RAD18 and poly(ADP-ribose) polymerase independently suppress the access of nonhomologous end joining to double-strand breaks and facilitate homologous recombination-mediated repair.
about
RNAi-based screening identifies the Mms22L-Nfkbil2 complex as a novel regulator of DNA replication in human cells.The Role of PCNA Posttranslational Modifications in Translesion SynthesisChemotherapeutic compounds targeting the DNA double-strand break repair pathways: the good, the bad, and the promisingHuman RAD18 interacts with ubiquitylated chromatin components and facilitates RAD9 recruitment to DNA double strand breaksExpanded roles of the Fanconi anemia pathway in preserving genomic stability53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaksGenetic evidence for single-strand lesions initiating Nbs1-dependent homologous recombination in diversification of Ig v in chicken B lymphocytes.Structure/function analysis of PARP-1 in oxidative and nitrosative stress-induced monomeric ADPR formation.GEMIN2 promotes accumulation of RAD51 at double-strand breaks in homologous recombinationThe BRCT domain of PARP-1 is required for immunoglobulin gene conversion.The alternative end-joining pathway for repair of DNA double-strand breaks requires PARP1 but is not dependent upon microhomologies.RAD18-mediated ubiquitination of PCNA activates the Fanconi anemia DNA repair network.Chronic treatment with cisplatin induces replication-dependent sister chromatid recombination to confer cisplatin-resistant phenotype in nasopharyngeal carcinoma.Nonhomologous end joining drives poly(ADP-ribose) polymerase (PARP) inhibitor lethality in homologous recombination-deficient cells.UbcH7 regulates 53BP1 stability and DSB repairDNA ligase IV and artemis act cooperatively to suppress homologous recombination in human cells: implications for DNA double-strand break repair.RNF8-independent Lys63 poly-ubiquitylation prevents genomic instability in response to replication-associated DNA damage.Impaired 53BP1/RIF1 DSB mediated end-protection stimulates CtIP-dependent end resection and switches the repair to PARP1-dependent end joining in G1.Cell cycle stage-specific roles of Rad18 in tolerance and repair of oxidative DNA damageHyper-active non-homologous end joining selects for synthetic lethality resistant and pathological Fanconi anemia hematopoietic stem and progenitor cells.Targeted radiosensitization of ETS fusion-positive prostate cancer through PARP1 inhibition.RAD18 transmits DNA damage signalling to elicit homologous recombination repairRole of multifunctional transcription factor TFII-I and putative tumour suppressor DBC1 in cell cycle and DNA double strand damage repair.Poly(ADP-ribosyl)ation polymerases: mechanism and new target of anticancer therapy.Ubiquitin family modifications and template switching.Charity begins at home: non-coding RNA functions in DNA repairEnd-joining, translocations and cancer.Targeted radiosensitization with PARP1 inhibition: optimization of therapy and identification of biomarkers of response in breast cancer.Chromosomal Rearrangements in Cancer: Detection and potential causal mechanisms.Regulatory cross-talk determines the cellular levels of 53BP1 protein, a critical factor in DNA repair.Rad18 and Rnf8 facilitate homologous recombination by two distinct mechanisms, promoting Rad51 focus formation and suppressing the toxic effect of nonhomologous end joining.ATR-Chk1-APC/CCdh1-dependent stabilization of Cdc7-ASK (Dbf4) kinase is required for DNA lesion bypass under replication stressMechanisms of DNA damage, repair, and mutagenesis.Rad18 E3 ubiquitin ligase activity mediates Fanconi anemia pathway activation and cell survival following DNA Topoisomerase 1 inhibition.DNA polymerases nu and theta are required for efficient immunoglobulin V gene diversification in chicken.Roles of human AND-1 in chromosome transactions in S phaseRAD18 promotes DNA double-strand break repair during G1 phase through chromatin retention of 53BP1.The 9-1-1 DNA clamp is required for immunoglobulin gene conversion.The RecQ helicase WRN is required for normal replication fork progression after DNA damage or replication fork arrest.ALC1/CHD1L, a chromatin-remodeling enzyme, is required for efficient base excision repair.
P2860
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P2860
RAD18 and poly(ADP-ribose) polymerase independently suppress the access of nonhomologous end joining to double-strand breaks and facilitate homologous recombination-mediated repair.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair.
@ast
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair.
@en
type
label
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair.
@ast
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair.
@en
prefLabel
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair.
@ast
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair.
@en
P2093
P2860
P50
P356
P1476
RAD18 and poly(ADP-ribose) pol ...... recombination-mediated repair
@en
P2093
Akira Yasui
Hirobumi Teraoka
Hiroshi Arakawa
Jean-Marie Buerstedde
Kyoko Yokomori
Shunichi Takeda
Weihua Zeng
Yasuhiro Murakawa
Yoshihito Taniguchi
P2860
P304
P356
10.1128/MCB.01243-06
P407
P577
2007-01-22T00:00:00Z