User:Orsolya Kiraly: Difference between revisions
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==Contact Info== | ==Contact Info== | ||
[[Image:OWWEmblem.png|thumb|right|Orsolya Kiraly (an artistic interpretation)]] | [[Image:OWWEmblem.png|thumb|right|Orsolya Kiraly (an artistic interpretation)]] | ||
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*[[Special:Emailuser/Orsolya Kiraly|Email me through OpenWetWare]] | *[[Special:Emailuser/Orsolya Kiraly|Email me through OpenWetWare]] | ||
I received my PhD for work on how rare mutations in pancreatic trypsin inhibitor contribute to chronic pancreatic inflammation. In the [http://web.mit.edu/engelward-lab/], my current work is aimed at homologous recombination in the pancreas in vivo. | I received my PhD for work on how rare mutations in pancreatic trypsin inhibitor contribute to chronic pancreatic inflammation. In the [http://web.mit.edu/engelward-lab/ Engelward lab], my current work is aimed at homologous recombination in the pancreas in vivo. | ||
While mitotic homologous recombination is an important DNA repair/tolerance mechanism, it can result in sequence rearrangements that can contribute to cancer. I am investigating the effects of DNA damaging chemicals, radiation, cell proliferation and DNA repair on homologous recombination in the pancreas. | While mitotic homologous recombination is an important DNA repair/tolerance mechanism, it can result in sequence rearrangements that can contribute to cancer. I am investigating the effects of DNA damaging chemicals, radiation, cell proliferation and DNA repair on homologous recombination in the pancreas. | ||
Revision as of 08:04, 1 September 2010
Contact Info
- Orsolya Kiraly
- Postdoctoral Associate
- Engelward laboratory
- Department of Biological Engineering
- Massachusetts Institute of Technology
- 77 Massachusetts Ave
- Lab: 617-750-7335 (Room 16-760)
- Cambridge, MA
- Email me through OpenWetWare
I received my PhD for work on how rare mutations in pancreatic trypsin inhibitor contribute to chronic pancreatic inflammation. In the Engelward lab, my current work is aimed at homologous recombination in the pancreas in vivo.
While mitotic homologous recombination is an important DNA repair/tolerance mechanism, it can result in sequence rearrangements that can contribute to cancer. I am investigating the effects of DNA damaging chemicals, radiation, cell proliferation and DNA repair on homologous recombination in the pancreas.
The next question in my project is whether homologous recombination is induced by inflammation, which is a major risk factor for cancer.
Education
- Year, PhD, Institute
- Year, MS, Institute
- Year, BS, Institute
Research interests
- Interest 1
- Interest 2
- Interest 3
Publications
- Goldbeter A and Koshland DE Jr. An amplified sensitivity arising from covalent modification in biological systems. Proc Natl Acad Sci U S A. 1981 Nov;78(11):6840-4. DOI:10.1073/pnas.78.11.6840 |
- JACOB F and MONOD J. Genetic regulatory mechanisms in the synthesis of proteins. J Mol Biol. 1961 Jun;3:318-56. DOI:10.1016/s0022-2836(61)80072-7 |
leave a comment about a paper here
- ISBN:0879697164
