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抗Human ERCC6 抗体:
抗Rat (Rattus) ERCC6 抗体:
抗Mouse (Murine) ERCC6 抗体:
CSB recruitment to DSBs is dependent upon an interaction between CSB's newly described winged-helix domain and the NHEJ factor RIF1 (显示 INSL6 抗体), but subsequent remodelling activity undertaken by CSB following DSB induction inhibits RIF1 (显示 INSL6 抗体) accumulation while promoting BRCA1-mediated HR repair. In vivo remodelling assays are used to demonstrate that CSB evicts histones following generation of DSBs in a manner controlled by ATM (显示 ATM 抗体) and CDK1 (显示 CDK1 抗体).
CSB regulates double strand break repair choice by recruiting HR factors BRCA1, RPA (显示 RPA1 抗体) and Rad51 (显示 RAD51 抗体) while suppressing NHEJ factors at damaged chromatin in S/G2 (显示 STRN3 抗体) cells. Loss of CSB impairs activation of ATM (显示 ATM 抗体) and downstream targets following induction of double strand breaks, and promotes premature exit from the G2/M checkpoint.
ERCC6 rs1917799, ERCC8 (显示 ERCC8 抗体) rs158572 and rs158916 demonstrated pairwise epistatic interactions to associate with chronic atrophic gastritis and gastric cancer risk. The ERCC6 rs1917799-ERCC8 (显示 ERCC8 抗体) rs158572 pair significantly influence ERCC6 and ERCC6-ERCC8 (显示 ERCC8 抗体) expression.
Let-7c-5p acted as a tumor suppressor in breast cancer possibly by negatively regulating ERCC6.
Loss of Cockayne syndrome group A protein (CSA (显示 ERCC8 抗体)) or Cockayne syndrome group B protein (CSB) leads to polymerase stalling at non-B DNA in a neuroblastoma (显示 ARHGEF16 抗体) cell line, in particular at G-quadruplex structures.
The present study reported two novel causative mutations on ERCC6 loci, and the clinical characteristics are described. These results add to clinical and molecular data for elucidating genotype-phenotype correlations in CS
Gene analysis showed mutations in exons 4 and 18 of the ERCC6 gene. Multiple ocular abnormalities were observed in a patient with Cockayne syndrome. A detailed ophthalmic evaluation of children with Cockayne syndrome is advised.
The role of ERCC6 in regulating response to 5-fluorouracil and drug resistance in colorectal cancer.Elevated expression of ERCC6 is associated with poor colorectal cancer patient survival.
NAP1L1 (显示 NAP1L1 抗体) increases CSB processivity by decreasing the pausing probability during translocation. Our study, therefore, uncovers the different steps of CSB-mediated chromatin remodeling that can be regulated by NAP1L1 (显示 NAP1L1 抗体).
pro-apoptotic effects observed after CSB ablation
Our data show that in addition to promoting repeat expansion, CSB does in fact protect the genome from germ line expansions in the FXD mouse model.
loss of CSB affects tandem-repeat expansions in a gender and cell-type-specific manner
CSB has been shown to regulate processes such as the transcriptional recovery after DNA damage, the p53 (显示 TP53 抗体) transcriptional response, the response to hypoxia, the response IGF-1 (显示 IGF1 抗体), transactivation of nuclear receptors, transcription of housekeeping genes
CSB and PCAF (显示 KAT2B 抗体) play cooperative roles to establish the active state of rRNA genes by histone acetylation
Csb-/- neural precursors exhibited defective self-renewal in the neurosphere assay.
Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a cs-b xp-c murine model of Cockayne syndrome
Testicular nuclear receptor 4 (TR4 (显示 NR2C2 抗体)) regulates UV light-induced responses via Cockayne syndrome B protein-mediated transcription-coupled DNA repair
Data suggest that Cockayne syndrome B protein protects CAG repeats from expansion by either active reduction of the tract length during parent-child transmission, or by antagonizing the action of OGG1 (显示 OGG1 抗体), which tends to promote expansion in somatic cells.
These results suggested that reduced repair of a DNA topoisomerase I-DNA covalent complex because of truncated CSB proteins is involved in the pathogenesis of CS-B.
MtDNA mutations are highly increased in cells from subcutaneous fat of aged Csb(m/m) mice
This gene encodes a DNA-binding protein that is important in transcription-coupled excision repair. The encoded protein has ATP-stimulated ATPase activity, interacts with several transcription and excision repair proteins, and may promote complex formation at DNA repair sites. Mutations in this gene are associated with Cockayne syndrome type B and cerebrooculofacioskeletal syndrome 1. Naturally-occurring readthrough transcription occurs between this gene and the adjacent PGBD3 gene (GeneID:267004), and results in a fusion protein that shares sequence with the product of each individual gene. The readthrough locus is represented by GeneID:101243544.
ATP-dependent helicase ERCC6
, Cockayne syndrome group B protein
, DNA excision repair protein ERCC-6
, cockayne syndrome protein CSB
, CS group B correcting
, excision repair cross-complementing rodent repair deficiency, complementation group 6