Chk1 loss creates replication barriers that compromise cell survival independently of excess origin firing

The effectiveness of checkpoint kinase 1 (Chk1) inhibitors at killing cancer cells is considered to be fully dependent on their effect on DNA replication initiation. Chk1 inhibition boosts origin firing, presumably limiting the availability of nucleotides and in turn provoking the slowdown and subse...

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Bibliographic Details
Published in:	The EMBO journal Vol. 38; no. 16; pp. e101284 - n/a
Main Authors:	González Besteiro, Marina A, Calzetta, Nicolás L, Loureiro, Sofía M, Habif, Martín, Bétous, Rémy, Pillaire, Marie‐Jeanne, Maffia, Antonio, Sabbioneda, Simone, Hoffmann, Jean‐Sébastien, Gottifredi, Vanesa
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 15.08.2019 Springer Nature B.V EMBO Press John Wiley and Sons Inc
Subjects:	Cdc45 protein Cell death Cell Line, Tumor Cell Proliferation Cell Survival Cell viability checkpoint kinase 1 Checkpoint Kinase 1 - genetics CHK1 protein Chromatin Collapse Damage accumulation Deoxyribonucleic acid DNA DNA biosynthesis DNA Damage DNA helicase DNA polymerase DNA Replication DNA-directed DNA polymerase DNA-Directed DNA Polymerase - metabolism Elongation EMBO13 Firing Gene Expression Regulation, Neoplastic Gene Knockdown Techniques - methods HCT116 Cells HEK293 Cells Humans Kinases Life Sciences Neoplasms - genetics Neoplasms - metabolism Nucleotides origin firing Phosphorylation Replication replication barrier Replication initiation Replication Origin Replication origins replicative helicase Survival Synergism translesion DNA polymerase eta Tumors replicative helicase checkpoint kinase 1 translesion DNA polymerase eta replication barrier origin firing Recombination Repair &amp translesion DNA polymerase eta Subject Categories DNA Replication checkpoint kinase 1 origin firing replication barrier replicative helicase translesion DNA polymerase eta Subject Categories DNA Replication
ISSN:	0261-4189, 1460-2075, 1460-2075
Online Access:	Get full text
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