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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
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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
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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
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
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 (zeige PARP1 Antikörper)) 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 (zeige GSTT1 Antikörper) null, XPD (zeige ERCC2 Antikörper) 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 (zeige SAG Antikörper) molecule, middle-loop and C-loop, enhanced or reduced arrestin-3 (zeige ARRB2 Antikörper) interactions with several GPCRs in receptor subtype and functional state-specific manner.
these studies found that carriers of the T allele of ERCC1 (zeige ERCC1 Antikörper) rs11615, XPC rs2228000 and rs50872, particularly in postmenopausal females, have an increased risk of breast cancer
Data suggest that a common TFIIH subunit (zeige GTF2H4 Antikörper) p62 (zeige GTF2H1 Antikörper) recruitment mechanism is shared by UV-stimulated scaffold protein A (UVSSA (zeige KIAA1530 Antikörper)) in transcription-coupled repair (TCR) and xeroderma pigmentosum, complementation group C protein (XPC) in global genome repair (GGR (zeige GCGR Antikörper)).
CHD1 (zeige CHD1 Antikörper) facilitates substrate handover from XPC to the downstream TFIIH (zeige GTF2H1 Antikörper) (transcription factor IIH).
results provide insights into an unexpected biological role of XPC in response to DNA replication stress
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) 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 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