MutYH (MYH) and colorectal cancer

2005 ◽  
Vol 33 (4) ◽  
pp. 679-683 ◽  
Author(s):  
J.R. Sampson ◽  
S. Jones ◽  
S. Dolwani ◽  
J.P. Cheadle
Keyword(s):  
Excision Repair ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Ras Genes ◽  
Stable Product ◽  
Base Excision ◽  
Mutyh Associated Polyposis ◽  
Inherited Mutations ◽  
Oxidative Damage To Dna

MAP (MutYH-associated polyposis) is a recently described colorectal adenoma and carcinoma predisposition syndrome that is associated with biallelic-inherited mutations of the human MutY homologue gene, MutYH. MutYH is often also termed MYH. MAP tumours display a mutational signature of somatic guanine-to-thymine transversion mutations in the adenomatous polyposis coli and K-ras genes, reflecting the normal role of MutYH in the base excision repair of adenines misincorporated opposite 7,8-dihydro-8-oxoguanine, a prevalent and stable product of oxidative damage to DNA. However, the full genetic pathway of MAP tumorigenesis has not been elucidated.

Structure/Function Analysis of the Interaction of Adenomatous Polyposis Coli with DNA Polymerase β and Its Implications for Base Excision Repair†

Biochemistry ◽  
2007 ◽  
Vol 46 (49) ◽  
pp. 13961-13974 ◽  
Author(s):  
Ramesh Balusu ◽  
Aruna S. Jaiswal ◽  
Melissa L. Armas ◽  
Chanakya N. Kundu ◽  
Linda B. Bloom ◽  
...  
Keyword(s):  
Structure Function ◽  
Adenomatous Polyposis Coli ◽  
Dna Polymerase ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Function Analysis ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Dna Polymerase Β ◽  
Base Excision

scholarly journals A distinct physiological role of MutY in mutation prevention in mycobacteria

Microbiology ◽  
2010 ◽  
Vol 156 (1) ◽  
pp. 88-93 ◽  
Author(s):  
Krishna Kurthkoti ◽  
Thiruneelakantan Srinath ◽  
Pradeep Kumar ◽  
Vidyasagar S. Malshetty ◽  
Pau Biak Sang ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Mycobacterium Smegmatis ◽  
Biochemical Characterization ◽  
Excision Repair ◽  
Physiological Role ◽  
Repair Enzymes ◽  
Base Excision ◽  
Oxidative Damage To Dna

Oxidative damage to DNA results in the occurrence of 7,8-dihydro-8-oxoguanine (8-oxoG) in the genome. In eubacteria, repair of such damage is initiated by two major base-excision repair enzymes, MutM and MutY. We generated a MutY-deficient strain of Mycobacterium smegmatis to investigate the role of this enzyme in DNA repair. The MutY deficiency in M. smegmatis did not result in either a noteworthy susceptibility to oxidative stress or an increase in the mutation rate. However, rifampicin-resistant isolates of the MutY-deficient strain showed distinct mutations in the rifampicin-resistance-determining region of rpoB. Besides the expected C to A (or G to T) mutations, an increase in A to C (or T to G) mutations was also observed. Biochemical characterization of mycobacterial MutY (M. smegmatis and M. tuberculosis) revealed an expected excision of A opposite 8-oxoG in DNA. Additionally, excision of G and T opposite 8-oxoG was detected. MutY formed complexes with DNA containing 8-oxoG : A, 8-oxoG : G or 8-oxoG : T but not 8-oxoG : C pairs. Primer extension reactions in cell-free extracts of M. smegmatis suggested error-prone incorporation of nucleotides into the DNA. Based on these observations, we discuss the physiological role of MutY in specific mutation prevention in mycobacteria.

scholarly journals Mechanism of Adenomatous Polyposis Coli (APC)-Mediated Blockage of Long-Patch Base Excision Repair†

Biochemistry ◽  
2006 ◽  
Vol 45 (51) ◽  
pp. 15903-15914 ◽  
Author(s):  
Aruna S. Jaiswal ◽  
Ramesh Balusu ◽  
Melissa L. Armas ◽  
Chanakya N. Kundu ◽  
Satya Narayan
Keyword(s):  
Adenomatous Polyposis Coli ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Base Excision
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