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Literature DB >> 21963239

BRCA1 is required for postreplication repair after UV-induced DNA damage.

Shailja Pathania¹, Jenna Nguyen, Sarah J Hill, Ralph Scully, Guillaume O Adelmant, Jarrod A Marto, Jean Feunteun, David M Livingston.

Abstract

BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.

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Year: 2011 PMID： 21963239 PMCID： PMC3200447 DOI： 10.1016/j.molcel.2011.09.002

Source DB: PubMed Journal: Mol Cell ISSN： 1097-2765 Impact factor: 17.970

68 in total

1. Regulation of ATR substrate selection by Rad17-dependent loading of Rad9 complexes onto chromatin.

Authors: Lee Zou; David Cortez; Stephen J Elledge
Journal: Genes Dev Date: 2002-01-15 Impact factor: 11.361

2. Analysis of nucleotide excision repair by detection of single-stranded DNA transients.

Authors: C P Rubbi; J Milner
Journal: Carcinogenesis Date: 2001-11 Impact factor: 4.944

3. Loading of the human 9-1-1 checkpoint complex onto DNA by the checkpoint clamp loader hRad17-replication factor C complex in vitro.

Authors: Vladimir P Bermudez; Laura A Lindsey-Boltz; Anthony J Cesare; Yoshimasa Maniwa; Jack D Griffith; Jerard Hurwitz; Aziz Sancar
Journal: Proc Natl Acad Sci U S A Date: 2003-02-10 Impact factor: 11.205

Review 4. Pathways of mammalian replication fork restart.

Authors: Eva Petermann; Thomas Helleday
Journal: Nat Rev Mol Cell Biol Date: 2010-09-15 Impact factor: 94.444

5. Genetic analysis of BRCA1 function in a defined tumor cell line.

Authors: R Scully; S Ganesan; K Vlasakova; J Chen; M Socolovsky; D M Livingston
Journal: Mol Cell Date: 1999-12 Impact factor: 17.970

6. RAP80-directed tuning of BRCA1 homologous recombination function at ionizing radiation-induced nuclear foci.

Authors: Yiduo Hu; Ralph Scully; Bijan Sobhian; Anyong Xie; Elena Shestakova; David M Livingston
Journal: Genes Dev Date: 2011-03-15 Impact factor: 11.361

7. Brca1 controls homology-directed DNA repair.

Authors: M E Moynahan; J W Chiu; B H Koller; M Jasin
Journal: Mol Cell Date: 1999-10 Impact factor: 17.970

8. Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions.

Authors: Vassilis G Gorgoulis; Leandros-Vassilios F Vassiliou; Panagiotis Karakaidos; Panayotis Zacharatos; Athanassios Kotsinas; Triantafillos Liloglou; Monica Venere; Richard A Ditullio; Nikolaos G Kastrinakis; Brynn Levy; Dimitris Kletsas; Akihiro Yoneta; Meenhard Herlyn; Christos Kittas; Thanos D Halazonetis
Journal: Nature Date: 2005-04-14 Impact factor: 49.962

9. Fork reversal and ssDNA accumulation at stalled replication forks owing to checkpoint defects.

Authors: José M Sogo; Massimo Lopes; Marco Foiani
Journal: Science Date: 2002-07-26 Impact factor: 47.728

10. BRCA1 induces DNA damage recognition factors and enhances nucleotide excision repair.

Authors: Anne-Renee Hartman; James M Ford
Journal: Nat Genet Date: 2002-08-26 Impact factor: 38.330

71 in total

1. Prediction of DNA Repair Inhibitor Response in Short-Term Patient-Derived Ovarian Cancer Organoids.

Authors: Sarah J Hill; Brennan Decker; Emma A Roberts; Neil S Horowitz; Michael G Muto; Michael J Worley; Colleen M Feltmate; Marisa R Nucci; Elizabeth M Swisher; Huy Nguyen; Chunyu Yang; Ryuji Morizane; Bose S Kochupurakkal; Khanh T Do; Panagiotis A Konstantinopoulos; Joyce F Liu; Joseph V Bonventre; Ursula A Matulonis; Geoffrey I Shapiro; Ross S Berkowitz; Christopher P Crum; Alan D D'Andrea
Journal: Cancer Discov Date: 2018-09-13 Impact factor: 39.397

2. USP1 Is Required for Replication Fork Protection in BRCA1-Deficient Tumors.

Authors: Kah Suan Lim; Heng Li; Emma A Roberts; Emily F Gaudiano; Connor Clairmont; Larissa Alina Sambel; Karthikeyan Ponnienselvan; Jessica C Liu; Chunyu Yang; David Kozono; Kalindi Parmar; Timur Yusufzai; Ning Zheng; Alan D D'Andrea
Journal: Mol Cell Date: 2018-12-20 Impact factor: 17.970

BRCA1 is required for postreplication repair after UV-induced DNA damage.

1. Regulation of ATR substrate selection by Rad17-dependent loading of Rad9 complexes onto chromatin.

2. Analysis of nucleotide excision repair by detection of single-stranded DNA transients.

3. Loading of the human 9-1-1 checkpoint complex onto DNA by the checkpoint clamp loader hRad17-replication factor C complex in vitro.

Review 4. Pathways of mammalian replication fork restart.

5. Genetic analysis of BRCA1 function in a defined tumor cell line.

6. RAP80-directed tuning of BRCA1 homologous recombination function at ionizing radiation-induced nuclear foci.

7. Brca1 controls homology-directed DNA repair.

8. Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions.

9. Fork reversal and ssDNA accumulation at stalled replication forks owing to checkpoint defects.

10. BRCA1 induces DNA damage recognition factors and enhances nucleotide excision repair.

1. Prediction of DNA Repair Inhibitor Response in Short-Term Patient-Derived Ovarian Cancer Organoids.

2. USP1 Is Required for Replication Fork Protection in BRCA1-Deficient Tumors.

3. BRCA1 forks over new roles in DNA-damage response- before and beyond the breaks.

Review 4. Exploiting replicative stress to treat cancer.

5. Augmented generation of protein fragments during wakefulness as the molecular cause of sleep: a hypothesis.

6. PARI overexpression promotes genomic instability and pancreatic tumorigenesis.

7. Tandem Affinity Purification and Mass Spectrometry (TAP-MS) for the Analysis of Protein Complexes.

Review 8. Mechanisms of BRCA1 tumor suppression.

9. BRCA1 pathway function in basal-like breast cancer cells.

10. RING domain-deficient BRCA1 promotes PARP inhibitor and platinum resistance.