Chk1 phosphorylation during mitosis: A new role for a master regulator

Deborah Wilsker; Fred Bunz

doi:10.4161/cc.8.8.8148

Chk1 phosphorylation during mitosis: A new role for a master regulator

Deborah Wilsker, Fred Bunz

School of Medicine

Research output: Contribution to journal › Review article › peer-review

8 Scopus citations

Abstract

The human DNA damage responses are modulated by both nonessential and essential pathways. The extensively studied ATM kinase and p53 are examples of the former. While loss-of-function mutations in genes that encode ATM and p53 cause marked predispositions to cancer, the loss of these proteins does not appear to impact basic cell growth and proliferation. In contrast, the checkpoint kinase Chk1 and its upstream activator ATR are essential. ^1-4 What do these proteins do in undamaged cells?

Original language	English (US)
Pages (from-to)	1161-1163
Number of pages	3
Journal	Cell Cycle
Volume	8
Issue number	8
DOIs	https://doi.org/10.4161/cc.8.8.8148
State	Published - Apr 15 2009

Keywords

ATR
Cell cycle
Chk1
Ionizing radiation
Mitosis
Phosphorylation

ASJC Scopus subject areas

Molecular Biology
Developmental Biology
Cell Biology

Access to Document

10.4161/cc.8.8.8148

Cite this

@article{55f6239ab9ca4feaa08b7a4d97b2d47b,

title = "Chk1 phosphorylation during mitosis: A new role for a master regulator",

abstract = "The human DNA damage responses are modulated by both nonessential and essential pathways. The extensively studied ATM kinase and p53 are examples of the former. While loss-of-function mutations in genes that encode ATM and p53 cause marked predispositions to cancer, the loss of these proteins does not appear to impact basic cell growth and proliferation. In contrast, the checkpoint kinase Chk1 and its upstream activator ATR are essential. 1-4 What do these proteins do in undamaged cells?",

keywords = "ATR, Cell cycle, Chk1, Ionizing radiation, Mitosis, Phosphorylation",

author = "Deborah Wilsker and Fred Bunz",

note = "Funding Information: The authors are supported by grants from the Flight Attendant Medical Research Institute and the NIH (CA104253 and CA119724).",

year = "2009",

month = apr,

day = "15",

doi = "10.4161/cc.8.8.8148",

language = "English (US)",

volume = "8",

pages = "1161--1163",

journal = "Cell Cycle",

issn = "1538-4101",

publisher = "Landes Bioscience",

number = "8",

}

TY - JOUR

T1 - Chk1 phosphorylation during mitosis

T2 - A new role for a master regulator

AU - Wilsker, Deborah

AU - Bunz, Fred

N1 - Funding Information: The authors are supported by grants from the Flight Attendant Medical Research Institute and the NIH (CA104253 and CA119724).

PY - 2009/4/15

Y1 - 2009/4/15

N2 - The human DNA damage responses are modulated by both nonessential and essential pathways. The extensively studied ATM kinase and p53 are examples of the former. While loss-of-function mutations in genes that encode ATM and p53 cause marked predispositions to cancer, the loss of these proteins does not appear to impact basic cell growth and proliferation. In contrast, the checkpoint kinase Chk1 and its upstream activator ATR are essential. 1-4 What do these proteins do in undamaged cells?

AB - The human DNA damage responses are modulated by both nonessential and essential pathways. The extensively studied ATM kinase and p53 are examples of the former. While loss-of-function mutations in genes that encode ATM and p53 cause marked predispositions to cancer, the loss of these proteins does not appear to impact basic cell growth and proliferation. In contrast, the checkpoint kinase Chk1 and its upstream activator ATR are essential. 1-4 What do these proteins do in undamaged cells?

KW - ATR

KW - Cell cycle

KW - Chk1

KW - Ionizing radiation

KW - Mitosis

KW - Phosphorylation

UR - http://www.scopus.com/inward/record.url?scp=65949087446&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=65949087446&partnerID=8YFLogxK

U2 - 10.4161/cc.8.8.8148

DO - 10.4161/cc.8.8.8148

M3 - Review article

C2 - 19282670

AN - SCOPUS:65949087446

SN - 1538-4101

VL - 8

SP - 1161

EP - 1163

JO - Cell Cycle

JF - Cell Cycle

IS - 8

ER -

Chk1 phosphorylation during mitosis: A new role for a master regulator

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this