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Human XPA Primary Antibody for SDS - ABIN1098757
Pan, Lee: UV-dependent interaction between Cep164 and XPA mediates localization of Cep164 at sites of DNA damage and UV sensitivity. in Cell cycle (Georgetown, Tex.) 2009
XPA reduction increased cell viability of a bladder cancer cell line RT4, while XPA re-expression decreased the cell viability of RT4 cells. Study suggests that downregulated XPA may promote carcinogenesis of bladder cancer via impairment of DNA repair.
The risk of esophageal squamous cell carcinoma associated with XPA rs-1800975 was determined. A high ESCC risk was found in subjects who carried the homozygous minor allele of XPA, especially in smokers, those in adobe houses, drinkers of salt tea, or those with a family history of cancer. Variant genotypes of both XPA and XPC (show XPC Proteins) in combination showed an increased risk towards ESCC.
The role of conformational selection in the molecular recognition of the wild type and mutants XPA67-80 peptides by ERCC1 (show ERCC1 Proteins) has been described.
We discovered four new XP-A patients and a novel XPA mutation resulting in two diverse patient alleles.
a specific XPA genotype is associated with mild phenotype in Xeroderma Pigmentosum in United Kingdom immigrants from India, Pakistan, and Afghanistan
Findings suggest that xeroderma pigmentosum complementation group-A (XPA) levels may be a potential predictor of prognosis in locally advanced nasopharyngeal carcinoma (NPC (show NPC1 Proteins)) patients treated with platinum-based chemoradiotherapy.
Upon UVC radiation, Nlp interacts with XPA and ERCC1 (show ERCC1 Proteins), and enhances their association
Data suggest an association of high mobility group box 1 (HMGB1 (show HMGB1 Proteins)) with xeroderma pigmentosum complementation group A (XPA) protein facilitates the formation of a favorable architectural environment for DNA interstrand crosslinks (ICLs) repair processing.
The lack of XPA significantly enhanced the mutant proportion of tandem 8-oxoG in the transcribed strand (12%) compared with that in TSCER122 cells (7.4%) but not in the non-transcribed strand.
Xeroderma pigmentosum syndrome is rarely associated with inherited disease-causing XPA mutations in the Brazilian population.
The authors' results suggest that lack of the DNA repair factor XPA may delay neurobehavioral recovery after TBI (show TBPL1 Proteins)
Oxidized glycerophosphocholines play a pivotal role in the photosensitivity associated with the deficiency of XPA.
The tissue-specific effect of Xpa deficiency represents a novel finding; it suggests that tissue-to-tissue variation in CAG repeat (show CELF3 Proteins) instability arises, in part, by different underlying mechanisms.
The circadian oscillation of XPA is achieved both by regulation of transcription by the core circadian clock proteins including cryptochrome and by regulation at the posttranslational level by the HERC2 ubiquitin ligase.
The Xpa/p53 (show TP53 Proteins)+/- mouse model is an excellent candidate for a future replacement of the chronic mouse bioassay for certain classes of chemicals.
Xeroderma pigmentosum group A (XPA) gene-deficient mice cannot repair UV-induced DNA damage and easily develop skin cancers by UV irradiation. UVB-induced local and systemic immunosuppression was greatly enhanced in the (-/-) mice.
Enhanced spontaneous and aflatoxin-induced liver tumorigenesis in xeroderma pigmentosum group A gene-deficient mice
XPA (-/-), SCF (show KITLG Proteins)-Tg mice did not develop skin cancers after repeated exposures to UVB for 30 wk at a total dose of 72 J per cm(2)
Xpa-/- keratinocytes (complete nucleotide excision repair deficiency) show a rapid depletion of DNA replicating S-phase cells, a transient increase in quiescent S-phase cells (not replicating DNA), followed by massive apoptosis.
The human carcinogen phenacetin acts as a weak genotoxic agent in an in vivo mouse model system in an Xpa deficient model.
This gene encodes a zinc finger protein involved in DNA excision repair. The encoded protein is part of the NER (nucleotide excision repair) complext which is responsible for repair of UV radiation-induced photoproducts and DNA adducts induced by chemical carcinogens. Mutations in this gene are associated with xeroderma pigmentosum complementation group A. Alternatively spliced transcript variants have been found for this gene.
, xeroderma pigmentosum group A-like
, DNA repair protein complementing XP-A cells
, excision repair-controlling
, xeroderma pigmentosum group A-complementing protein
, DNA repair protein complementing XP-A cells homolog
, xeroderma pigmentosum group A-complementing protein homolog
, xpacch protein
, xpacx1 protein