Genomes and Genes
Affiliation: Harvard University
- Bad-deficient mice develop diffuse large B cell lymphomaAnn M Ranger
Howard Hughes Medical Institute and Department of Pathology, Harvard Medical School and Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 100:9324-9. 2003..Exposure of Bad-null mice to sublethal gamma-irradiation resulted in an increased incidence of pre-T cell and pro-/pre-B cell lymphoblastic leukemia/lymphoma. Thus, proapoptotic BAD suppresses tumorigenesis in the lymphocyte lineage...
- Homeostatic functions of BCL-2 proteins beyond apoptosisNika N Danial
Department of Pathology, Harvard Medical School, Boston, Massachusetts, USA
Adv Exp Med Biol 687:1-32. 2010....
- BAD modulates counterregulatory responses to hypoglycemia and protective glucoprivic feedingMayowa A Osundiji
Department of Cancer Biology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
PLoS ONE 6:e28016. 2011..Together, these data indicate a previously unappreciated role for BAD in the control of central glucose sensing...
- BCL-2 family proteins: critical checkpoints of apoptotic cell deathNika N Danial
Department of Pathology, Harvard Medical School and Department of Cancer Biology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Clin Cancer Res 13:7254-63. 2007....
- Dual role of proapoptotic BAD in insulin secretion and beta cell survivalNika N Danial
Department of Pathology, Harvard Medical School, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
Nat Med 14:144-53. 2008..Furthermore, we show that BAD regulates the physiologic adaptation of beta cell mass during high-fat feeding. Our findings provide genetic proof of the bifunctional activities of BAD in both beta cell survival and insulin secretion...
- BAD: undertaker by night, candyman by dayN N Danial
Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
Oncogene 27:S53-70. 2008..By executing its 'day' and 'night' jobs in metabolism and apoptosis, respectively, BAD helps coordinate mitochondrial fuel metabolism and the apoptotic machinery...
- BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosisNika N Danial
Howard Hughes Medical Institute, Dana Faber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 424:952-6. 2003..This combination of proteomics, genetics and physiology indicates an unanticipated role for BAD in integrating pathways of glucose metabolism and apoptosis...
- Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemiaAnna C Schinzel
Howard Hughes Medical Institute and Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:12005-10. 2005....
- Targeting the cell death-survival equationEdward J Benz
Dana Farber Cancer Institute, Harvard University, Boston, MA 02115, USA
Clin Cancer Res 13:7250-3. 2007
- beta-Cell mitochondria exhibit membrane potential heterogeneity that can be altered by stimulatory or toxic fuel levelsJakob D Wikstrom
Tufts University, Department of Pharmacology and Experimental Therapeutics, 136 Harrison Ave, Boston, MA 02111, USA
Diabetes 56:2569-78. 2007..This study offers insight into the different metabolic states of beta-cell mitochondria...
- Fast kinase domain-containing protein 3 is a mitochondrial protein essential for cellular respirationMaria Simarro
Division of Rheumatology, Immunology and Allergy, Brigham and Women s Hospital, and Department of Medicine, Harvard Medical School, Boston, MA 02115, United States
Biochem Biophys Res Commun 401:440-6. 2010..Our results introduce FASTKD3 as an essential component of mitochondrial respiration that may modulate energy balance in cells exposed to adverse conditions by functionally coupling mitochondrial protein synthesis to respiration...
- Bad targets the permeability transition pore independent of Bax or Bak to switch between Ca2+-dependent cell survival and deathSoumya Sinha Roy
Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
Mol Cell 33:377-88. 2009..Thus, phospho-regulatory mechanisms converge on Bad to switch between the survival and apoptotic functions of mitochondrial calcium signaling by activating a mechanism whereby a BH3-only protein bypasses Bax/Bak and engages the PTP...
- Cell death: critical control pointsNika N Danial
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cell 116:205-19. 2004..The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics...
- Behavioral stress accelerates prostate cancer development in miceSazzad Hassan
Department of Cancer Biology, Wake Forest School of Medicine, Medical Center Blvd, Winston Salem, North Carolina 27157, USA
J Clin Invest 123:874-86. 2013..Our findings could be used to identify prostate cancer patients who could benefit from stress reduction or from pharmacological inhibition of stress-induced signaling...
- Loss of Mcl-1 protein and inhibition of electron transport chain together induce anoxic cell deathJoslyn K Brunelle
Department of Medicine, Northwestern University Medical School, 240 East Huron Avenue, Chicago, IL 60611, USA
Mol Cell Biol 27:1222-35. 2007..Collectively, these results demonstrate that anoxia-induced cell death requires the loss of Mcl-1 protein and inhibition of the electron transport chain to negate Bcl-X(L)/Bcl-2 proteins...
- Transplacental exposure to the vacuolar-ATPase inhibitor bafilomycin disrupts survival signaling in beta cells and delays neonatal remodeling of the endocrine pancreasKalindi D Hettiarachchi
Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia
Exp Toxicol Pathol 60:295-306. 2008....
- OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusionChristian Frezza
Dulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Padova, Italy
Cell 126:177-89. 2006..The proapoptotic BCL-2 family member BID, which widens cristae junctions, also disrupts OPA1 oligomers. Thus, OPA1 has genetically and molecularly distinct functions in mitochondrial fusion and in cristae remodeling during apoptosis...
- Dissecting the Death Pathway in the Islet beta-cellNika Danial; Fiscal Year: 2005..abstract_text> ..
- BAD Intergrates Glycolysis and ApoptosisNika Danial; Fiscal Year: 2008..Danial's development as an independent investigator. Dr. Korsmeyer, a world leader in the fields of oncogenesis and apoptosis, has an excellent record of training and fostering independent investigators. ..