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

Bad targets the permeability transition pore independent of Bax or Bak to switch between Ca2+-dependent cell survival and death.
Authors: Authors: Roy SS, Madesh M, Davies E, Antonsson B, Danial N, Hajnóczky G.
Mol Cell
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BAD: undertaker by night, candyman by day.
Authors: Authors: Danial NN.
Oncogene
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Transplacental exposure to the vacuolar-ATPase inhibitor bafilomycin disrupts survival signaling in beta cells and delays neonatal remodeling of the endocrine pancreas.
Authors: Authors: Hettiarachchi KD, Zimmet PZ, Danial NN, Myers MA.
Exp Toxicol Pathol
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Dual role of proapoptotic BAD in insulin secretion and beta cell survival.
Authors: Authors: Danial NN, Walensky LD, Zhang CY, Choi CS, Fisher JK, Molina AJ, Datta SR, Pitter KL, Bird GH, Wikstrom JD, Deeney JT, Robertson K, Morash J, Kulkarni A, Neschen S, Kim S, Greenberg ME, Corkey BE, Shirihai OS, Shulman GI, Lowell BB, Korsmeyer SJ.
Nat Med
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BCL-2 family proteins: critical checkpoints of apoptotic cell death.
Authors: Authors: Danial NN.
Clin Cancer Res
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Targeting the cell death-survival equation.
Authors: Authors: Benz EJ, Nathan DG, Amaravadi RK, Danial NN.
Clin Cancer Res
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beta-Cell mitochondria exhibit membrane potential heterogeneity that can be altered by stimulatory or toxic fuel levels.
Authors: Authors: Wikstrom JD, Katzman SM, Mohamed H, Twig G, Graf SA, Heart E, Molina AJ, Corkey BE, de Vargas LM, Danial NN, Collins S, Shirihai OS.
Diabetes
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Loss of Mcl-1 protein and inhibition of electron transport chain together induce anoxic cell death.
Authors: Authors: Brunelle JK, Shroff EH, Perlman H, Strasser A, Moraes CT, Flavell RA, Danial NN, Keith B, Thompson CB, Chandel NS.
Mol Cell Biol
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OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion.
Authors: Authors: Frezza C, Cipolat S, Martins de Brito O, Micaroni M, Beznoussenko GV, Rudka T, Bartoli D, Polishuck RS, Danial NN, De Strooper B, Scorrano L.
Cell
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Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia.
Authors: Authors: Schinzel AC, Takeuchi O, Huang Z, Fisher JK, Zhou Z, Rubens J, Hetz C, Danial NN, Moskowitz MA, Korsmeyer SJ.
Proc Natl Acad Sci U S A
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