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dc.contributor.authorWong, H.en
dc.contributor.authorShaukat, Z.en
dc.contributor.authorWang, J.en
dc.contributor.authorSaint, R.en
dc.contributor.authorGregory, S.en
dc.identifier.citationCell Cycle, 2014; 13(4):622-631en
dc.descriptionPublished Online 12 Dec 2013en
dc.description.abstractChromosomal instability (CIN), as a common feature of tumors, represents a potential therapeutic target if ways can be found to specifically cause apoptosis in unstably dividing cells. We have previously shown that if signaling through the JNK pathway is reduced, apoptosis is triggered in models of chromosomal instability induced by loss of the spindle checkpoint. Here we identify components upstream and downstream of JNK that are able to mediate this effect, and test the involvement of p53 and DNA damage in causing apoptosis when JNK signaling is reduced in CIN cells. We show that cell cycle progression timing has a strong effect on the apoptosis seen when JNK signaling is reduced in genetically unstable cells: a shortened G₂ phase enhances the apoptosis, while lengthening G₂ rescues the JNK-deficient CIN cell death phenotype. Our findings suggest that chromosomal instability represents a significant stress to dividing cells, and that without JNK signaling, cells undergo apoptosis because they lack a timely and effective response to DNA damage.en
dc.description.statementofresponsibilityHeidi W-S Wong, Zeeshan Shaukat, Jianbin Wang, Robert Saint, and Stephen L Gregoryen
dc.publisherLandes Bioscienceen
dc.rights© 2014 Landes Bioscienceen
dc.subjectChromosomal instability; JNK; Drosophila; apoptosis; Mad2en
dc.titleJNK signaling is needed to tolerate chromosomal instabilityen
dc.typeJournal articleen
pubs.library.collectionMolecular and Biomedical Science publicationsen
dc.identifier.orcidGregory, S. [0000-0002-0046-5815]en
Appears in Collections:Molecular and Biomedical Science publications

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