Research Topics
Genomes and Genes
| Stanley KorsmeyerSummaryAffiliation: Harvard University Country: USA Publications
Research Grants
| Collaborators
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Detail Information
Publications
Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome cS J Korsmeyer
Department of Pathology, Harvard Medical School, Dana Farber Cancer Institute, Howard Hughes Medical Institute, Boston, Massachusetts, MA 02115, USA
Cell Death Differ 7:1166-73. 2000..Thus, an activation cascade of pro-apoptotic proteins from BID to BAK or BAX integrates the pathway from surface death receptors to the irreversible efflux of cytochrome c. Cell Death and Differentiation (2000) 7, 1166 - 1173..- Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family membersMichael Certo
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
Cancer Cell 9:351-65. 2006..Our data allow us to distinguish a cellular state we call "primed for death," which can be determined by BH3 profiling and which correlates with dependence on antiapoptotic family members for survival... 
The BCL2A1 gene as a pre-T cell receptor-induced regulator of thymocyte survivalMalay Mandal
Department of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL 60637, USA
J Exp Med 201:603-14. 2005..Finally, we suggest that pre-TCR-induced A1 overexpression can contribute to T cell leukemia in both mice and humans...- Obligate role of anti-apoptotic MCL-1 in the survival of hematopoietic stem cellsJoseph T Opferman
Howard Hughes Medical Institute, Department of Cancer Immunology and AIDS, Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Science 307:1101-4. 2005..Deletion of Mcl-1 in other tissues, including liver, did not impair survival. Thus, MCL-1 is a critical and specific regulator essential for ensuring the homeostasis of early hematopoietic progenitors... - Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulumScott A Oakes
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:105-10. 2005..These findings support a model in which BCL-2 family members regulate IP3R-1 phosphorylation to control the rate of ER Ca(2+) leak from intracellular stores... - Conformational changes in BID, a pro-apoptotic BCL-2 family member, upon membrane binding. A site-directed spin labeling studyKyoung Joon Oh
Howard Hughes Medical Institute, the Department of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Biol Chem 280:753-67. 2005..Our study presents a more detailed model for the reorganization of the structure of tBID on membranes... - Survival factor-induced extracellular signal-regulated kinase phosphorylates BIM, inhibiting its association with BAX and proapoptotic activityHisashi Harada
Department of Internal Medicine, Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA
Proc Natl Acad Sci U S A 101:15313-7. 2004..Thus, ERK/mitogen-activated protein kinase-dependent phosphorylation of BIM in response to survival factor regulates BIM/BAX interaction and the pro-death activity of BIM... - Untangling the web: mitochondrial fission and apoptosisScott A Oakes
Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Dev Cell 7:460-2. 2004..A new study by Szabadkai et al. in the October 8th issue of Molecular Cell shows that dynamin-related protein 1 (Drp1)-induced scission hinders the ability of mitochondria to transport calcium across the cell and mediate apoptosis... - Inhibition of both the extrinsic and intrinsic death pathways through nonhomotypic death-fold interactionsYoung Jae Nam
Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
Mol Cell 15:901-12. 2004..Conversely, physiological levels of ARC suppress these events. These studies establish a critical role for nonhomotypic death-fold interactions in the regulation of apoptosis... - Antiapoptotic BCL-2 is required for maintenance of a model leukemiaAnthony Letai
Howard Hughes Medical Institute, Department of Pathology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 6:241-9. 2004..This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s)... - Activation of apoptosis in vivo by a hydrocarbon-stapled BH3 helixLoren D Walensky
Howard Hughes Medical Institute, Department of Pediatric Hematology Oncology and Children s Hospital Boston, Massachusetts, USA
Science 305:1466-70. 2004..Hydrocarbon stapling of native peptides may provide a useful strategy for experimental and therapeutic modulation of protein-protein interactions in many signaling pathways... - BAD is a pro-survival factor prior to activation of its pro-apoptotic functionSo Young Seo
W Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD21205, USA
J Biol Chem 279:42240-9. 2004..These findings suggest that BAD is more than an inert death factor in healthy cells; it is also a pro-survival factor, prior to its role in promoting cell death... - Definitive hematopoiesis requires the mixed-lineage leukemia genePatricia Ernst
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115 USA
Dev Cell 6:437-43. 2004..These results demonstrate an intrinsic requirement for MLL in definitive hematopoiesis, where it is essential for the generation of HSCs in the embryo... - Phosphorylation of BCL-2 regulates ER Ca2+ homeostasis and apoptosisMichael C Bassik
Department of Pathology and Medicine, Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
EMBO J 23:1207-16. 2004..Unexpectedly, the regulation of ER Ca(2+) dynamics is a principal avenue whereby BCL-2 phosphorylation alters susceptibility to apoptosis... - Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channelLaurent M Dejean
Department of Basic Sciences, College of Dentistry, New York University, New York, NY 10010, USA
Mol Biol Cell 16:2424-32. 2005..These findings indicate Bax is a component of MAC in staurosporine-treated HeLa cells and suggest Bax and Bak are functionally redundant as components of MAC... - Proapoptotic BAX and BAK control multiple initiator caspasesAntonio Ruiz-Vela
Howard Hughes Medical Institute, Department of Pathology and Medicine, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
EMBO Rep 6:379-85. 2005..Thus, BAX and BAK confer an essential gateway for the activation of caspases in the intrinsic apoptotic pathway... 
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...- Multiple signaling pathways promote B lymphocyte stimulator dependent B-cell growth and survivalRobert T Woodland
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655, USA
Blood 111:750-60. 2008..Because BlyS is required for the normal homeostasis of all B cells, these data suggest a therapeutic strategy simultaneously inhibiting mTOR and Pim 2 could target pathogenic B cells... - A spatially and temporally restricted mouse model of soft tissue sarcomaDavid G Kirsch
Center for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA
Nat Med 13:992-7. 2007..Therefore, the intrinsic pathway of apoptosis seems sufficient to mediate p53 tumor suppression in an epithelial cancer, but not in this model of soft tissue sarcoma... - A stapled BID BH3 helix directly binds and activates BAXLoren D Walensky
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children s Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cell 24:199-210. 2006..We further demonstrate that membrane targeting of stapled BID BH3 optimizes its ability to activate BAX, supporting a model in which BID directly engages BAX to trigger mitochondrial apoptosis... - A membrane-targeted BID BCL-2 homology 3 peptide is sufficient for high potency activation of BAX in vitroKyoung Joon Oh
Howard Hughes Medical Institute, the Department of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Biol Chem 281:36999-7008. 2006..These results highlight the importance of membrane targeting of the BID BH3 domain in tBID-mediated BAX activation and support a model in which tBID engages BAX to trigger its pro-apoptotic activity... - PP2A regulates BCL-2 phosphorylation and proteasome-mediated degradation at the endoplasmic reticulumStephen S Lin
Howard Hughes Medical Institute, Department of Cancer Immunology and AIDS, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 281:23003-12. 2006..These studies support the hypothesis that PP2A-mediated dephosphorylation of BCL-2 is required to protect BCL-2 from proteasome-dependent degradation, affecting resistance to ER stress... - Essential role of BAX,BAK in B cell homeostasis and prevention of autoimmune diseaseOsamu Takeuchi
Howard Hughes Medical Institute, Dana Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:11272-7. 2005..Furthermore, inducible deletion of Bax and Bak in adult mice results in the development of severe autoimmune disease... - Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alphaClaudio Hetz
Howard Hughes Medical Institute, Dana Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA
Science 312:572-6. 2006..Thus, BAX and BAK function at the ER membrane to activate IRE1alpha signaling and to provide a physical link between members of the core apoptotic pathway and the UPR... - Bax channel inhibitors prevent mitochondrion-mediated apoptosis and protect neurons in a model of global brain ischemiaClaudio Hetz
Serono Pharmaceutical Research Institute, 14 Chemin des Aulx, CH 1228 Plan les Ouates, Geneva, Switzerland
J Biol Chem 280:42960-70. 2005..The protective effect in the animal model correlated with decreased cytochrome c release in the infarcted area. This is the first demonstration that Bax channel activity is required in apoptosis... - p600, a unique protein required for membrane morphogenesis and cell survivalYoshihiro Nakatani
Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:15093-8. 2005..Consequently, knockdown of p600 sensitizes cells to apoptosis induced by cell detachment. These findings provide mechanistic insight into the regulation of membrane-proximal events in tumorigenesis... - A role for proapoptotic BID in the DNA-damage responseSandra S Zinkel
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cell 122:579-91. 2005..We further demonstrate that this role is mediated through BID phosphorylation by the DNA-damage kinase ATM. These results establish a link between proapoptotic Bid and the DNA-damage response... - 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.... - 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... - Switching mechanisms of cell death in mdm2- and mdm4-null mice by deletion of p53 downstream targetsArturo Chavez-Reyes
Department of Molecular Genetics, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
Cancer Res 63:8664-9. 2003..Thus, in both examples, deletion of a p53 downstream target gene allows p53 to redirect its efforts, highlighting a high degree of plasticity in p53 function... - Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1Joseph T Opferman
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Department of Pathology and Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 426:671-6. 2003..Thus, MCL-1, which selectively inhibits the proapoptotic protein BIM, is essential both early in lymphoid development and later on in the maintenance of mature lymphocytes... - Role of proapoptotic BAX in propagation of Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis) and the host inflammatory responseJean Luc Perfettini
Universite Paris 7, Institut Pasteur, Unité de Biologie Moléculaire du Gène, INSERM U277, Paris, France
J Biol Chem 278:9496-502. 2003..Bax deficiency results in lower infection and an increased inflammatory cytokine response associated with more severe pathology... - Bax, caspase-2, and caspase-3 are required for ovarian follicle loss caused by 4-vinylcyclohexene diepoxide exposure of female mice in vivoYasushi Takai
Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital Harvard Medical School, Boston, Massachusetts 02114, USA
Endocrinology 144:69-74. 2003.... - Proteolytic cleavage of MLL generates a complex of N- and C-terminal fragments that confers protein stability and subnuclear localizationJames J D Hsieh
Howard Hughes Medical Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cell Biol 23:186-94. 2003..This predicts that MLL fusion proteins of leukemia which would lose the ability to complex with C180 have their stability conferred instead by the fusion partners, thus providing one mechanism for altered target gene expression... - Survival factor-mediated BAD phosphorylation raises the mitochondrial threshold for apoptosisSandeep Robert Datta
Division of Neuroscience, Children s Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA
Dev Cell 3:631-43. 2002..These findings establish a function for endogenous BAD phosphorylation, and elucidate a mechanism by which survival kinases block apoptosis in vivo... - BID regulation by p53 contributes to chemosensitivityJoanna K Sax
Laboratory of Molecular Oncology and Cell Cycle Regulation, Howard Hughes Medical Institute, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Nat Cell Biol 4:842-9. 2002..Our results indicate that BID is a p53-responsive 'chemosensitivity gene' that may enhance the cell death response to chemotherapy... - Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeuticsAnthony Letai
Howard Hughes Medical Institute, Department of Pathology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 2:183-92. 2002..These data support a two-class model for BH3 domains: BID-like domains that "activate" BAX, BAK and BAD-like domains that "sensitize" by occupying the pocket of antiapoptotic members... - Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viabilityGael G McGill
Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cell 109:707-18. 2002..This linkage helps explain the vital roles of both Mitf and Bcl2 in the melanocyte lineage and the well-known treatment resistance of melanoma... - Activation of BAD by therapeutic inhibition of epidermal growth factor receptor and transactivation by insulin-like growth factor receptorAndrew P Gilmore
School of Biological Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, United Kingdom
J Biol Chem 277:27643-50. 2002..Our results indicate that by targeting a growth factor-mediated survival signaling pathway, BAD phosphorylation can be manipulated therapeutically to induce apoptosis... - Bax-dependent spermatogonia apoptosis is required for testicular development and spermatogenesisLonnie D Russell
Department of Physiology, Southern Illinois University School of Medicine, Carbondale, IL 62901, USA
Biol Reprod 66:950-8. 2002..The massive hyperplasia that occurs in Bax-deficient mice subsequently results in Bax independent cell death that may be triggered by overcrowding of the seminiferous epithelium... - Function of BID -- a molecule of the bcl-2 family -- in ischemic cell death in the brainNikolaus Plesnila
Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
Eur Surg Res 34:37-41. 2002..The findings indicate that the proapoptotic molecule BID may contribute to the demise of nerve cells from cerebral ischemia by release of cytochrome c and activation of caspase... - BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosisLuca Scorrano
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Department of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Science 300:135-9. 2003..Thus, BAX and BAK operate in both the ER and mitochondria as an essential gateway for selected apoptotic signals... - Enhanced oligodendrocyte survival after spinal cord injury in Bax-deficient mice and mice with delayed Wallerian degenerationHongxin Dong
Department of Neurology, Spinal Cord Injury Neuro Rehabilitation Section, Restorative Treatment and Research Program, and Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63108, USA
J Neurosci 23:8682-91. 2003..On the basis of these data, we hypothesize that the Wallerian degeneration of white matter axons that follows SCI removes axonal support and induces apoptotic death in oligodendrocytes by triggering Bax expression... - Regulation of endoplasmic reticulum Ca2+ dynamics by proapoptotic BCL-2 family membersScott A Oakes
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Boston, USA
Biochem Pharmacol 66:1335-40. 2003..Thus, BAX and BAK control apoptosis not only at the mitochondria, but also at the ER, an obligate checkpoint for Ca(2+)-dependent apoptotic stimuli... - 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... - VDAC2 inhibits BAK activation and mitochondrial apoptosisEmily H Y Cheng
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Science 301:513-7. 2003..Thus, VDAC2, an isoform restricted to mammals, regulates the activity of BAK and provides a connection between mitochondrial physiology and the core apoptotic pathway... - 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... - Mechanisms of cytochrome c release by proapoptotic BCL-2 family membersLuca Scorrano
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Biochem Biophys Res Commun 304:437-44. 2003..This mitochondrial remodelling insures complete release of cytochrome c and the onset of mitochondrial dysfunction that is a typical feature of many apoptotic deaths... - Involvement of proapoptotic molecules Bax and Bak in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced mitochondrial disruption and apoptosis: differential regulation of cytochrome c and Smac/DIABLO releaseKarthikeyan Kandasamy
Department of Pharmaceutical Sciences, University of Maryland, School of Pharmacy, Greenebaum Cancer Center, Baltimore, Maryland 21201 1180, USA
Cancer Res 63:1712-21. 2003.... - Taspase1: a threonine aspartase required for cleavage of MLL and proper HOX gene expressionJames J D Hsieh
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cell 115:293-303. 2003..Taspase1 coevolved with MLL/trithorax as Arthropoda and Chordata emerged from Metazoa suggesting that Taspase1 originated to regulate complex segmental body plans in higher organisms... - Proapoptotic histone H1.2 induces CASP-3 and -7 activation by forming a protein complex with CYT c, APAF-1 and CASP-9Antonio Ruiz-Vela
Howard Hughes Medical Institute, Department of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
FEBS Lett 581:3422-8. 2007..In cell-free systems, we show that histone H1.2 triggers activation of CASP-3 and -7 via APAF-1 and CASP-9. We therefore conclude that upon DNA damage histone H1.2 acts as a positive regulator of apoptosome formation... - Reactivation of the p53 tumor suppressor pathway by a stapled p53 peptideFederico Bernal
Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA
J Am Chem Soc 129:2456-7. 2007 - Loss of Bax alters tumor spectrum and tumor numbers in ARF-deficient miceChristine M Eischen
Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Cancer Res 62:2184-91. 2002.... - Caspase regulation of genotoxin-induced neural precursor cell deathBarbara J Klocke
Division of Neuropathology, Department of Pathology, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294, USA
J Neurosci Res 74:435-45. 2003..These studies suggest that caspase-9 activation is both necessary and sufficient for genotoxin-induced neural precursor cell reactive oxygen species generation and death... - Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative diseaseJing Wang
Department of Pathology and Medicine, Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
EMBO J 24:368-81. 2005..This model of MLL-CBP therapy-related myeloproliferative disease demonstrates the selectivity of this MLL fusion for GMP cells and its ability to initiate leukemogenesis in conjunction with cooperating mutations... - A novel mitochondriotoxic small molecule that selectively inhibits tumor cell growthValeria R Fantin
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Cell 2:29-42. 2002..Mitochondrial hyperpolarization is a shared feature of many tumor cell lines, explaining the broad action spectrum of this novel delocalized lipophilic cation... - cdx4 mutants fail to specify blood progenitors and can be rescued by multiple hox genesAlan J Davidson
Department of Medicine, Division of Hematology Oncology, Children s Hospital and Dana Farber Cancer Institute, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA
Nature 425:300-6. 2003..Taken together, these findings demonstrate that cdx4 regulates hox genes and is necessary for the specification of haematopoietic cell fate during vertebrate embryogenesis... - Traumatic brain injury in mice deficient in Bid: effects on histopathology and functional outcomeDaniela Bermpohl
Neuroscience Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
J Cereb Blood Flow Metab 26:625-33. 2006..The data show that Bid deficiency decreases early posttraumatic brain cell death and tissue damage, but does not reduce functional outcome deficits after CCI in mice... - Differential mRNA expression of Ara-C-metabolizing enzymes explains Ara-C sensitivity in MLL gene-rearranged infant acute lymphoblastic leukemiaRonald W Stam
University Hospital Rotterdam Sophia Children s Hospital, Department of Pediatric Oncology Hematology, Erasmus Medical Center, The Netherlands
Blood 101:1270-6. 2003..046) mRNA expression in patients with MLL gene-rearranged ALL. We conclude that an elevated expression of hENT1, which transports Ara-C across the cell membrane, contributes to Ara-C sensitivity in MLL gene-rearranged infant ALL... - Stanley J. Korsmeyer (1950-2005)Luca Scorrano
J Bioenerg Biomembr 37:109. 2005 - An inhibitor of Bcl-2 family proteins induces regression of solid tumoursTilman Oltersdorf
Idun Pharmaceuticals, 9380 Judicial Drive, San Diego, California 92121, USA
Nature 435:677-81. 2005.... - Cell death induced by granzyme CHillary Johnson
Division of Oncology, Department of Medicine, Siteman Cancer Center, Washington University School of Medicine, St Louis, MO 63110, USA
Blood 101:3093-101. 2003..These results suggest that granzyme C rapidly induces target cell death by attacking nuclear and mitochondrial targets and that these targets are distinct from those used by granzyme B to cause classical apoptosis... - Proapoptotic BID is required for myeloid homeostasis and tumor suppressionSandra S Zinkel
Howard Hughes Medical Institute, Department of Pathology, Harvard Medical School, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Genes Dev 17:229-39. 2003..Moreover, progression to CMML indicates that an upstream BH3-only molecule, BID, is required to suppress tumorigenesis... - A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosisLuca Scorrano
Howard Hughes Medical Institute, Department of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, 02115, Boston, MA, USA
Dev Cell 2:55-67. 2002..This reorganization does not require tBID's BH3 domain and is independent of BAK, but is inhibited by CsA. During this process, individual cristae become fused and the junctions between the cristae and the intermembrane space are opened...
Research Grants
- PROTEIN INTERACTION EXTENDS THE CELL DEATH PATHWAYStanley Korsmeyer; Fiscal Year: 2001..2) The functional role of BID within apoptosis will be delineated, and 3) A minimal death domain will be defined and the mechanism of killing by each BCL-2 family death agonist will be detailed. ..