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Human Polyclonal MPG Primary Antibody pour ICC, IF - ABIN4335346
Ström, Johansson, Uhlén, Szigyarto, Erixon, Helleday: Poly (ADP-ribose) polymerase (PARP) is not involved in base excision repair but PARP inhibition traps a single-strand intermediate. dans Nucleic acids research 2011
Show all 2 Pubmed References
Human Monoclonal MPG Primary Antibody pour IF, IHC (p) - ABIN561837
Chou, Wang, Wong, Ding, Wu, Shieh, Shen: Chk2-dependent phosphorylation of XRCC1 in the DNA damage response promotes base excision repair. dans The EMBO journal 2008
Human Polyclonal MPG Primary Antibody pour ELISA, WB - ABIN268629
Samson, Derfler, Boosalis, Call: Cloning and characterization of a 3-methyladenine DNA glycosylase cDNA from human cells whose gene maps to chromosome 16. dans Proceedings of the National Academy of Sciences of the United States of America 1991
high levels of APNG were associated with better overall survival in patients with glioblastoma
Data indicate that DNA glycosylases MYH (Montrer MUTYH Anticorps), UNG2 (Montrer CCNO Anticorps), MPG, NTH1, NEIL1 (Montrer NEIL1 Anticorps), 2 and 3 on nascent DNA.
Data suggest that the change in tryptophan fluorescence of Y162W mutant of AAG (alkyladenine DNA glycosylase) is extremely rapid upon binding to either damaged or undamaged DNA, much faster than lesion-recognition and nucleotide flipping steps; thus, intercalation by tyrosine may be one of the earliest steps in search for/recognition of DNA damage.
Rheumatoid arthritis is associated with a polymorphism in the MPG gene (rs2858056) and increased serum level of the MPG protein.
Role of MPG protein in the DNA damage response through the base excision repair pathway
results suggest that individuals carrying R120C and R141Q MPG variants may be at risk for genomic instability and associated diseases as a consequence.
Elevated MPG activity is associated with lung cancer, possibly by creating an imbalance in the base excision repair pathway.
High MPG DNA repair assays for two different oxidative DNA lesions reveal associations with increased lung cancer risk.
disease-stage-specific alterations in the expression of MPG may highlight a potential role for MPG in determining EAC (Montrer CYLD Anticorps) onset and thus potentially be of clinical relevance for early disease detection and increased patient survival.
AAG has a flexible amino terminus that tunes its affinity for nonspecific DNA, but we find that it is not required for intersegmental transfer. As AAG has only a single DNA binding site, this argues against the bridging model for intersegmental transfer
The depletion of Aag (Montrer C16orf35 Anticorps) did not significantly change the transcriptional inhibitory or mutagenic properties of all five examined lesions, suggesting a negligible role of Aag (Montrer C16orf35 Anticorps) in the repair of these DNA adducts in mammalian cells.
This study demonstrates for the first time a non-linear dose-response for alkylation-induced colorectal carcinogenesis and reveals DNA repair by MGMT (Montrer MGMT Anticorps), but not AAG (Montrer C16orf35 Anticorps), as a key node in determining a carcinogenic threshold.
the detrimental effects of Aag (Montrer C16orf35 Anticorps)-initiated BER during I/R and sterile inflammation, and present a novel target for controlling I/R-induced injury.
Toxicity, induced by tert (Montrer TERT Anticorps)-butyl-hydroperoxide and potassium bromate, differs in base excision repair proficient (Mpg (+/+), Nth1 (+/+)) and deficient (Mpg (-/-), Nth1 (-/-)) mouse embryonic fibroblasts following Msh2 (Montrer MSH2 Anticorps) knockdown, was examined.
These results provide in vivo evidence that Aag (Montrer C16orf35 Anticorps)-initiated BER may play a critical role in determining the side-effects of alkylating agent chemotherapies and that Parp1 (Montrer PARP1 Anticorps) plays a crucial role in Aag (Montrer C16orf35 Anticorps)-mediated tissue damage.
ALKBH2 (Montrer ALKBH2 Anticorps) and ALKBH3 (Montrer ALKBH3 Anticorps) provide cancer protection similar to that of the DNA glycosylase AAG (Montrer C16orf35 Anticorps) and display apparent epistasis with Aag (Montrer C16orf35 Anticorps)
AAG (Montrer C16orf35 Anticorps) is a mammalian enzyme that can act on all three purine deamination bases, hypoxanthine, xanthine, and oxanine
the N-terminal tail in MPG plays a critical role in overcoming product inhibition, which is achieved by reducing the differences of MPG binding affinity toward hypoxanthine and apurinic/apyrimidinic sites
Aag (Montrer C16orf35 Anticorps)-mediated DNA repair prevents colonic epithelial damage and reduces the severity of dextran sulfate sodium-induced colon tumorigenesis.
Aag (Montrer C16orf35 Anticorps)-initiated base excision repair drives alkylation-induced retinal degeneration.
enzyme that cleaves 3-methyladenine and 7-methylguanine residues from DNA
3' end of the Mid1 gene, localized 68 kb upstream the humanzeta globin gene on 16p
, 3-alkyladenine DNA glycosylase
, 3-methyladenine DNA glycosidase
, CRA36.1 (3-methyl-adenine DNA glycosylase)
, DNA-3-methyladenine glycosylase
, N-methylpurine-DNA glycosylase, MPG
, proliferation-inducing protein 11
, proliferation-inducing protein 16
, N-methylpurine-DNA glycocylase
, 3-methyladenine DNA glycosylase
, N-methylpurine-DNA glycosylase