Photo of Robb E. Moses, M.D.

Robb E. Moses M.D.

    • Professor Emeritus of Molecular and Medical Genetics School of Medicine
    • Molecular and Medical Genetics Graduate Program School of Medicine

My lab studies DNA crosslink repair using two model systems. Fanconi anemia is a recessive disease affecting multiple organ systems and results in severe anemia and an increased risk of leukemia. Cells from the patients are hypersensitive to DNA crosslinkers. The Moses group is part of a program project on Fanconi anemia and has participated in the positional cloning of one of the genes, from among at least twelve. The role of the FA genes inrepair of DNA cross links is intriguing not just because of the association with disease, but because the FA cells are competent in all other types of DNA repair tested. Our current work is focused on the role of chromatin remodeling in FA and potential defects in remodeling which might affect ICL repair. A second project investigates the function a mammalian gene responsible for crosslink repair, the hSNM1 gene. We have isolated the protein encoded by the gene and it is a 5’-exonuclease which is required for intermediate processing in the repair of ICLs.


  • M.D., Johns Hopkins University Medical School 1966
  • Residency:

    • Johns Hopkins Hospital, Baltimore
  • Fellowship:

    • Fellowship in biochemistry, Harvard Medical School, Boston

Memberships and associations

  • Medical genetics, 1982


  • "REGg controls hippo signaling and reciprocal NF-kB–YAP regulation to promote colon cancer." Clinical Cancer Research  In: , Vol. 24, No. 8, 15.04.2018, p. 2015-2025.
  • "Upregulation of GSK3β Contributes to Brain Disorders in Elderly REGγ-knockout Mice." Neuropsychopharmacology  In: , Vol. 41, No. 5, 01.04.2016, p. 1340-1349.
  • "The REGγ 3-proteasome forms a regulatory circuit with Iκ BIκ and NFκB in experimental colitis." Nature Communications  In: , Vol. 7, 10761, 22.02.2016.
  • "REGγ 3 is critical for skin carcinogenesis by modulating the Wnt/β 2-catenin pathway." Nature Communications  In: , Vol. 6, 6875, 24.04.2015.
  • "KLF17 empowers TGF-β/Smad signaling by targeting Smad3-dependent pathway to suppress tumor growth and metastasis during cancer progression." Cell Death and Disease  In: , Vol. 6, No. 3, e1681, 12.03.2015.
  • "Stresses, aging, and age-related disorders." Oxidative Medicine and Cellular Longevity  In: , Vol. 2014, 320564, 30.12.2014.
  • "Bloom syndrome radials are predominantly non-homologous and are suppressed by phosphorylated BLM." Cytogenetic and Genome Research  In: , Vol. 144, No. 4, 24.04.2014, p. 255-263.
  • "Steroid receptor coactivator 1 is an integrator of glucose and NAD+/NADH homeostasis." Molecular Endocrinology  In: , Vol. 28, No. 3, 03.2014, p. 395-405.
  • "REGγ deficiency promotes premature aging via the casein kinase 1 pathway." Proceedings of the National Academy of Sciences of the United States of America  In: , Vol. 110, No. 27, 02.07.2013, p. 11005-11010.
  • "DNA transcription and repair : A confluence." Journal of Biological Chemistry  In: , Vol. 287, No. 28, 06.07.2012, p. 23266-23270.
  • "A FANCD2 domain activates Tip60-dependent apoptosis." Cell Biology International  In: , Vol. 34, No. 9, 09.2010, p. 893-899.
  • "DNA interstrand crosslink repair in mammalian cells." Journal of Cellular Physiology  In: , Vol. 220, No. 3, 09.2009, p. 569-573.
  • "Topo IIIα and BLM act within the fanconi anemia pathway in response to DNA-crosslinking agents." Cytogenetic and Genome Research  In: , Vol. 125, No. 3, 09.2009, p. 165-175.
  • "ERCC1 is required for FANCD2 focus formation." Molecular Genetics and Metabolism  In: , Vol. 95, No. 1-2, 09.2008, p. 66-73.
  • "Loss of homologous recombination or non-homologous end-joining leads to radial formation following DNA interstrand crosslink damage." Cytogenetic and Genome Research  In: , Vol. 121, No. 3-4, 08.2008, p. 174-180.
  • "Role for DNA polymerase κ in the processing of N2-N 2-guanine interstrand cross-links." Journal of Biological Chemistry  In: , Vol. 283, No. 25, 20.06.2008, p. 17075-17082.
  • "Mammalian SNM1 is required for genome stability." Molecular Genetics and Metabolism  In: , Vol. 94, No. 1, 05.2008, p. 38-45.
  • "Tip60 is required for DNA interstrand cross-link repair in the fanconi anemia pathway." Journal of Biological Chemistry  In: , Vol. 283, No. 15, 11.04.2008, p. 9844-9851.
  • "The hSNM1 protein is a DNA 5′-exonuclease." Nucleic Acids Research  In: , Vol. 35, No. 18, 09.2007, p. 6115-6123.
  • "The yeast Snm1 protein is a DNA 5′-exonuclease." DNA Repair  In: , Vol. 4, No. 2, 03.02.2005, p. 163-170.
  • "Direct interaction of FANCD2 with BRCA2 in DNA damage response pathways." Human Molecular Genetics  In: , Vol. 13, No. 12, 15.06.2004, p. 1241-1248.
  • "siRNA depletion of BRCA1, but not BRCA2, causes increased genome instability in Fanconi anemia cells." DNA Repair  In: , Vol. 2, No. 9, 18.09.2003, p. 1007-1013.
  • "The β-lactamase motif in Snm1 is required for repair of DNA double-strand breaks caused by interstrand crosslinks in S. cerevisiae." DNA Repair  In: , Vol. 2, No. 1, 02.01.2003, p. 121-129.
  • "BRCA1 interacts directly with the Fanconi anemia protein FANCA." Human Molecular Genetics  In: , Vol. 11, No. 21, 01.10.2002, p. 2591-2597.
  • "S. cerevisiae has three pathways for DNA interstrand crosslink repair." Mutation Research - DNA Repair  In: , Vol. 487, No. 3-4, 19.12.2001, p. 73-83.
  • "DNA damage processing defects and disease." Annual Review of Genomics and Human Genetics  In: , Vol. 2, 2001, p. 41-68.
  • "Positional cloning of a novel Fanconi anemia gene, FANCD2." Molecular Cell  In: , Vol. 7, No. 2, 2001, p. 241-248.
  • "Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S- phase but arrest permanently in G2 after cisplatin treatment." Mutation Research - DNA Repair  In: , Vol. 461, No. 1, 15.09.2000, p. 1-13.
  • "Localization of the fanconi anemia complementation group D gene to a 200-kb region on chromosome 3p25.3." American Journal of Human Genetics  In: , Vol. 66, No. 5, 2000, p. 1540-1551.
  • "Cisplatin DNA cross-links do not inhibit S-phase and cause only a G2/M arrest in Saccharomyces cerevisiae." Mutation Research - DNA Repair  In: , Vol. 434, No. 1, 14.05.1999, p. 29-39.

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