Activation of BRCA1/BRCA2-associated helicase BACH1 is required for timely progression through S phase.
about
Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndromeHow the fanconi anemia pathway guards the genomeThe Fanconi anemia pathway and DNA interstrand cross-link repairCellular and molecular consequences of defective Fanconi anemia proteins in replication-coupled DNA repair: mechanistic insightsMitotic homologous recombination maintains genomic stability and suppresses tumorigenesisFancJ (Brip1) loss-of-function allele results in spermatogonial cell depletion during embryogenesis and altered processing of crossover sites during meiotic prophase I in miceFANCJ helicase uniquely senses oxidative base damage in either strand of duplex DNA and is stimulated by replication protein A to unwind the damaged DNA substrate in a strand-specific manner.Overexpression of RAD51 suppresses recombination defects: a possible mechanism to reverse genomic instability.BACH1/FANCJ acts with TopBP1 and participates early in DNA replication checkpoint control.Mechanistic and biological aspects of helicase action on damaged DNA.Insight into the roles of helicase motif Ia by characterizing Fanconi anemia group J protein (FANCJ) patient mutationsMutations in the BRCT binding site of BRCA1 result in hyper-recombinationNovel function of the Fanconi anemia group J or RECQ1 helicase to disrupt protein-DNA complexes in a replication protein A-stimulated manner.G-quadruplex nucleic acids and human diseaseBRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair.MicroRNA profiling of follicular lymphoma identifies microRNAs related to cell proliferation and tumor response.BRCA1-directed, enhanced and aberrant homologous recombination: mechanism and potential treatment strategies.Poly (ADP-ribose) polymerase as a novel therapeutic target in cancer.Fanconi anemia group J mutation abolishes its DNA repair function by uncoupling DNA translocation from helicase activity or disruption of protein-DNA complexes.Genome-wide analysis reveals a role for BRCA1 and PALB2 in transcriptional co-activationMolecular and cellular functions of the FANCJ DNA helicase defective in cancer and in Fanconi anemiaFANCB is essential in the male germline and regulates H3K9 methylation on the sex chromosomes during meiosis.Mutation of the BRCA1 SQ-cluster results in aberrant mitosis, reduced homologous recombination, and a compensatory increase in non-homologous end joining.Helicase-inactivating mutations as a basis for dominant negative phenotypes.Hereditary breast cancer and the BRCA1-associated FANCJ/BACH1/BRIP1.A distinct triplex DNA unwinding activity of ChlR1 helicaseOncogenic RAS regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence.BRCA1 tumor suppressor network: focusing on its tail.DNA helicases involved in DNA repair and their roles in cancerDNA helicase and helicase-nuclease enzymes with a conserved iron-sulfur cluster.The Q motif of Fanconi anemia group J protein (FANCJ) DNA helicase regulates its dimerization, DNA binding, and DNA repair function.BRCA1 regulation of epidermal growth factor receptor (EGFR) expression in human breast cancer cells involves microRNA-146a and is critical for its tumor suppressor function.FANCJ helicase defective in Fanconia anemia and breast cancer unwinds G-quadruplex DNA to defend genomic stabilityFANCJ couples replication past natural fork barriers with maintenance of chromatin structure.BRCA1 in the DNA damage response and at telomeresFANCJ at the FORK.Fanconi anemia proteins, DNA interstrand crosslink repair pathways, and cancer therapy.FANCJ uses its motor ATPase to destabilize protein-DNA complexes, unwind triplexes, and inhibit RAD51 strand exchange.Welcome the family of FANCJ-like helicases to the block of genome stability maintenance proteins.Specialization among iron-sulfur cluster helicases to resolve G-quadruplex DNA structures that threaten genomic stability.
P2860
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P2860
Activation of BRCA1/BRCA2-associated helicase BACH1 is required for timely progression through S phase.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh
2007年學術文章
@zh-hant
name
Activation of BRCA1/BRCA2-asso ...... y progression through S phase.
@en
type
label
Activation of BRCA1/BRCA2-asso ...... y progression through S phase.
@en
prefLabel
Activation of BRCA1/BRCA2-asso ...... y progression through S phase.
@en
P2860
P356
P1476
Activation of BRCA1/BRCA2-asso ...... y progression through S phase.
@en
P2093
Easwari Kumaraswamy
Ramin Shiekhattar
P2860
P304
P356
10.1128/MCB.00961-07
P407
P577
2007-07-30T00:00:00Z