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anti-Human XPA Antibodies:
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Human Monoclonal XPA Primary Antibody for IP, WB - ABIN967532
Aboussekhra, Biggerstaff, Shivji, Vilpo, Moncollin, Podust, Protić, Hübscher, Egly, Wood: Mammalian DNA nucleotide excision repair reconstituted with purified protein components. in Cell 1995
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Human Monoclonal XPA Primary Antibody for Inhibition, ELISA - ABIN3200998
Tanaka, Miura, Satokata, Miyamoto, Yoshida, Satoh, Kondo, Yasui, Okayama, Okada: Analysis of a human DNA excision repair gene involved in group A xeroderma pigmentosum and containing a zinc-finger domain. in Nature 1990
Show all 2 Pubmed References
Human Polyclonal XPA Primary Antibody for IHC (p), WB - ABIN2477157
Jones, Wood: Preferential binding of the xeroderma pigmentosum group A complementing protein to damaged DNA. in Biochemistry 1993
Show all 3 Pubmed References
Human Monoclonal XPA Primary Antibody for ICC, IF - ABIN4219741
ODowd, Zavala, Brown, Mori, Fortunato: HCMV-infected cells maintain efficient nucleotide excision repair of the viral genome while abrogating repair of the host genome. in PLoS pathogens 2012
Data suggest that the multi-protein interactions involved in the nucleotide excision repair (NER (show NR1H2 Antibodies)) process and potential cytotoxic mechanism associated with Ni(2 (show VMP1 Antibodies)+) binding in xeroderma pigmentosum complementation group A protein (XPA) may facilitate rational anti-cancer drug design based on the NER (show NR1H2 Antibodies) mechanism.
XPA status does not globally influence human gene transcription. However, XPA significantly influences expression of a small subset of genes important for mitochondrial functions and steroid hormone metabolism.
These results suggest that for XPA mutants exhibiting altered DNA-binding properties, a correlation exists between the extent of reduction in DNA-binding affinity and the severity of symptoms in XP patients.
These results illustrate that EZH2 (show EZH2 Antibodies) may promote carcinogenesis and cancer development of nasopharyngeal carcinoma by transcriptional repression of XPA gene and inactivation of nucleotide excision repair pathway.
SNP rs10817938 in promoter region associated with poor prognosis of oral squamous cell carcinoma in Chinese Han population
We showed that loss of HERC2 function leads to the accumulation of XPA and BRCA1 in the patient's fibroblasts and generates decreased sensitivity to apoptosis and increased level of DNA repair
Accumulating evidence suggests that XPA and the helicase activity of transcription factor IIH (TFIIH (show GTF2H1 Antibodies)) cooperate to verify abnormalities in damaged DNA chemistry. (Review)
XPA is a key scaffold protein (show HOMER1 Antibodies) for human nucleotide excision repair. (Review)
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 Antibodies) in combination showed an increased risk towards ESCC.
The authors' results suggest that lack of the DNA repair factor XPA may delay neurobehavioral recovery after TBI
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 Antibodies) 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 Antibodies)+/- 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 Antibodies)-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