Recombinant Escherichia coli A/G-specific adenine glycosylase (mutY)

1. Studies indicate that the DNA repair gene MUTYH, which is a homologue of the E. coli gene mutY, is responsible for colorectal carcinoma (CRC). PMID: 23933175
2. MutY mutations reduced the point-mutation rate by 40-60%. PMID: 23248287
3. ability of MUTYH and the variants to suppress mutations and complement for the absence of MutY in Escherichia coli was assessed using rifampicin resistance assays. PMID: 19836313
4. catalytic analysis of Escherichia coli MutY DNA glycosylase PMID: 15326180
5. Mutant MutY(Delta26-134), which lacks the six-helix barrel domain, cannot complement the mutator phenotype of a mutY mutant in vivo. However, the mutant can still bind DNA and has weak catalytic activity at high enzyme concentrations. PMID: 15456766
6. Electrochemical measurement of MutY using DNA-modified electrodes demonstrates that this base excision repair enzyme containing a [4Fe-4S] cofactor is redox-active when bound to DNA. PMID: 15938629
7. 8-oxoG-derived lesions are equally miscoding when replicated in E. coli lacking MutY; no significant change in mutation identity or frequency is observed. Yet, in the presence of MutY, Sp1 and Sp2 are more toxic than in cells lacking this repair enzyme PMID: 17260974
8. Data show a lack of interaction of mutY with dnaX36 since the double dnaX36 mutY strains did not show any major changes in the frequency of G.CT.A transversions compared to the single dnaX36 strain. PMID: 18156258
9. HPs and SSAs are a common finding in MAP patients. The detection of almost exclusively G:C-->T:A transversions in the K-ras gene of HPs/SSAs strongly suggests that these polyps are related causally to MYH deficiency. PMID: 19013464
10. V45A and Q182L mutants had reduced binding for A/G and A/8-oxoG mismatches and increased affinities towards T/G mismatch. PMID: 19523222

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KEGG: ecj:JW2928

STRING: 316385.ECDH10B_3136