression of Jab1/CSN5 in cancer provides evidence that it is involved in the tumorigenic process. In this review, we highlight our current knowledge of Jab1/CSN5 function and the recent discoveries in dissecting the Jab1 signaling pathway. Further, we also discuss the regulation of Jab1/CSN5 in cancers and its potential as a therapeutic target.
AB - c-Jun activation domain-binding protein-1 (Jab1) acts as a modulator of intracellular signaling and affects cellular proliferation and apoptosis, through its existence as a monomer or as the fifth component of the constitutive photomorphogenic-9 signalosome (CSN5). Jab1/CSN5 is involved in transcription factor specificity, deneddylation of NEDD8, and nuclear-to-cytoplasmic shuttling of key molecules. Jab1/CSN5 activities positively and negatively affect a number of pathways, including integrin signaling, cell cycle control, and apoptosis. Also, more recent studies have demonstrated the intriguing roles of Jab1/CSN5 in regulating genomic instability and DNA repair. The effects of Jab1/CSN5's multiple protein interactions are generally oncogenic in nature, and overexpression of Jab1/CSN5 in cancer provides evidence that it is involved in the tumorigenic process. In this review, we highlight our current knowledge of Jab1/CSN5 function and the recent discoveries in dissecting the Jab1 signaling pathway. Further, we also discuss the regulation of Jab1/CSN5 in cancers and its potential as a therapeutic target.
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U2 - 10.1186/1747-1028-5-26
DO - 10.1186/1747-1028-5-26
M3 - Review article
C2 - 20955608
AN - SCOPUS:77957914630
SN - 1747-1028
VL - 5
JO - Cell Division
JF - Cell Division
M1 - 26
ER -