Recombinant Mouse A/G-specific adenine DNA glycosylase (Mutyh)

1. results suggested that MYH, which interacts with TRADD, inhibits TNF-alpha necroptotic signaling. Therefore, MYH inactivation is essential for necroptosis via the downregulation of caspase-8. PMID: 28059467
2. Ogg1 and Mutyh regulate hippocampal gene expression related to cognition and behavior, suggesting a role for the glycosylases in regulating adaptive behavior. PMID: 26711335
3. MUTYH loss is associated with an increase in inflammation associated colorectal cancer risk, which involves immunosuppression and altered inflammatory response. PMID: 26109431
4. Results show that MYH is a vital DNA repair enzyme that protects cells from oxidative DNA damage and is critical for a proper cellular response to DNA damage. PMID: 24315136
5. 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 Promoter for transcription. PMID: 24291244
6. Data indicate that maternal folate depletion during pregnancy and high-fat feeding from weaning altered gene expression of Ogg1, Neil1, Mutyh and Xrcc1 in the brain of adult offspring. PMID: 23603834
7. The action of MUTYH, which initiates excision repair of adenine opposite 8-oxoG, triggers neurodegeneration in mice. PMID: 23143307
8. OGG1 and MYH appear to be dispensable for antimutator function in mitochondria. PMID: 22209780
9. Mutyh plays a major role in maintaining intestinal integrity by affecting the inflammatory response. PMID: 20706593
10. 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 PMID: 19953527
11. Replication-associated repair of adenine:8-oxoguanine mispairs by MYH PMID: 11864576
12. a specific germ-line mutation (G382D) is identified in mutyH which may be responsible for the mutator phenotype PMID: 12917422
13. MUTYHalpha and MUTYHbeta were detected in wild-type embryonic stem (ES) cells or thymocytes prepared from wild-type mice PMID: 14742662
14. The C-terminal domain of MUTYH is necessary for its ability to prevent OGG1 or APEX1 from inappropriately processing its substrate. PMID: 15199168
15. Because there is an increased incidence of lung and small intestine cancer in Myh(-/-)/Ogg1(-/-) mice, these findings support a causal role for unrepaired oxidized DNA bases in cancer development. PMID: 15231648
16. MUTYH has a DNA glycosylase activity excising not only adenine opposite 8-oxoguanine (8-oxoG) but also 2-hydroxyadenine (2-OH-A) opposite guanine. PMID: 15681617
17. MUTYH suppresses spontaneous tumorigenesis in mice, thus providing experimental evidence for the association between biallelic germ-line MUTYH mutations and a recessive form of human hereditary colorectal adenoma and carcinoma PMID: 17638869
18. Required for normal cell-cycle progression and nuclear division, suggesting multiple roles of Myh in the maintenance of genome stability and tumor prevention. PMID: 18258604
19. A large fraction of the cancer-prone phenotype of Msh2 deficient mice depends on Mutyh activity. PMID: 19435918

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KEGG: mmu:70603

STRING: 10090.ENSMUSP00000099760

UniGene: Mm.180333