Physician
Medical Genetics
Dr. Robb E. Moses, MD
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Dr. Robb E. Moses is an expert in the field of Medical Genetics. He attended Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is a top medical university. Johns Hopkins University School of Medicine is ranked 3 in research and 29 in primary care medicine He has 1 awards "CMS Meaningful Use Stage 1 Certification". Doctor Robb E. Moses, MD is a published doctor. He published 70 publications, including: 'Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation.' Robb Moses accepts Medicare payments and is registered with Medicare.gov.
Publications
- Bloom Syndrome Radials Are Predominantly Non-Homologous and Are Suppressed by Phosphorylated BLM.
- Steroid Receptor Coactivator 1 is an Integrator of Glucose and NAD(+)/NADH Homeostasis.
- DNA interstrand crosslink repair in mammalian cells.
- ERCC1 is required for FANCD2 focus formation.
- Role for DNA polymerase kappa in the processing of N2-N2-guanine interstrand cross-links.
- Tip60 is required for DNA interstrand cross-link repair in the Fanconi anemia pathway.
- A new DNA polymerase activity of Escherichia coli. I. Purification and properties of the activity present in E. coli polA1.
- Holoenzyme DNA polymerase III fixes mutations.
- Replication at restrictive temperatures in Escherichia coli containing a polCts mutation.
- Alternate pathways of DNA replication: DNA polymerase I-dependent replication.
- Molecular structure of uvrC gene of Escherichia coli: identification of DNA sequences required for transcription of the uvrC gene.
- Ultraviolet irradiation inhibition of replicative deoxyribonucleic acid synthesis in toluene-treated Escherichia coli.
- Polynucleotide phosphorylase of Micrococcus luteus. Studies on the polymerization reaction catalyzed by primer-dependent and primer-independent enzymes.
- The ovalbumin gene. Insertion of ovalbumin gene sequences in chimeric bacterial plasmids.
- Cloning the polB gene of Escherichia coli and identification of its product.
- Intermolecular plasmid recombination in fibroblasts from humans with DNA damage-processing defects.
- Repair response of human fibroblasts to bleomycin damage.
- Synthesis by DNA polymerase I on bleomycin-treated deoxyribonucleic acid: a requirement for exonuclease III.
- Map location of the pcbA mutation and physiology of the mutant.
- Abnormal response of xeroderma pigmentosum cells to bleomycin.
- Expression of the cDNA for the beta subunit of human casein kinase II confers partial UV resistance on xeroderma pigmentosum cells.
- Ethyl methane sulfonate- and bleomycin-generated deletion mutations at HPRT locus in xeroderma pigmentosum complementation group D fibroblasts.
- DNA polymerase III of Escherichia coli is required for UV and ethyl methanesulfonate mutagenesis.
- Immortalization of Werner syndrome and progeria fibroblasts.
- DNA polymerase III-dependent repair synthesis in response to bleomycin in toluene-treated Escherichia coli.
- Repair response of Escherichia coli to hydrogen peroxide DNA damage.
- Multiple pathways for repair of hydrogen peroxide-induced DNA damage in Escherichia coli.
- Diseases with DNA damage-processing defects.
- Transformation of DNA repair-deficient human diploid fibroblasts with a simian virus 40 plasmid.
- Apurinic DNA endonuclease activities in repair-deficient human cell lines.
- Functional complementation by electroporation of human BACs into mammalian fibroblast cells.
- DNA damage processing defects and disease.
- Replication and repair of DNA in cells of Escherichia coli treated with toluene.
- Replicative deoixyribonucleic acid synthesis in a system diffusible for macromolecules.
- DNA polymerase I-mediated ultraviolet repair synthesis in toluene-treated Escherichia coli.
- Role of DNA polymerases in excision repair in Escherichia coli.
- Conversion of replicative intermediates in human DNA-repair defective cells.
- DNA polymerase III requirement for repair of DNA damage caused by methyl methanesulfonate and hydrogen peroxide.
- Reactivation of psoralen-reacted plasmid DNA in Fanconi anemia, xeroderma pigmentosum, and normal human fibroblast cells.
- Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S-phase but arrest permanently in G2 after cisplatin treatment.
- Growth factors and insulin stimulate tyrosine phosphorylation of the 51C/SHIP2 protein.
- The effect of low oxygen tension on the in vitro-replicative life span of human diploid fibroblast cells and their transformed derivatives.
- Permeabilized cells.
- Inactivation of the 5''-3'' exonuclease of Thermus aquaticus DNA polymerase.
- Direct interaction of FANCD2 with BRCA2 in DNA damage response pathways.
- The hSNM1 protein is a DNA 5''-exonuclease.
- S. cerevisiae has three pathways for DNA interstrand crosslink repair.
- Cloning and characterization of a human cDNA (INPPL1) sharing homology with inositol polyphosphate phosphatases.
- Replisome pausing in mutagenesis.
- DNA repair synthesis dependent on the uvrA,B gene products in toluene-treated cells.
- Escherichia coli DNA polymerase II is stimulated by DNA polymerase III holoenzyme auxiliary subunits.
- Hypersensitivity to oxygen is a uniform and secondary defect in Fanconi anemia cells.
- Localization of the Fanconi anemia complementation group D gene to a 200-kb region on chromosome 3p25.3.
- The Ashkenazi Jewish Fanconi anemia mutation: incidence among patients and carrier frequency in the at-risk population.
- A common mutation in the FACC gene causes Fanconi anaemia in Ashkenazi Jews.
- Cisplatin DNA cross-links do not inhibit S-phase and cause only a G2/M arrest in Saccharomyces cerevisiae.
- Topo IIIalpha and BLM act within the Fanconi anemia pathway in response to DNA-crosslinking agents.
- Positional cloning of a novel Fanconi anemia gene, FANCD2.
- siRNA depletion of BRCA1, but not BRCA2, causes increased genome instability in Fanconi anemia cells.
- Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation.
- BRCA1 interacts directly with the Fanconi anemia protein FANCA.
- Complementation group assignments in Fanconi anemia fibroblast cell lines from North America.
- Immortalization of four new Fanconi anemia fibroblast cell lines by an improved procedure.
- Fanconi anemia cells have a normal gene structure for topoisomerase I.
- Mammalian SNM1 is required for genome stability.
- Loss of homologous recombination or non-homologous end-joining leads to radial formation following DNA interstrand crosslink damage.
- The yeast Snm1 protein is a DNA 5''-exonuclease.
- The beta-lactamase motif in Snm1 is required for repair of DNA double-strand breaks caused by interstrand crosslinks in S. cerevisiae.
- A FANCD2 domain activates Tip60-dependent apoptosis.
Schools
Johns Hopkins Univ Sch Of Med
Johns Hopkins Hospital
National Insthlth
Doctors Specialties
- Clinical Genetics
- Medical Genetics
Accepted Insurances
Awards
- CMS Meaningful Use Stage 1 Certification
Education
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Johns Hopkins University -
Johns Hopkins University School of Medicine
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1912915471 |
| Last Name Of The Provider | MOSES |
| First Name Of The Provider | ROBB |
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