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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 ELISA Kits)) patients treated with platinum-based chemoradiotherapy.
Upon UVC radiation, Nlp interacts with XPA and ERCC1 (show ERCC1 ELISA Kits), and enhances their association
Data suggest an association of high mobility group box 1 (HMGB1 (show HMGB1 ELISA Kits)) 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.
This study identified 13 novel mutations and extended the mutation spectrum of XP in the Chinese Han population
A tripartite lesion verification mechanism involving XPC (show XPC ELISA Kits), TFIIH (show GTF2H1 ELISA Kits), and XPA is necessary for efficient nucleotide excision repair.
Homozygous mutations in the XPA gene were seen in xeroderma pigmentosum patients with moderate to severe mental retardation (6/10 families) but not in those without neurological features.
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 ELISA Kits) 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 ELISA Kits)+/- 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 ELISA Kits)-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