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Richard Pomerantz, PhD

 

Richard Pomerantz, PhD

 

Assistant Professor, Biochemistry

Assistant Professor, Fels Institute for Cancer Research and Molecular Biology

Email: richard.pomerantz@temple.edu

 

Department of Biochemistry

Fels Institute for Cancer Research and Molecular Biology

 

Educational Background:

 

Undergraduate degree, Arizona State University, Tempe, AZ, 1992

 

PhD, State University of New York Downstate Medical Center, Brooklyn, NY, 2006

 

Postdoctoral fellowship, The Rockefeller University, New York, NY, 2006-2013

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Research Interests:

 

DNA Repair, Genome Instability and Cancer

 

Genome instability is a hallmark of cancer cells and it is well established that defects in DNA repair pathways such as homologous recombination predispose to cancer.  My laboratory is interested in understanding the underlying mechanisms of DNA repair in human cells and how proper genome maintenance reduces the risks of cancer.  Understanding how proteins function within DNA repair pathways provides important insights into the etiology of certain cancers and is necessary for the development of novel cancer drugs.

 

Double-strand and single-strand breaks in DNA are repaired by a highly conserved pathway called homologous recombination which directs the replication machinery to copy sequence information from a homologous DNA donor.  Homologous recombination is necessary for maintaining genome integrity and suppressing tumorigenesis.  For example, mutations of important factors within this pathway such as tumor suppressor proteins BRCA1 and BRCA2 predispose to breast and ovarian cancers.  BRCA2, which is considered a pro-recombination factor, loads RAD51 recombinase onto DNA which is necessary for the initiation of homologous recombination.  Anti-recombination factors which dissociate RAD51 from DNA, however, are also important for genome maintenance.  For example, defects in factors that dissociate recombination intermediates results in hyper-recombination and gross chromosomal rearrangements which are thought to promote cancer.  Current research is focused on identifying anti-recombination factors in human cells and investigating their mechanisms and role in the regulation of DNA repair.

 

Most DNA repair processes including homologous recombination require the activity of DNA polymerases.  Although several DNA polymerases have been discovered is human cells, many of their functions remain obscure.  For example, DNA polymerase theta is a relatively newly discovered error-prone translesion DNA polymerase this is implicated in multiple DNA repair pathways including translesion synthesis, DNA double-strand break repair, base excision repair and interstrand crosslink repair.  Importantly, DNA polymerase theta is significantly upregulated in 70% of breast cancers and such upregulation corresponds to a poor clinical outcome.  Reducing the expression level of DNA polymerase theta has been shown to specifically sensitize cancer cells to radiation.  Drugs that inhibit DNA polymerase theta may therefore be used as radiosensitizers and potentially increase the survival rate of breast cancer patients.  Current research is focused on understanding the mechanism of action of DNA polymerase theta and identifying and developing small-molecule inhibitors of the polymerase for potential use in cancer therapy.


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PUBMED PUBLICATIONS :


Recent Medically Related Publications, Obtained from PubMed (Click on PubMed ID to view abstract)

23907132. Pomerantz RT, Goodman MF, O'Donnell ME, DNA polymerases are error-prone at RecA-mediated recombination intermediates. Cell Cycle 12:16(2558-63)2013 Aug 15

23686288. Pomerantz RT, Kurth I, Goodman MF, O'Donnell ME, Preferential D-loop extension by a translesion DNA polymerase underlies error-prone recombination. Nat Struct Mol Biol 20:6(748-55)2013 Jun

21326887. Pomerantz RT, O'Donnell M, Polymerase trafficking: A role for transcription factors in preventing replication fork arrest. Transcription 1:3(136-139)2010 Nov

20581460. Pomerantz RT, O'Donnell M, What happens when replication and transcription complexes collide? Cell Cycle 9:13(2537-43)2010 Jul 1

20436399. Pomerantz RT, O'Donnell M, Direct restart of a replication fork stalled by a head-on RNA polymerase. J Vis Exp :38()2010 Apr 29

20110508. Pomerantz RT, O'Donnell M, Direct restart of a replication fork stalled by a head-on RNA polymerase. Science 327:5965(590-2)2010 Jan 29

19020502. Pomerantz RT, O'Donnell M, The replisome uses mRNA as a primer after colliding with RNA polymerase. Nature 456:7223(762-6)2008 Dec 11

17350265. Pomerantz RT, O'Donnell M, Replisome mechanics: insights into a twin DNA polymerase machine. Trends Microbiol 15:4(156-64)2007 Apr

17052459. Kashkina E, Anikin M, Brueckner F, Pomerantz RT, McAllister WT, Cramer P, Temiakov D, Template misalignment in multisubunit RNA polymerases and transcription fidelity. Mol Cell 24:2(257-66)2006 Oct 20

17052458. Pomerantz RT, Temiakov D, Anikin M, Vassylyev DG, McAllister WT, A mechanism of nucleotide misincorporation during transcription due to template-strand misalignment. Mol Cell 24:2(245-55)2006 Oct 20

16159208. Pomerantz RT, Ramjit R, Gueroui Z, Place C, Anikin M, Leuba S, Zlatanova J, McAllister WT, A tightly regulated molecular motor based upon T7 RNA polymerase. Nano Lett 5:9(1698-703)2005 Sep

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