A5003203263- DNA Repair Mechanisms
- DNA and Nucleic Acid Chemistry
- CRISPR and Genetic Engineering
- Carcinogens and Genotoxicity Assessment
- Bacterial Genetics and Biotechnology
- Genomics and Chromatin Dynamics
- RNA and protein synthesis mechanisms
- Cancer-related Molecular Pathways
- RNA modifications and cancer
- Cancer therapeutics and mechanisms
- Advanced biosensing and bioanalysis techniques
- RNA Interference and Gene Delivery
- Plant Genetic and Mutation Studies
- Light effects on plants
- bioluminescence and chemiluminescence research
- Skin Protection and Aging
- Bacteriophages and microbial interactions
- Genetically Modified Organisms Research
- Epigenetics and DNA Methylation
- Photosynthetic Processes and Mechanisms
- Protist diversity and phylogeny
- Genetic factors in colorectal cancer
- RNA Research and Splicing
- Mitochondrial Function and Pathology
- Science, Research, and Medicine
Stanford University
2014-2024
Pennsylvania State University
2018
Arizona State University
2013
The University of Texas MD Anderson Cancer Center
1989-2008
University of Sheffield
2006
Northwestern University
2006
Cancer Research UK
2006
Vanderbilt University
2004
Mississippi State University
2001-2003
National Institute of Environmental Health Sciences
2002
Abstract The SOS response in UV-irradiated Escherichia coli includes the upregulation of several dozen genes that are negatively regulated by LexA repressor. Using DNA microarrays containing amplified fragments from 95.5% all open reading frames identified on E. chromosome, we have examined changes gene expression following UV exposure both wild-type cells and lexA1 mutants, which unable to induce under control. We report here time courses surrounding 26 documented lexA-regulated regions...
In human cells, efficient global genomic repair of DNA damage induced by ultraviolet radiation requires the p53 tumor suppressor, but mechanism has been unclear. The p48 gene is required for expression an radiation-damaged binding activity and disrupted mutations in subset xeroderma pigmentosum group E cells that lack this activity. Here, we show mRNA levels strongly depend on basal increase further after a p53-dependent manner. Furthermore, like p53(-/-) are deficient repair. These results...
Removal of pyrimidine dimers was measured in defined sequences human cells amplified for the dihydrofolate reductase (DHFR) gene. We quantitated repair specific restriction fragments by using dimer-specific bacteriophage T4 endonuclease V and analysis Southern blotting. Within 4 hr after 5- or 10-J/m2 UV irradiation, more than 60% had been removed from a 20-kilobase fragment that lies entirely within transcription unit DHFR gene 25-kilobase located 5' flanking region Repair overall genome...
Human cells lacking functional p53 exhibit a partial deficiency in nucleotide excision repair (NER), the pathway for of UV-induced DNA damage. The global genomic (GGR) subpathway NER, but not transcription-coupled (TCR), is mainly affected by loss or inactivation. We have utilized mouse embryo fibroblasts (MEFs) genes downstream effector pathway, gadd45 (Gadd45a) p21 (Cdkn1a), as well MEFs both and to address potential contribution these effectors p53-associated repair. Loss had pronounced...
We have shown previously that Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in the removal of UV-induced cyclobutane pyrimidine dimers from genomic DNA, but still proficient transcription-coupled repair pathway (Ford, J. M., and Hanawalt, P. C. (1995) Proc. Natl. Acad. Sci. U. S. A. 92, 8876–8880). now utilized monoclonal antibodies specific or 6-4 photoproducts, respectively, to measure their UV-irradiated human fibroblasts. Cells were both whereas cells...
A current model for transcription-coupled DNA repair is that RNA polymerase, arrested at a lesion, directs the machinery to transcribed strand of an active gene. To help elucidate this role we constructed templates containing major late promoter adenovirus and cyclobutane pyrimidine dimer (CPD) specific site. CPDs, predominant lesions formed by ultraviolet radiation, are good substrates repair. CPD located on template was strong block polymerase movement, whereas nontranscribed had no effect...
We have developed a method for efficiently generating transient pores in the outer membranes of Escherichia coli K-12 derivatives by using new type electroporation apparatus. The are large enough and persist long to facilitate equilibration plasmid molecules between intracellular extracellular spaces. has been used transform bacterial cells with an efficiency greater than 10(9) transformants per microgram plasmid. It also extract intact from transformed efficiencies comparable those...