A role for dormant origins in tumor suppression

Kathleen Klotz-Noack; J. Julian Blow

doi:10.1016/j.molcel.2011.02.014

A role for dormant origins in tumor suppression

Kathleen Klotz-Noack, J. Julian Blow

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

In this issue of Molecular Cell, Kawabata et al. (2011) show that mice hypomorphic for the replication licensing protein Mcm4 show spontaneous DNA replication defects due to a lack of dormant origins, potentially explaining why these mice are cancer prone.

Original language	English
Pages (from-to)	495-496
Number of pages	2
Journal	Molecular Cell
Volume	41
Issue number	5
DOIs	https://doi.org/10.1016/j.molcel.2011.02.014
Publication status	Published - 4 Mar 2011

Keywords

REPLICATIVE STRESS
EXCESS MCM2-7
CANCER
MICE

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.molcel.2011.02.014Licence: Other

Cite this

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title = "A role for dormant origins in tumor suppression",

abstract = "In this issue of Molecular Cell, Kawabata et al. (2011) show that mice hypomorphic for the replication licensing protein Mcm4 show spontaneous DNA replication defects due to a lack of dormant origins, potentially explaining why these mice are cancer prone.",

keywords = "REPLICATIVE STRESS, EXCESS MCM2-7, CANCER, MICE",

author = "Kathleen Klotz-Noack and Blow, {J. Julian}",

year = "2011",

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AU - Blow, J. Julian

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AB - In this issue of Molecular Cell, Kawabata et al. (2011) show that mice hypomorphic for the replication licensing protein Mcm4 show spontaneous DNA replication defects due to a lack of dormant origins, potentially explaining why these mice are cancer prone.

KW - REPLICATIVE STRESS

KW - EXCESS MCM2-7

KW - CANCER

KW - MICE

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DO - 10.1016/j.molcel.2011.02.014

M3 - Article

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EP - 496

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

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