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This study suggested that the XPA gene rs1800975 Polymorphism was associated with lung cancer susceptibility. By performing multiple separate pairwise comparisons, carriers with AG genotype under the codominant genetic model (AG vs. AA) might play actually the leading role in associating with lung cancer susceptibility in overall and in Asians.
We have suggested that the nuclear localization signal on XPA is masked, perhaps in a complex with a cytosolic XPA sequestration protein, and that this complex is disrupted by methanol fixation in non-stressed cells and as part of the DNA damage response following UV irradiation
It can be concluded that A23G XPA polymorphism might contribute to increased lung cancer risk in North Indian population emphasizing on poor survival among females
molecular analysis of the 5 other exons of the XPA gene, showed that the 2 negative siblings carried no mutation in the XPA gene. This finding suggests that c.682C>T (p.Arg228X) mutation is relatively associated with moderate phenotype in XP group A Moroccan families
XPA rs1800975 polymorphism may decrease the risk of breast cancer in both non-Asians and population-based patients
Our results indicate that increased XP-1 levels were associated with PCOS after adjustment for potential confounders, which has been shown to be effective in the function of the insulin (show INS Proteins) signaling pathway.
data obtained allow us to suggest that XPA can be involved in the post-incision NER stages via its interaction with RPA
Data suggest that the multi-protein interactions involved in the nucleotide excision repair (NER (show NR1H2 Proteins)) process and potential cytotoxic mechanism associated with Ni(2 (show VMP1 Proteins)+) binding in xeroderma pigmentosum complementation group A protein (XPA) may facilitate rational anti-cancer drug design based on the NER (show NR1H2 Proteins) 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.
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 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