Ali Senejani, Ph.D.
Post-doctoral training, Yale University School of Medicine
Ph.D., Genetics, University of Connecticut
M.S., Biotechnology, Mannheim University of Applied Science, Germany
My broad research objective is to study DNA damage and repair. I would like to contribute to our understanding of how different environmental factors, chemotherapies, and radiations can damage DNA. Also, to study how the genetic variants in DNA repair pathway genes in the normal population and in patients can influence individual susceptibility and development of diseases such as cancer and autoimmunity.
Environmental and genetic factors are both important to promote genomic instability that lead to a series of mutations, some of which trigger initiation and/or progression of many diseases. The maintenance of genome integrity is dependent on numerous mechanisms, which notably allow fidelity of DNA replication and repair of damaged DNA. Those processes require a large number of proteins including DNA repair proteins to proceed. There are several hundreds of DNA repair protein variants in the germline of the human population and even more in aged populations and people with diseases; therefore it is important to uncover the correlation between altered DNA repair genes and human diseases. I am very interested to contribute to the in-depth understanding of the cellular, biochemical, and molecular genetic aspects of DNA repair, mutagenesis, cell cycle regulation, apoptosis and other biological responses in cells exposed to genomic insult.
Peer Reviewed Publications
- Lokanga R., Senejani A.G., Sweasy J.B., Usdin K. “Heterozygosity for a hypomorphic Polβ mutation reduces the expansion frequency in a mouse model of the repeat expansion disease Fragile X syndrome” 2015 PLoS Genetics. 2015 Apr 17;11(4)
- Park H.J., Kim D.H., Choi J.Y., Kim W.J., Kim J.Y., Senejani A.G., Hwang S.S., Kim, L.K., Tobiasova Z., Lee G.R., Craft J., Choi J., Bothwell A.L., Choi J.M. “PPARγ negatively regulates T cell activation to prevent follicular helper T cells and germinal center formation” PLoS One 2014 June 12;9(6)
- Senejani A.G., Liu Y., Kidane D., Maher S.E., Zeiss C.J., Park H., Kashgarian M., McNiff J.M., Zelterman D., Bothwell A., Sweasy J.B. “Mutation of A DNA Repair Enzyme Causes Lupus in Mice” Cell reports (CELL PRESS) 2014 Jan 16;6(1):1-8. doi: 10.1016/j.celrep.2013.12.017. Epub 2014 Jan 2
- Ray S., Menezes M.R., Senejani A., Sweasy J.B. “Cellular Roles of DNA Polymerase Beta” Yale J Biol Med 2013 Dec 13;86(4):463-469
- Sjolund A.B., Senejani A.G., Sweasy J.B. “MBD4 and TDG: Multifaceted DNA Glycosylases With Ever Expanding Biological Roles” Mutation Research (ELSEVIER) 2013 Mar-Apr;743-744:12-25
- Senejani A.G., Dalal S., Liu Y., Nottoli, T., McGrath J., Clairmont C.S., Sweasy J.B. “Y265C DNA Polymerase Beta Knockin Mice Survive Past Birth and Accumulate Base Excision Repair Intermediate Substrates” Proc Natl Acad Sci USA 2012 Apr 24; 109(17): 6632-7
- Senejani, A.G. and Sweasy, J.B. “Eukaryotic gene invasion by a bacterial mobile Insertion sequence element IS2 during cloning into a plasmid vector” Genome Integrity 2010 May 26; 1(1):2.
- Swithers K.S., Senejani A.G, Fournier G.P., Gogarten J.P. “Conservation of intron and intein insertion sites: implications for life histories of parasitic genetic elements” BMC Evol Biol. 2009; 9:303 “BMC Highly accessed article”
- Senejani, A.G. and Gogarten, J.P. “Structural stability and endonuclease activity of PI-SceI GFP-fusion protein” Int J Biol Sci2007; 3:205-211
- Gogarten, J.P., Senejani, A.G., Zhaxybayeva, O., Olendzenski, L. and Hilario, E. “Inteins: Structure, Function, and Evolution” Annul. Review of Microbiology. 2002; 56: 263-287
- Senejani, A.G., Hilario, E., and Gogarten, J.P. “The intein of the Thermoplasma A-ATPase A subunit: Structure, evolution and expression in E. coli” BMC Biochemistry. 2001; 2(1): 13, 1-10