A5028234632- DNA Repair Mechanisms
- Advanced biosensing and bioanalysis techniques
- DNA and Nucleic Acid Chemistry
- RNA Interference and Gene Delivery
- RNA and protein synthesis mechanisms
- Carcinogens and Genotoxicity Assessment
- CRISPR and Genetic Engineering
- Fungal and yeast genetics research
- Bacteriophages and microbial interactions
- Viral gastroenteritis research and epidemiology
- Metalloenzymes and iron-sulfur proteins
- X-ray Diffraction in Crystallography
- Coordination Chemistry and Organometallics
- Viral Infectious Diseases and Gene Expression in Insects
- RNA modifications and cancer
- Asymmetric Hydrogenation and Catalysis
- Bacterial Genetics and Biotechnology
- Protist diversity and phylogeny
- Virus-based gene therapy research
- Genomics and Chromatin Dynamics
- Genetics and Neurodevelopmental Disorders
- Plant Genetic and Mutation Studies
- Crystallography and molecular interactions
- Transgenic Plants and Applications
- Cancer Research and Treatments
Lawrence Berkeley National Laboratory
2006-2021
University of California, Berkeley
2002
The ability to express or deplete proteins in living cells is crucial for the study of biological processes. Viral vectors are often useful deliver DNA constructs that difficult transfect by other methods. Lentiviruses have additional advantage being able integrate into genomes non-dividing mammalian cells. However, existing viral expression systems generally require different vector backbones cDNA, small hairpin RNA (shRNA) microRNA (miRNA) and provide limited drug selection markers....
Damaged bases in DNA are known to lead errors replication and transcription, compromising the integrity of genome. We have proposed a model where repair proteins containing redox-active [4Fe-4S] clusters utilize charge transport (CT) as first step finding lesions. In this model, population sites search is reduced by localization protein vicinity Here, we examine using single-molecule atomic force microscopy (AFM). XPD, 5′-3′ helicase involved nucleotide excision repair, contains cluster...
DNA polymerase ε (pol ε) has been implicated in replication, repair, and cell cycle control, but its precise roles are unclear. When the subcellular localization of human pol was examined by indirect immunofluorescence, appeared discrete nuclear foci that colocalized with proliferating antigen (PCNA) sites synthesis only late S phase. Early phase, were adjacent to PCNA foci. In contrast present throughout mitosis G1 phase cycling cells. It is hypothesized from these observations have...
Using DNA-modified electrodes, we show DNA-mediated signaling by XPD, a helicase that contains [4Fe-4S] cluster and is critical for nucleotide excision repair transcription. The redox signal resembles of base proteins, with DNA-bound potential ∼80 mV versus NHE. Significantly, this increases ATP hydrolysis. Moreover, the substrate-dependent, reports on DNA conformational changes associated enzymatic function, may reflect general biological role charge transport.
You probably weren't thinking about your body's cellular DNA repair systems the last time you sat on beach in bright sunshine. Fortunately, however, while were subjecting to harmful effects of ultraviolet light, cells busy repairing damage. The idea that our genetic material could be damaged by sun was not appreciated early days molecular biology. When Watson and Crick discovered structure 1953 [1], it assumed is fundamentally stable since carries blueprint life. However, over 50 years...
Human DNA polymerase η (HsPol ) plays an important role in translesion synthesis (TLS), which allows for replication past damage such as UV‐induced cis-syn cyclobutane pyrimidine dimers (CPDs). Here, we characterized ApPol from the thermophilic worm Alvinella pompejana , inhabits deep‐sea hydrothermal vent chimneys. shares sequence homology with HsPol and contains domains binding ubiquitin proliferating cell nuclear antigen. Sun‐induced UV does not penetrate Alvinella′s environment; however,...
Human damaged DNA-binding protein (DDB) is a heterodimer of p48/DDB2 and p127/DDB1 subunits. Mutations in DDB2 are responsible for Xeroderma Pigmentosum group E, but no mutants mammalian DDB1 have been described. To study DDB1, the Schizosaccharomyces pombe sequence homologue (ddb1(+)) was cloned, ddb1 deletion strain constructed. The gene not essential; however, mutant cells showed 37% impairment colony-forming ability, an elongated phenotype, abnormal nuclei. ddb1Delta sensitive to UV...
The title complex, [RuCp*(OSO2CF3){P(iPr)3}(CO)] or [Ru(CF3O3S)(C10H15)(C9H21P)(CO)], consists of an Ru atom coordinated by inner sphere trifluoromethanesulfonate, a carbonyl, and triisopropylphosphine in `three-legged stool' fashion.
DNA is constantly threatened by internal and external pressures. Xeroderma Pigmentosum (XP) complementation groups D (XPD) B (XPB) are helicases that unwind helix‐distorting lesions in damaged allowing for repair to occur. These proteins critical components of the Transcription Factor II H complex, essential nucleotide excision repair. Three rare genetic diseases characterized cancer premature aging caused mutations genes code these helicase enzymes. In order understand how function at...
Abstract The general transcription factor TFIIH contains three ATP-dependent catalytic activities. functions in nucleotide excision repair primarily as a DNA helicase and Pol II initiation dsDNA translocase protein kinase. During initiation, the XPB/Ssl2 subunit of couples ATP hydrolysis to translocation facilitating promoter opening kinase module phosphorylates C-terminal domain facilitate transition elongation. These are conserved between metazoans yeast; however, yeast also drives...