Please use this identifier to cite or link to this item: https://doi.org/10.1042/BSR20160152
Title: APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway
Authors: Ramanujan, Ajeena 
Tiwari, Swati
Keywords: Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Cell Biology
anaphase promoting complex/cyclosome
cell cycle
FZR1
human papilloma virus
LxCxE
retinoblastoma
ANAPHASE-PROMOTING COMPLEX
PAPILLOMAVIRUS TYPE-16 E7
CELL-CYCLE PROGRESSION
TUMOR-SUPPRESSOR
LOW-PENETRANCE
GENE-PRODUCT
COMPLEX/CYCLOSOME APC/C
S-PHASE
D-BOX
TRANSCRIPTIONAL REPRESSOR
Issue Date: 1-Oct-2016
Publisher: PORTLAND PRESS LTD
Citation: Ramanujan, Ajeena, Tiwari, Swati (2016-10-01). APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway. BIOSCIENCE REPORTS 36 (5). ScholarBank@NUS Repository. https://doi.org/10.1042/BSR20160152
Abstract: The ubiquitin (Ub) ligase anaphase promoting complex/cyclosome (APC/C) and the tumour suppressor retinoblastoma protein (pRB) play key roles in cell cycle regulation. APC/C is a critical regulator of mitosis and G1-phase of the cell cycle whereas pRB keeps a check on proliferation by inhibiting transition to the S-phase. APC/C and pRB interact with each other via the co-activator of APC/C, FZR1, providing an alternative pathway of regulation of G1 to S transition by pRB using a post-translational mechanism. Both pRB and FZR1 have complex roles and are implicated not only in regulation of cell proliferation but also in differentiation, quiescence, apoptosis, maintenance of chromosomal integrity and metabolism. Both are also targeted by transforming viruses. We discuss recent advances in our understanding of the involvement of APC/C and pRB in cell cycle based decisions and how these insights will be useful for development of anti-cancer and anti-viral drugs.
Source Title: BIOSCIENCE REPORTS
URI: https://scholarbank.nus.edu.sg/handle/10635/219116
ISSN: 0144-8463
1573-4935
DOI: 10.1042/BSR20160152
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