Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/90081
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Type: Journal article
Title: The role of JNK signalling in responses to oxidative DNA damage
Author: Shaukat, Z.
Liu, D.
Hussain, R.
Khan, M.
Gregory, S.
Citation: Current drug targets, 2016; 17(2):154-163
Publisher: Bentham Science Publishers
Issue Date: 2016
ISSN: 1389-4501
1873-5592
Statement of
Responsibility: 
Zeeshan Shaukat, Dawei Liu, Rashid Hussain, Mahwish Khan and Stephen L. Gregory
Abstract: The production of reactive oxygen species is a normal part of cell physiology, but many internal and external stimuli are able to trigger the production of excess levels of oxidants that are potentially damaging. The threat of oxidative damage is particularly significant to DNA, as damaged bases can interfere with replication to generate lasting mutations. Signalling through the JNK pathway is a key cellular response to oxidative damage. Depending on the intensity and duration of the damage signal, JNK signalling can lead to distinct alternative responses including DNA repair, anti-oxidant production or cell death. These responses are highly relevant to cancer therapy, as tumours are often under oxidative stress that produces elevated JNK levels and therapy often involves inducing DNA damage with the intention of driving cell death. In this review we examine the causes and consequences of JNK activation that relate to oxidative DNA damage, with a focus on the potential therapeutic implications.
Keywords: Animals; Humans; Neoplasms; DNA Damage; Antineoplastic Agents; MAP Kinase Signaling System; Oxidative Stress
RMID: 0030022662
DOI: 10.2174/1389450116666150126111055
Grant ID: http://purl.org/au-research/grants/nhmrc/1027878
Published version: http://benthamscience.com/journal/abstracts.php?journalID=cdt&articleID=127995
Appears in Collections:Genetics publications

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