Recruitment of fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication - Wikidata - wikimedia - TriplyDB

Recruitment of fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication

Recruitment of fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication

http://www.wikidata.org/entity/Q33502468

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Rif1 provides a new DNA-binding interface for the Bloom syndrome complex to maintain normal replication INO80 chromatin remodeling complex promotes the removal of UV lesions by the nucleotide excision repair pathway A histone-fold complex and FANCM form a conserved DNA-remodeling complex to maintain genome stability Fanconi anemia (FA) binding protein FAAP20 stabilizes FA complementation group A (FANCA) and participates in interstrand cross-link repair A ubiquitin-binding protein, FAAP20, links RNF8-mediated ubiquitination to the Fanconi anemia DNA repair network Susceptibility pathways in Fanconi's anemia and breast cancer High mobility group protein 1: A collaborator in nucleosome dynamics and estrogen-responsive gene expression Structure of the FANCI-FANCD2 Complex: Insights into the Fanconi Anemia DNA Repair Pathway Fanconi anaemia and the repair of Watson and Crick DNA crosslinks Mammalian nucleotide excision repair proteins and interstrand crosslink repair Advances in understanding the complex mechanisms of DNA interstrand cross-link repair Human variation databases The FANCM/FAAP24 complex is required for the DNA interstrand crosslink-induced checkpoint response CtIP maintains stability at common fragile sites and inverted repeats by end resection-independent endonuclease activity.Mutagenic repair of DNA interstrand crosslinks.The BRCA1-interacting protein Abraxas is required for genomic stability and tumor suppression.Using synthetic DNA interstrand crosslinks to elucidate repair pathways and identify new therapeutic targets for cancer chemotherapy.Orchestrating the nucleases involved in DNA interstrand cross-link (ICL) repair.Repair of cisplatin-induced DNA interstrand crosslinks by a replication-independent pathway involving transcription-coupled repair and translesion synthesis DNA double strand breaks but not interstrand crosslinks prevent progress through meiosis in fully grown mouse oocytes.Fanconi anemia group J helicase and MRE11 nuclease interact to facilitate the DNA damage response.The Fanconi anemia pathway and ICL repair: implications for cancer therapy.BRCA1 is required for postreplication repair after UV-induced DNA damage Alcohol metabolism in human cells causes DNA damage and activates the Fanconi anemia-breast cancer susceptibility (FA-BRCA) DNA damage response network.Rescue of replication failure by Fanconi anaemia proteins.Single Molecule Analysis of Laser Localized Interstrand Crosslinks.Personalized therapy for urothelial cancer: review of the clinical evidence.UHRF1 contributes to DNA damage repair as a lesion recognition factor and nuclease scaffold.FANCM and FAAP24 maintain genome stability via cooperative as well as unique functions FANCJ at the FORK.Construction of plasmids containing site-specific DNA interstrand cross-links for biochemical and cell biological studies.DNA crosslinking damage and cancer - a tale of friend and foe.Ubiquitylation and the Fanconi anemia pathway.BRCA1 and its toolbox for the maintenance of genome integrity Repair of DNA interstrand cross-links during S phase of the mammalian cell cycle.The Fanconi anemia pathway in replication stress and DNA crosslink repair.REV1 and DNA polymerase zeta in DNA interstrand crosslink repair.The roles of DNA polymerase ζ and the Y family DNA polymerases in promoting or preventing genome instability.The yin and yang of repair mechanisms in DNA structure-induced genetic instability.The differences between ICL repair during and outside of S phase

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P2860

Recruitment of fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication

http://www.wikidata.org/entity/Q33502468

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2009 nî lūn-bûn

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2009 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2009 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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Recruitment of fanconi anemia ...... tially governed by replication

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Recruitment of fanconi anemia ...... tially governed by replication

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Recruitment of fanconi anemia ...... tially governed by replication

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J.MOLCEL.2009.06.034

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Recruitment of fanconi anemia ...... tially governed by replication

@en

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Bing Xia

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Huong Do

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Johan P de Winter

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Lei Li

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Maria Tomasz

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Stephen J Elledge

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Weidong Wang

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Woo-Hyun Chung

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Xi Shen

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Yongjiang Li

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P2860

Mechanistic insight into site-restricted monoubiquitination of FANCD2 by Ube2t, FANCL, and FANCI

Nucleotide excision repair- and polymerase eta-mediated error-prone removal of mitomycin C interstrand cross-links

PALB2, which encodes a BRCA2-interacting protein, is a breast cancer susceptibility gene

Identification of the FANCI protein, a monoubiquitinated FANCD2 paralog required for DNA repair

Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway

A novel ubiquitin ligase is deficient in Fanconi anemia

Biallelic inactivation of BRCA2 in Fanconi anemia

Involvement of nucleotide excision repair in a recombination-independent and error-prone pathway of DNA interstrand cross-link repair.

Human RPA (hSSB) interacts with EBNA1, the latent origin binding protein of Epstein-Barr virus

Human DNA replication initiation factors, ORC and MCM, associate with oriP of Epstein-Barr virus.

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