Richard Kolodner

About

Richard Kolodner is a Professor of Cellular and Molecular Medicine at UC San Diego. His laboratory studies the genetic and biochemical mechanisms of genetic recombination, DNA repair, and suppression of spontaneous mutations, primarily using Saccharomyces cerevisiae as a model system. His research focuses on analyzing the proteins and genes involved in DNA mismatch repair and elucidating pathways that prevent translocations and other types of gross chromosomal rearrangements. Additionally, he investigates the genetics of cancer susceptibility and development, particularly in relation to Lynch Syndrome, a common cancer susceptibility syndrome caused by inherited defects in DNA mismatch repair genes. His work aims to understand whether genes that prevent genome instability act as tumor suppressors in humans and whether defects in these genes can be targeted therapeutically.

Research topics

• Biology
• Cancer research
• Genetics
• Molecular biology

Selected publications

• Tumour predisposition and cancer syndromes as models to study gene–environment interactions

  Nature reviews. Cancer · 2020 · 194 citations

  PublisherOA PDFDOI

• FEN1 endonuclease as a therapeutic target for human cancers with defects in homologous recombination

  Proceedings of the National Academy of Sciences · 2020 · 99 citations

  Senior authorCorresponding

  mutations, and other genetic defects.

  PublisherOA PDFDOI

• Alternative splicing regulates stochastic NLRP3 activity

  Nature Communications · 2019-07-19 · 68 citations

  articleOpen access

  Leucine-rich repeat (LRR) domains are evolutionarily conserved in proteins that function in development and immunity. Here we report strict exonic modularity of LRR domains of several human gene families, which is a precondition for alternative splicing (AS). We provide evidence for AS of LRR domain within several Nod-like receptors, most prominently the inflammasome sensor NLRP3. Human NLRP3, but not mouse NLRP3, is expressed as two major isoforms, the full-length variant and a variant lacking…

  PublisherOA PDFDOI

• Ligation of newly replicated DNA controls the timing of DNA mismatch repair

  Current Biology · 2021-01-09 · 30 citations

  articleOpen access
  PublisherOA PDFDOI

• Rad27 and Exo1 function in different excision pathways for mismatch repair in Saccharomyces cerevisiae

  Nature Communications · 2021-09-22 · 25 citations

  articleOpen accessSenior authorCorresponding

  Eukaryotic DNA Mismatch Repair (MMR) involves redundant exonuclease 1 (Exo1)-dependent and Exo1-independent pathways, of which the Exo1-independent pathway(s) is not well understood. The exo1Δ440-702 mutation, which deletes the MutS Homolog 2 (Msh2) and MutL Homolog 1 (Mlh1) interacting peptides (SHIP and MIP boxes, respectively), eliminates the Exo1 MMR functions but is not lethal in combination with rad27Δ mutations. Analyzing the effect of different combinations of the exo1Δ440-702 mutation,…

  PublisherOA PDFDOI

Recent grants

• NIH Grant T32CA009361

  NIH · $13.0M · 2017

• NIH Grant R01HG000305

  NIH · $619k · 1994

• Enzymatic Mechanisms of Genetic Recombination

  NIH · $11.4M · 1978–2027

Frequent coauthors

• Bert Vogelstein

  Howard Hughes Medical Institute

  195 shared

• Christopher D. Putnam

  Ludwig Cancer Research

  193 shared

• Annika Lindblom

  Karolinska University Hospital

  175 shared

• Païvi Peltomäki

  University of Helsinki

  171 shared

• K. W. Kinzler

  Johns Hopkins University

  170 shared

• Jana Vandrovcová

  University College London

  169 shared

• T. Liu

  University of Helsinki

  169 shared

• Mef Nilbert

  Lund University

  169 shared

Education

• Ph.D., Molecular Biology

  University of California, San Diego

  1983

• M.S., Molecular Biology

  University of California, San Diego

  1979

• B.S., Biology

  University of California, San Diego

  1977

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