Open Access. Powered by Scholars. Published by Universities.®
- Keyword
-
- ATPase (1)
- Adenosine Triphosphate (1)
- Amino Acid Substitution (1)
- Astrocytes (1)
- Brain Neoplasms (1)
-
- CRISPR-Cas Systems (1)
- CTG•CAG (1)
- Cell Line (1)
- Cell biology (1)
- Colorectal Neoplasms (1)
- DNA Mismatch Repair (1)
- Dimerization (1)
- Gene Knockout Techniques (1)
- Genes, Reporter (1)
- Genetic Vectors (1)
- Humans (1)
- Hydrolysis (1)
- Melatonin (1)
- Metabolites (1)
- Molecular biology (1)
- Msh3 (1)
- MutS Homolog 2 Protein (1)
- MutS Homolog 3 Protein (1)
- MutSβ (1)
- Mutation, Missense (1)
- NRF2-mediated pathways (1)
- Neoplastic Syndromes, Hereditary (1)
- Neurological diseases (1)
- Point Mutation (1)
- Trinucleotide Repeat Expansion (1)
Articles 1 - 2 of 2
Full-Text Articles in Medical Toxicology
Mutsβ Abundance And Msh3 Atp Hydrolysis Activity Are Important Drivers Of Ctg•Cag Repeat Expansions, Norma Keogh, Kara Y. Chan, Guo-Min Li, Robert S. Lahue
Mutsβ Abundance And Msh3 Atp Hydrolysis Activity Are Important Drivers Of Ctg•Cag Repeat Expansions, Norma Keogh, Kara Y. Chan, Guo-Min Li, Robert S. Lahue
Toxicology and Cancer Biology Faculty Publications
CTG•CAG repeat expansions cause at least twelve inherited neurological diseases. Expansions require the presence, not the absence, of the mismatch repair protein MutSβ (Msh2-Msh3 heterodimer). To evaluate properties of MutSβ that drive expansions, previous studies have tested under-expression, ATPase function or polymorphic variants of Msh2 and Msh3, but in disparate experimental systems. Additionally, some variants destabilize MutSβ, potentially masking the effects of biochemical alterations of the variations. Here, human Msh3 was mutated to selectively inactivate MutSβ. Msh3−/− cells are severely defective for CTG•CAG repeat expansions but show full activity on contractions. Msh3−/− cells provide a single, isogenic system …
Melatonin And Its Metabolites Protect Human Melanocytes Against Uvb-Induced Damage: Involvement Of Nrf2-Mediated Pathways, Zorica Janjetovic, Stuart G. Jarrett, Elizabeth F. Lee, Cory Duprey, Russel J. Reiter, Andrzej T. Slominski
Melatonin And Its Metabolites Protect Human Melanocytes Against Uvb-Induced Damage: Involvement Of Nrf2-Mediated Pathways, Zorica Janjetovic, Stuart G. Jarrett, Elizabeth F. Lee, Cory Duprey, Russel J. Reiter, Andrzej T. Slominski
Toxicology and Cancer Biology Faculty Publications
Ultraviolet light (UV) is an inducer of reactive oxygen species (ROS) as well as 6-4-photoproducts and cyclobutane pyrimidine dimers (CPD) in the skin, which further cause damage to the skin cells. Irradiation of cultured human melanocytes with UVB stimulated ROS production, which was reduced in cells treated with melatonin or its metabolites: 6-hydroxymelatonin (6-OHM), N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK), N-acetylserotonin (NAS), and 5-methoxytryptamine (5-MT). Melatonin and its derivatives also stimulated the expression of NRF2 (nuclear factor erythroid 2 [NF-E2]-related factor 2) and its target enzymes and proteins that play an important role in cell protection from different damaging factors including UVB. Silencing …