• Title Research Assistant Professor of Biology
  • Education Ph.D., Neurobiology/Neuroendocrinology, Mount Sinai School of Medicine of New York University, 2001
  • Office BRB523
  • Phone 617-358-2995
  • Area of Interest growth factor-mediated cell survival, cancer biology, transcription network mapping, gene regulation, neuroscience, endocrinology, neuroendocrinology, physiology, carcinogenesis, cell biology, molecular biology, transcription regulation
  • CV

Current Research

Professor Tullai is not currently accepting applicants for graduate study or postdoctoral appointments

My previous work was done in collaboration with Prof. Geoffrey Cooper, integrating experimental and systems biological/genomic methodologies. My focus was on the transcription regulation of phosphatidylinositol-3-kinase (PI3K)/Akt-mediated survival signals and induction of apoptosis in human cell models. My more recent work investigated PI3K/Akt/Glycogen synthase kinase-3 (GSK-3)-mediated transcription regulating the induction of cardiomyocyte hypertrophy and apoptosis in primary culture models.

While in Prof. Cooper’s laboratory, I was heavily engaged in mentoring and training undergraduate and graduate students, as well as participating in formal teaching as a guest lecturer. Because of the satisfaction I have derived from these activities, my primary focus has since shifted to science education and teaching within the College of Arts and Sciences at Boston University.
My research activity likewise continues in studying the regulation of transcription factor LSF and its involvement in cancer, supported by my role in mentoring and training undergraduate and graduate researchers in the laboratory of Prof. Ulla Hansen.

Selected Publications

  • Tullai JW†, Moss ME, Sepulveda SM, Brennan JF, Naya FJ, Cooper GM (2016) Role of GSK-3 in CREB-mediated transcription regulation, hypertrophy and survival in cardiomyocytes. In revision. PLoS ONE. †Corresponding Author
  • Tullai JW, Graham JR, Cooper GM(2011) A GSK-3-mediated transcription network maintains repression of immediate early genes in quiescent cells. Cell Cycle. 10 (18): 3072-3077. Review Article.
  • Tullai JW, Owens LJ, Tacheva S, Graham JR, Cooper GM (2011) AP-1 is a Component of the Transcriptional Network Regulated by GSK-3 in Quiescent Cells. PLoS ONE. 6(5): e20150.
  • Graham JR, Tullai JW, Cooper GM (2010) GSK-3 represses growth factor-inducible genes by inhibiting NF-kB in quiescent cells. J. Biol. Chem. 285: 4472-4480.
  • Terragni J, Graham JR, Schaffer ME, Tullai JW, Cooper GM (2008) The roles of forkhead and NF-kB in the transcription regulation of the phosphatidylinositol 3-kinase pathway. BMC Cell Biol. 9: 6.
  • Tullai JW, Schaffer ME, Mullenbrock S, Sholder G, Kasif S,Cooper GM (2007) Immediate-early and delayed primary response genes are distinct in function and genomic architecture. J. Biol. Chem. 282: 23981-95.
  • Tullai JW, Chen J, Schaffer ME, Kamenetsky E, Kasif S, Cooper GM (2007) Glycogen synthase kinase-3 represses cyclic AMP response element-binding protein (CREB)-targeted immediate early genes in quiescent cells. J. Biol. Chem. 282: 9482-91.
  • Tullai JW, Schaffer ME, Mullenbrock S, Kasif S, Cooper GM (2004) Identification of transcription factor binding sites upstream of human genes regulated by the phosphatidylinositol 3-kinase and MEK/ERK signaling pathways. J. Biol. Chem. 279: 20167-77.

Courses Taught:

  • BI 576 Carcinogenesis
  • BI 315 Systems Physiology Laboratory
  • BI 203 Cell Biology
  • BI 108 Biology II: Cells, Genetics, Development, and Physiology
  • BI 211 Human Physiology (Guest Lecturer)
  • BI 753 Advanced Molecular Biology (Guest Lecturer)
  • BI 553 Molecular Biology II (Guest Lecturer)

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