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anti-Human XPC Antikörper:
anti-Mouse (Murine) XPC Antikörper:
anti-Rat (Rattus) XPC Antikörper:
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Human Monoclonal XPC Primary Antibody für ICC, IF - ABIN151924
Aboussekhra, Biggerstaff, Shivji, Vilpo, Moncollin, Podust, Protić, Hübscher, Egly, Wood: Mammalian DNA nucleotide excision repair reconstituted with purified protein components. in Cell 1995
Show all 18 Pubmed References
Human Polyclonal XPC Primary Antibody für IP, WB - ABIN188792
Rageul, Frëmin, Ezan, Baffet, Langouët: The knock-down of ERCC1 but not of XPF causes multinucleation. in DNA repair 2011
Show all 2 Pubmed References
Human Polyclonal XPC Primary Antibody für WB - ABIN1882000
Stern, Lin, Figueroa, Kelsey, Kiltie, Yuan, Matullo, Fletcher, Benhamou, Taylor, Placidi, Zhang, Steineck, Rothman, Kogevinas, Silverman, Malats, Chanock, Wu, Karagas: Polymorphisms in DNA repair genes, smoking, and bladder cancer risk: findings from the international consortium of bladder cancer. in Cancer research 2009
Human Polyclonal XPC Primary Antibody für IF (p), IHC (p) - ABIN719171
Biswas, Mitchell, Johnson: E2F1 responds to ultraviolet radiation by directly stimulating DNA repair and suppressing carcinogenesis. in Cancer research 2014
Allelic variants in the gene XPC are not associated with an increased risk for developing pre-senile cataract
XPC dissociation from the damage site could become a rate-limiting step in nucleotide excision repair (NER (zeige NR1H2 Antikörper)) of certain types of DNA adducts, leading to repression of NER (zeige NR1H2 Antikörper).
Histone deacetylation plays a significant role in the process of DNA damage recognition for nucleotide excision repair and the localization and functions of XPC can be regulated by acetylated states of histones.
The risk of esophageal squamous cell carcinoma associated with XPC rs-2228000 was determined. A homozygous minor allele showed strong association with ESCC risk, especially in smokers, those in adobe houses, and drinkers of salt tea. Variant genotypes of both XPA (zeige XPA Antikörper) and XPC in combination showed an increased risk towards ESCC.
the associations between three XPC gene polymorphisms (rs2228001 A>C, rs2228000 C>T, and rs2229090 G>C) and neuroblastoma risk with 256 neuroblastoma patients and 531 healthy controls in a Chinese Han population, were investigated.
XPC polymorphisms are associated with gastric cancer and atrophic gastritis risks.
A chirality change in XPC- and Sfi1 (zeige SFI1 Antikörper)-derived peptides affects their affinity for centrin (zeige CETN1 Antikörper).
XPC intron11 C/A polymorphism was associated with an increased risk of prostate cancer. Among non-smokers, the A/A genotype was significantly more prevalent in prostate cancer patients than in controls.
No association between XPC polymorphisms and grades/stages of tumors, but report significant association between XPC PAT and reduction of prostate cancer risk in this group of patients.
Structural insight into the mechanism of TFIIH (zeige GTF2H1 Antikörper) recognition by the acidic string of the nucleotide excision repair factor XPC has been uncovered.
results suggest that XPC may help repair DNA damage caused by KRAS-mediated production of ROS (zeige ROS1 Antikörper).
OCT4 (zeige POU5F1 Antikörper) and SOX2 (zeige SOX2 Antikörper) are the primary transcription factors recruiting SCC (zeige CYP11A1 Antikörper) to regulatory regions of pluripotency genes; the XPC subunit is essential for interaction with the two proteins
progerin and p16(INK4a (zeige CDKN2A Antikörper)) expression, beta-galactosidase (zeige GLB1 Antikörper) activity, and reactive oxygen species, which increase with age, were higher in young Xpc(-/-) mice than in young Xpc(+/+) ones
Study indicates that Xpc(-/-) mice have an increased mutational load upon induction of oxidative stress. The effect of non-functional XPC in vivo appears to have implications in mutagenesis, which can contribute to the carcinogenesis process.
The C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 (zeige POU5F1 Antikörper) in mouse embryonic stem cells.
BRAF (zeige BRAF Antikörper)(V600E) and ARF (zeige CDKN2A Antikörper) deletion synergize to inhibit nucleotide excision repair by epigenetically repressing XPC.
Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a cs-b xp-c murine model of Cockayne syndrome
analysis of mHR23A/B double-mutant cells showed that HR23 proteins function in nucleotide excision repair by governing xeroderma pigmentosum group C protein stability via partial protection against proteasomal degradation
mutational hot spot is not at a dipyrimidine site and is apparently Xpc-specific, suggesting some form of non-dipyrimidine base damage is normally repaired in a manner distinct from conventional nucleotide excision repair, but that requires XPC protein
Deletion of Gadd45a (zeige GADD45A Antikörper) alone does not lead to increased lung tumors in mice, but coupled with an XPC deletion, it results in lung tumor progression
This gene encodes a component of the nucleotide excision repair (NER) pathway. There are multiple components involved in the NER pathway, including Xeroderma pigmentosum (XP) A-G and V, Cockayne syndrome (CS) A and B, and trichothiodystrophy (TTD) group A, etc. This component, XPC, plays an important role in the early steps of global genome NER, especially in damage recognition, open complex formation, and repair protein complex formation. Mutations in this gene or some other NER components result in Xeroderma pigmentosum, a rare autosomal recessive disorder characterized by increased sensitivity to sunlight with the development of carcinomas at an early age. Alternatively spliced transcript variants have been found for this gene.
xeroderma pigmentosum, complementation group C
, DNA repair protein complementing XP-C cells
, mutant xeroderma pigmentosum group C
, DNA repair protein complementing XP-C cells homolog
, xeroderma pigmentosum group C-complementing protein homolog