HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
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Remodeling and Control of Homologous Recombination by DNA Helicases and Translocases that Target Recombinases and SynapsisA structure-specific nucleic acid-binding domain conserved among DNA repair proteinsDNA Polymerase θ: A Unique Multifunctional End-Joining MachineCSB-PGBD3 Mutations Cause Premature Ovarian FailureGenetic variants in DNA repair pathways and risk of upper aerodigestive tract cancers: combined analysis of data from two genome-wide association studies in European populations.Analysis of DNA polymerase ν function in meiotic recombination, immunoglobulin class-switching, and DNA damage tolerance.Hypersensitivity of primordial germ cells to compromised replication-associated DNA repair involves ATM-p53-p21 signalingRad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells.Conserved overlapping gene arrangement, restricted expression, and biochemical activities of DNA polymerase ν (POLN).FANCJ suppresses microsatellite instability and lymphomagenesis independent of the Fanconi anemia pathway.Structure-function analysis of DNA helicase HELQ: A new diagnostic marker in ovarian cancer.Hrq1, a homolog of the human RecQ4 helicase, acts catalytically and structurally to promote genome integrity.Association of breast cancer risk with genetic variants showing differential allelic expression: Identification of a novel breast cancer susceptibility locus at 4q21.Replication fork reversal in eukaryotes: from dead end to dynamic response.Overexpression of thymidylate synthase (TYMS) is associated with aggressive tumor features and early PSA recurrence in prostate cancer.Pan-cancer analysis of homozygous deletions in primary tumours uncovers rare tumour suppressors.The helicase domain of Polθ counteracts RPA to promote alt-NHEJ.A Role for the Twins Protein Phosphatase (PP2A-B55) in the Maintenance of Drosophila Genome Integrity.AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in MiceHigh expression of the breast cancer susceptibility gene BRCA1 in long-lived termite kingsPolymerase θ-helicase efficiently unwinds DNA and RNA-DNA hybridsCRISPR-Cas immunity, DNA repair and genome stability
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HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 04 September 2013
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
@en
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
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type
label
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
@en
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
@nl
prefLabel
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
@en
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
@nl
P2093
P2860
P50
P356
P1433
P1476
HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis.
@en
P2093
Alan D'Andrea
Carrie A Adelman
Gordon Stamp
J Mark Skehel
Kalindi Parmar
Kenichiro Matsuzaki
Rafal L Lolo
Simon J Boulton
Valérie Borel
P2860
P2888
P304
P356
10.1038/NATURE12565
P407
P577
2013-09-04T00:00:00Z
P5875
P6179
1015344515