MUTYH
MUTYH (mutY DNA glycosylase, also known as MYH) is an adenine DNA glycosylase involved in the repair of oxidative DNA damage. It removes adenine misincorporated opposite oxidised guanine, and mutations in the MUTYH gene are linked to heritable colorectal cancer predisposition. Browse Assay Genie's current range of MUTYH research reagents below, or read on for the biology behind the target.
MUTYH is a DNA glycosylase that takes part in oxidative DNA damage repair. It initiates repair of A*oxoG to C*G by removing the inappropriately paired adenine base from the DNA backbone. The enzyme excises adenine from sites where it is mispaired with guanine, cytosine or 8-oxo-7,8-dihydroguanine, a major oxidatively damaged DNA lesion. UniProt annotates it with both adenine and 2-OH-A DNA glycosylase activities.
The protein is also called adenine DNA glycosylase and is classified under EC 3.2.2.31. It belongs to the Nth/MutY family and sits within the HGNC DNA glycosylases gene group. MUTYH is localised to both the nucleus and the mitochondria, so it can act on nuclear and mitochondrial DNA. The gene has previously been known as MYH and as mutY homolog (E. coli), reflecting its relationship to the bacterial MutY enzyme. Mouse and rat both carry a Mutyh ortholog, and multiple transcript variants encoding different isoforms have been reported for the human MUTYH gene.
Beyond repair, MUTYH is thought to play a role in signalling apoptosis through the introduction of single-strand breaks following oxidative damage. Mutations in the gene cause a heritable predisposition to colorectal cancer, termed MUTYH-associated polyposis (MAP), which makes the protein a frequent subject in DNA repair and cancer genetics research.
MUTYH removes adenine mispaired with 8-oxoguanine, making it a central enzyme for studying how cells handle oxidative lesions in DNA.
Mutations in MUTYH cause MUTYH-associated polyposis, a heritable predisposition to colorectal cancer, so the gene is widely studied in hereditary cancer research.
MUTYH localises to mitochondria as well as the nucleus, which supports work on how oxidative damage to mitochondrial DNA is recognised and repaired.
MUTYH is thought to signal apoptosis by introducing single-strand breaks after oxidative damage, linking DNA repair to cell fate decisions.
MUTYH is a DNA glycosylase that initiates repair of A*oxoG to C*G by removing the mispaired adenine from the DNA backbone. It acts on adenine opposite guanine, cytosine or 8-oxoguanine and also has 2-OH-A DNA glycosylase activity.
The HGNC name is mutY DNA glycosylase, and UniProt lists the protein as adenine DNA glycosylase. The previous symbol is MYH and the earlier name was mutY homolog (E. coli). Multiple transcript variants encoding different isoforms have been described for the gene.
Yes. Mutations in MUTYH cause MUTYH-associated polyposis, a heritable predisposition to colorectal cancer. Mouse and rat have a Mutyh ortholog, and the protein belongs to the Nth/MutY family; check the datasheet of any product for its validated reactivity.
Other DNA glycosylases, base excision repair enzymes and colorectal cancer predisposition genes with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9UIF7; product specifications from Assay Genie datasheets.