John Abrams graduated from Cornell University in 1982 and received a National Science Foundation Fellowship for graduate work at Stanford University the following year. Under the mentorship of Dr. Robert Schimke, he analyzed the regulation, amplification and mutagenesis of transfected genes, receiving a PhD. in 1989. Later that year, Dr. Abrams moved to MIT as an American Cancer Society fellow, where he joined the lab of Hermann Steller and launched molecular studies on programmed cell death. Using the Drosophila model, he uncovered the first global cell death defective mutation in this animal and later he identified the gene ’reaper’ as the relevant locus encoding the predicted apoptotic function. Small molecules that simulate the activity encoded by this gene are now attracting widespread attention as promising anti-cancer drugs. In 1994, Dr. Abrams joined the faculty at UT Southwestern, where he continues research on the molecular physiology of cell death. In related efforts, his group is exploring biological links between tumor suppressor genes commonly mutated in human cancers and moible genetic elements. Dr. Abrams received the Research Scholar award from the American Cancer Society and the Senior Scholar award from the Ellison Medical Foundation. He is currently a Professor in the department of Cell Biology.
- Cornell University (1982), Biology
- Graduate School
- Stanford University (1989), Molecular & Cell Biology
- Chromatin Assembly, 3D Genome Organization and Gene Regulation
- Mobile Genetic Elements, Transposons
- Programmed Cell Death; Apoptosis
- Tumor Suppressor genes, Tumor Protein p53
- Retrotransposons Mimic Germ Plasm Determinants to Promote Transgenerational Inheritance.
- Tiwari B, Kurtz P, Jones AE, Wylie A, Amatruda JF, Boggupalli DP, Gonsalvez GB, Abrams JM Curr. Biol. 2017 Oct 27 19 3010-3016.e3
- p53 in the game of transposons.
- Wylie A, Jones AE, Abrams JM Bioessays 2016 Sep
- A platform for interrogating cancer-associated p53 alleles.
- D'Brot A, Kurtz P, Regan E, Jakubowski B, Abrams JM Oncogene 2016 Mar
- p53 genes function to restrain mobile elements.
- Wylie A, Jones AE, D'Brot A, Lu WJ, Kurtz P, Moran JV, Rakheja D, Chen KS, Hammer RE, Comerford SA, Amatruda JF, Abrams JM Genes Dev. 2015 Dec
- p53 activity is selectively licensed in the Drosophila stem cell compartment.
- Wylie A, Lu WJ, D'Brot A, Buszczak M, Abrams JM Elife 2014 3 e01530
- A p53 enhancer region regulates target genes through chromatin conformations in cis and in trans.
- Link N, Kurtz P, O'Neal M, Garcia-Hughes G, Abrams JM Genes Dev. 2013 Nov 27 22 2433-8
- Tango7 directs cellular remodeling by the Drosophila apoptosome.
- D'Brot A, Chen P, Vaishnav M, Yuan S, Akey CW, Abrams JM Genes Dev. 2013 Aug 27 15 1650-5
- Meiotic Recombination Provokes Functional Activation of the p53 Regulatory Network
- Lu, WJ Chapo, J. Roig, I. Abrams, J.M. Science June 2010 328 1278-81
- Genome-Wide Silencing Captures Obligate Apoptotic Components in Drosophila
- Chew, S.,Chen, P., Link, N., Galindo, K., Pogue, K. and Abrams, J.M. Nature July 2009 460 123-127
- A Collective Form of Cell Death Requires Homeodomain Interacting Protein Kinase
- Link, N., Chen, P., Lu, WJ, Pogue, K., Chuong, A., Mata, M., Checketts, J., Abrams, J.M J. Cell Biol August 2007 4 (178) 567-74
Honors & Awards
- Ellison Medical Foundation
Senior Scholar (2011)
- American Cancer Society
Research Scholar (2001)
- Howard Hughes Medical Institute
Postdoctoral Fellowship (1992)
- American Cancer Society
Postdoctoral Fellowsip (1989)
- National Science Foundation
Graduate Fellowship (1983)
- American Association for Cancer Research, Genetics Society of America
- American Association for the Advancement of Science
- BioMedcentral Faculty of 1000 reviewer, F1000 Faculty member
- Editorial Board: Apoptosis. Rapid Science Publishers.
- Editorial Board: Cell Death & Differentiation. Nature Publishing Group