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Bacteria Polyclonal MUTYH Primary Antibody für ICC, IF - ABIN153079
Bonde, Gao, Chen, Miyashita, Montgomery, Harmon, Wei: Duodenal reflux leads to down regulation of DNA mismatch repair pathway in an animal model of esophageal cancer. in The Annals of thoracic surgery 2007
Show all 9 Pubmed References
Human Monoclonal MUTYH Primary Antibody für IP, RNAi - ABIN561883
van der Post, Kets, Ligtenberg, van Krieken, Hoogerbrugge: Immunohistochemistry is not an accurate first step towards the molecular diagnosis of MUTYH-associated polyposis. in Virchows Archiv : an international journal of pathology 2008
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Human Polyclonal MUTYH Primary Antibody für ELISA, WB - ABIN188666
Russo, De Luca, Casorelli, Degan, Molatore, Barone, Mazzei, Pannellini, Musiani, Bignami: Role of MUTYH and MSH2 in the control of oxidative DNA damage, genetic instability, and tumorigenesis. in Cancer research 2009
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qPCR analysis of cDNA from the cerebella of affected and unaffected horses suggested that MUTYH expression is down-regulated in affected horses.
Acetohexamide exerted this protective function by antagonizing expression of the DNA glycosylase, MUTYH. Together, our data reveal the existence of an NER (zeige NR1H2 Antikörper)-independent mechanism to remove UV-induced DNA damage and prevent cell death.
Data indicate that DNA glycosylases MYH, UNG2 (zeige CCNO Antikörper), MPG (zeige MPG Antikörper), NTH1, NEIL1 (zeige NEIL1 Antikörper), 2 and 3 on nascent DNA.
No biallelic mutation carriers for the MUTYH variants c.536A.G p.Tyr179Cys (Y179C) in exon 7 and c.1187G.A p.Gly396Asp (G396D) in exon 13 was found, after screening with a novel high resolution melt curve (HRM) analysis assay.
MUTYH p.Y179C mutation was associated with an increased risk of colorectal cancer among Egyptian patients rather than MUTYH p.G396D mutation.
The majority (18/23) of patients with Familial Adenomatous Polyposis and all of the patients with Attenuated Familial Adenomatous Polyposis with an Adrenal Lesion had a genetically proven syndrome.All of the patients with MUTYH-Associated Polyposis had a biallelic germline MUTYH mutation.
These results suggested that reduced MUTYH expression is associated with somatic mutation loads via a reduction in DNA repair capacity in prostate adenocarcinoma.
MTH1 (zeige NUDT1 Antikörper) together with MYH plays an important role in protection against mutations induced by modified dNTPs during chronic oxidative stress.
Reduced MUTYH, MTH1 (zeige NUDT1 Antikörper), and OGG1 (zeige OGG1 Antikörper) expression and TP53 (zeige TP53 Antikörper) mutations occur in diffuse-type adenocarcinoma of gastric cardia.
Authors identified 266 probands (91% Caucasians) with a MUTYH mutation (41 biallelic and 225 monoallelic) from the Colon Cancer Family Registry. Mutation status, sex, age and histories of cancer from their 1,903 first- and 3,255 second-degree relatives were analyzed using modified segregation analysis conditioned on the ascertainment criteria.
A high heterogeneity of MUTYH variants and a high rate of variants of unknown significance were identified in a cohort of Italian patients with suspected MUTYH-associated polyposis. Genotype-phenotype analysis suggests that the p.Glu480del variant is associated with a severe phenotype.
results suggested that MYH, which interacts with TRADD (zeige TRADD Antikörper), inhibits TNF-alpha (zeige TNF Antikörper) necroptotic signaling. Therefore, MYH inactivation is essential for necroptosis via the downregulation of caspase-8 (zeige CASP8 Antikörper).
Ogg1 (zeige OGG1 Antikörper) and Mutyh regulate hippocampal gene expression related to cognition and behavior, suggesting a role for the glycosylases in regulating adaptive behavior.
MUTYH loss is associated with an increase in inflammation associated colorectal cancer risk, which involves immunosuppression and altered inflammatory response.
Results show that MYH is a vital DNA repair enzyme (zeige LIG4 Antikörper) that protects cells from oxidative DNA damage and is critical for a proper cellular response to DNA damage.
a 5-methylcytosine glycosylase activity for the murine DNA base excision repair enzyme Myh is described and shown that it is critically involved in remodeling the IL-2 (zeige IL2 Antikörper) Promoter for transcription.
Data indicate that maternal folate depletion during pregnancy and high-fat feeding from weaning altered gene expression of Ogg1 (zeige OGG1 Antikörper), Neil1 (zeige NEIL1 Antikörper), Mutyh and Xrcc1 (zeige XRCC1 Antikörper) in the brain of adult offspring.
The action of MUTYH, which initiates excision repair of adenine opposite 8-oxoG, triggers neurodegeneration in mice.
OGG1 (zeige OGG1 Antikörper) and MYH appear to be dispensable for antimutator function in mitochondria.
Mutyh plays a major role in maintaining intestinal integrity by affecting the inflammatory response.
Aim of this study was to characterize the biological effects, in a mammalian cell background, of human MUTYH mutations identified in MUTYH-associated polyposis patients
This gene encodes a DNA glycosylase involved in oxidative DNA damage repair. The enzyme excises adenine bases from the DNA backbone at sites where adenine is inappropriately paired with guanine, cytosine, or 8-oxo-7,8-dihydroguanine, a major oxidatively damaged DNA lesion. The protein is localized to the nucleus and mitochondria. Mutations in this gene result in heritable predisposition to colon and stomach cancer. Multiple transcript variants encoding different isoforms have been found for this gene.
mutY homolog (E. coli)
, A/G-specific adenine DNA glycosylase
, A/G-specific adenine DNA glycosylase-like
, mutY homolog
, adenine-DNA glycosylase
, mutY homolog alpha
, the full-length form type A, 5' region