Nika Danial

Nika Danial, Ph.D.

Associate Professor of Medicine (Dana-Farber Cancer Institute)
Affiliate Member of Cell Biology (HMS)

Nika Danial, Ph.D., is an Associate Professor of Cancer Biology and Medicine (DFCI) , and an affiliate member of the Cell Biology Department (HMS). She received an undergraduate degree in Biological Sciences from Stanford University, and a Ph.D. in Molecular, Cellular and Biophysical Studies from Columbia University. Her postdoctoral studies in the laboratory of Stanley J. Korsmeyer at the Dana-Farber Cancer Institute focused on the role of BCL-2 family proteins in mitochondrial apoptosis, where she discovered a molecular link between cell survival/death regulatory pathways and metabolism. She joined the faculty of the Dana-Farber Cancer Institute and Harvard Medical School in 2005.

The Danial Lab focuses on molecular mechanisms and biologic consequences of cellular fuel choices. Different cell states have distinct anabolic and catabolic needs that are fulfilled by processing specific metabolic substrates. As such, cells’ fuel choice can influence transitions in and out of quiescence, resistance/sensitivity to oxidative stress, metabolic adaptations to nutrient changes, and cell identity, including epigenetic regulation. Understanding how these fuel preferences are controlled and defining their specific metabolic outputs will provide a molecular handle on modulating cell behavior in normal physiology and in pathologic conditions. The Danial lab uses multi-disciplinary in vitro and in vivo approaches that draw on mitochondrial metabolism, biochemistry, chemical biology, proteomics, metabolomics and genetically engineered mouse models to identify molecular determinants of cellular fuel choices and their effects on cell fate and function. This research program has led to discoveries linking fuel utilization pathways to cellular stress outcomes in diseases such as cancer, diabetes and seizure disorders.

Dana Farber Cancer Institute

Dept. of Cell Biology, LC-6313

360 Longwood Avenue

Boston, MA 02115

Lab Phone: 617-632-6436

Lab Fax: 617-632-5363

v-Abl signaling disrupts SOCS-1 function in transformed pre-B cells.
Authors: Authors: Limnander A, Danial NN, Rothman PB.
Mol Cell
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Cell death: critical control points.
Authors: Authors: Danial NN, Korsmeyer SJ.
Cell
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BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis.
Authors: Authors: Danial NN, Gramm CF, Scorrano L, Zhang CY, Krauss S, Ranger AM, Datta SR, Greenberg ME, Licklider LJ, Lowell BB, Gygi SP, Korsmeyer SJ.
Nature
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Bad-deficient mice develop diffuse large B cell lymphoma.
Authors: Authors: Ranger AM, Zha J, Harada H, Datta SR, Danial NN, Gilmore AP, Kutok JL, Le Beau MM, Greenberg ME, Korsmeyer SJ.
Proc Natl Acad Sci U S A
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Functional involvement of Akt signaling downstream of Jak1 in v-Abl-induced activation of hematopoietic cells.
Authors: Authors: Oki S, Limnander A, Danial NN, Rothman PB.
Blood
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Positive regulation of interleukin-4-mediated proliferation by the SH2-containing inositol-5'-phosphatase.
Authors: Authors: Giallourakis C, Kashiwada M, Pan PY, Danial N, Jiang H, Cambier J, Coggeshall KM, Rothman P.
J Biol Chem
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JAK-STAT signaling activated by Abl oncogenes.
Authors: Authors: Danial NN, Rothman P.
Oncogene
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A thrombopoietin receptor mutant deficient in Jak-STAT activation mediates proliferation but not differentiation in UT-7 cells.
Authors: Authors: Dorsch M, Danial NN, Rothman PB, Goff SP.
Blood
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Transcriptional repression of Stat6-dependent interleukin-4-induced genes by BCL-6: specific regulation of iepsilon transcription and immunoglobulin E switching.
Authors: Authors: Harris MB, Chang CC, Berton MT, Danial NN, Zhang J, Kuehner D, Ye BH, Kvatyuk M, Pandolfi PP, Cattoretti G, Dalla-Favera R, Rothman PB.
Mol Cell Biol
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Direct interaction of Jak1 and v-Abl is required for v-Abl-induced activation of STATs and proliferation.
Authors: Authors: Danial NN, Losman JA, Lu T, Yip N, Krishnan K, Krolewski J, Goff SP, Wang JY, Rothman PB.
Mol Cell Biol
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