A5053418058- DNA Repair Mechanisms
- DNA and Nucleic Acid Chemistry
- Advanced biosensing and bioanalysis techniques
- RNA modifications and cancer
- Genetic factors in colorectal cancer
- RNA and protein synthesis mechanisms
- Acute Lymphoblastic Leukemia research
- Trace Elements in Health
- Carcinogens and Genotoxicity Assessment
University of California, Davis
2018-2024
The base excision repair glycosylase MUTYH prevents mutations associated with the oxidatively damaged base, 8-oxo-7,8-dihydroguanine (OG), by removing undamaged misincorporated adenines from OG:A mispairs. Defects in individuals inherited variants are correlated colorectal cancer predisposition syndrome known as MUTYH-associated polyposis (MAP). Herein, we reveal key structural features of OG required for efficient human using structure–activity relationships (SAR). We developed a GFP-based...
The oxidative base damage, 8-oxo-7,8-dihydroguanine (8-oxoG) is a highly mutagenic lesion because replicative DNA polymerases insert adenine (A) opposite 8-oxoG. In mammalian cells, the removal of A incorporated across from 8-oxoG mediated by glycosylase MUTYH during excision repair (BER). After excision, binds avidly to abasic site and thus product inhibited. We have previously reported that UV-DDB plays non-canonical role in BER glycosylase, OGG1 presented preliminary data can also...
The human DNA base excision repair enzyme MUTYH (MutY homolog glycosylase) excises undamaged adenine that has been misincorporated opposite the oxidatively damaged 8-oxoG, preventing transversion mutations and serving as an important defense against deleterious effects of this damage. Mutations in gene predispose patients to MUTYH-associated polyposis colorectal cancer, expression documented a biomarker for pancreatic cancer. Measuring activity is therefore critical evaluating diagnosing...
The DNA base excision repair (BER) glycosylase MUTYH prevents mutations by catalyzing adenine (A) from inappropriately formed 8-oxoguanine (8-oxoG):A mismatches. importance of this mutation suppression activity in tumor suppressor genes is underscored the association inherited variants with colorectal polyposis a hereditary cancer syndrome known as MUTYH-associated polyposis, or MAP. Many MAP encompass amino acid changes that occur at positions surrounding two-metal cofactor-binding sites...