Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Human XPC Antikörper:
anti-Mouse (Murine) XPC Antikörper:
anti-Rat (Rattus) XPC Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
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
XPC is an RNA polymerase II cofactor recruiting ATAC coactivator complex to promoters by interacting with E2F1.
CC genotype for XPC A>C polymorphism is associated with the risk of squamous cell carcinoma head and neck.
Results show that XPC deficiency leads to alterations in mitochondrial redox balance with a respiratory complex CI/CII shift as a possible adaptation to lower CI activity, but at the cost of sensitizing XP-C cells to mitochondrial oxidative stress.
Chronic low-dose of UVB (CLUV) treatment activates p53, which corroborate with the increased level of DDB2 and XPC proteins. DDB2 and XPC recruited at chromatin bound, suggesting a more efficient cyclobutane pyrimidine dimer (CPD) recognition by NER and more efficient repair of CDP.
Demethylation using decitabine increased XPC and apoptosis after sequential carboplatin. These results confirm that sequential decitabine and carboplatin requires further investigation as a combination treatment for melanoma.
These findings support that loss of XPC, possibly due to chronic Cigarette smoke exposure, promotes emphysema development and further supports a link between DNA damage, impaired DNA repair, and development of emphysema.
Poly(ADP-ribose) polymerase-1 (PARP1) interacts with xeroderma pigmentosum, complementation group C protein (XPC) in the nucleoplasmic and chromatin fractions in UV irradiated HEK293 cells.
hospital workers as a category are at risk for genotoxic damage caused by chronic exposure to xenobiotics. The higher levels of cytogenetic damage observed among GSTT1 null, XPD 751 and XPC 939 CC homozygote subjects confirm the importance of the genetic polymorphisms analysis associated to genotoxicological studies.
XPC Ala499Val substitution increases urinary bladder cancer risk, but Lys939Gln appears to be neutral. (Meta-analysis)
low XPC and global genome repair have roles in reduced repair of UVB-induced DNA damage in melanoma
Several mutations in the two parts of the central "crest" of the arrestin molecule, middle-loop and C-loop, enhanced or reduced arrestin-3 interactions with several GPCRs in receptor subtype and functional state-specific manner.
these studies found that carriers of the T allele of ERCC1 rs11615, XPC rs2228000 and rs50872, particularly in postmenopausal females, have an increased risk of breast cancer
analysis confirms that XP-C patients without increased sun sensitivity develop non-melanoma skin cancers earlier than sun-sensitive XP-C patients. Reduced cellular mRNA levels are characteristic for XP complementation group C and qRT-PCR represents a rapid diagnostic tool.
Data suggest that a common TFIIH subunit p62 recruitment mechanism is shared by UV-stimulated scaffold protein A (UVSSA) in transcription-coupled repair (TCR) and xeroderma pigmentosum, complementation group C protein (XPC) in global genome repair (GGR).
CHD1 facilitates substrate handover from XPC to the downstream TFIIH (transcription factor IIH).
results provide insights into an unexpected biological role of XPC in response to DNA replication stress
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) of certain types of DNA adducts, leading to repression of NER.
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 and XPC in combination showed an increased risk towards ESCC.
results suggest that XPC may help repair DNA damage caused by KRAS-mediated production of ROS.
OCT4 and SOX2 are the primary transcription factors recruiting SCC to regulatory regions of pluripotency genes; the XPC subunit is essential for interaction with the two proteins
progerin and p16(INK4a) expression, beta-galactosidase 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 in mouse embryonic stem cells.
BRAF(V600E) and ARF 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 alone does not lead to increased lung tumors in mice, but coupled with an XPC deletion, it results in lung tumor progression
In irradiated Xpc-/- keratinocytes (GG-nucleotide excision repair deficient) the loss of replicating S-phase cells is associated with a gradual build-up of both QS-phase cells and cells arrested in late-S phase, in complete absence of apoptosis.
Xpc-deficient mice possess a mutator phenotype in their germ line and somatic tissues that may significantly enhance carcinogenesis across multiple tissues.
XPC, but not XPA, plays a significant role in the removal of oxidative DNA damage and preventing development of lung tumors
Xpc gene status and genomic nucleotide excision repair may be determinants of response to DNA-damaging agents including carboplatin
these results indicate that there may be diverse roles or mechanisms through which XPC participates in genome maintenance in different tissues.
results point to an important 'care-taker'-type tumour-suppression function for alternative reading frame in nucleotide excision repair through the increased expression of XPC.
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