Cdc20 control of cell fate during prolonged mitotic arrest: do Cdc20 protein levels affect cell fate in response to antimitotic compounds?
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Cdc20 control of cell fate during prolonged mitotic arrest : do Cdc20 protein levels affect cell fate in response to antimitotic compounds? / Nilsson, Jakob.
I: BioEssays, Bind 33, Nr. 12, 2011, s. 903-9.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Cdc20 control of cell fate during prolonged mitotic arrest
T2 - do Cdc20 protein levels affect cell fate in response to antimitotic compounds?
AU - Nilsson, Jakob
N1 - Copyright © 2011 WILEY Periodicals, Inc.
PY - 2011
Y1 - 2011
N2 - The fate of cells arrested in mitosis by antimitotic compounds is complex but is influenced by competition between pathways promoting cell death and pathways promoting mitotic exit. As components of both of these pathways are regulated by Cdc20-dependent degradation, I hypothesize that variations in Cdc20 protein levels, rather than mutations in checkpoint genes, could affect cell fate during prolonged mitotic arrest. This hypothesis is supported by experiments where manipulation of Cdc20 levels affects the response to antimitotic compounds. The observed differences in Cdc20 levels between cell lines likely reflects differences in the rate of synthesis or degradation of the protein; therefore, understanding these pathways at a molecular level could pave the way for modulating the activity of Cdc20, in turn presenting novel therapeutic possibilities.
AB - The fate of cells arrested in mitosis by antimitotic compounds is complex but is influenced by competition between pathways promoting cell death and pathways promoting mitotic exit. As components of both of these pathways are regulated by Cdc20-dependent degradation, I hypothesize that variations in Cdc20 protein levels, rather than mutations in checkpoint genes, could affect cell fate during prolonged mitotic arrest. This hypothesis is supported by experiments where manipulation of Cdc20 levels affects the response to antimitotic compounds. The observed differences in Cdc20 levels between cell lines likely reflects differences in the rate of synthesis or degradation of the protein; therefore, understanding these pathways at a molecular level could pave the way for modulating the activity of Cdc20, in turn presenting novel therapeutic possibilities.
KW - Antimitotic Agents
KW - Calcium-Binding Proteins
KW - Cell Cycle Proteins
KW - Cell Line
KW - Cell Line, Tumor
KW - Humans
KW - M Phase Cell Cycle Checkpoints
KW - Mitosis
KW - Mutation
KW - Phosphorylation
KW - Protein-Serine-Threonine Kinases
KW - Repressor Proteins
U2 - 10.1002/bies.201100094
DO - 10.1002/bies.201100094
M3 - Journal article
C2 - 22045620
VL - 33
SP - 903
EP - 909
JO - BioEssays
JF - BioEssays
SN - 0265-9247
IS - 12
ER -
ID: 40288994