Genomes and Genes
proto oncogene proteins c bcl 2
Summary: Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Publications310 found, 100 shown here
- Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptorsX Luo
Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 75235, USA
Cell 94:481-90. 1998..The cytochrome c releasing activity of Bid was antagonized by Bcl2. A mutation at the BH3 domain diminished its cytochrome c releasing activity. Bid, therefore, relays an apoptotic signal from the cell surface to mitochondria...
- 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...
- Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and deathM C Wei
Howard Hughes Medical Institute, Departments of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
Science 292:727-30. 2001..Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli...
- 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....
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell deathZ N Oltvai
Howard Hughes Medical Institute Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110
Cell 74:609-19. 1993..Overexpressed Bax also counters the death repressor activity of Bcl-2. These data suggest a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus...
- Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosisH Li
Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
Cell 94:491-501. 1998..Coexpression of BclxL inhibits all the apoptotic changes induced by tBID. Our results indicate that BID is a mediator of mitochondrial damage induced by Casp8...
- The Bcl2 family: regulators of the cellular life-or-death switchSuzanne Cory
The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Victoria 3050, Australia
Nat Rev Cancer 2:647-56. 2002..Apoptosis is often impaired in cancer and can limit conventional therapy. A better understanding of how the Bcl2 family controls caspase activation should result in new, more effective therapeutic approaches...
- The Bcl-2 apoptotic switch in cancer development and therapyJ M Adams
Department of Molecular Genetics of Cancer, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia
Oncogene 26:1324-37. 2007..Better understanding of the Bcl-2 family is clarifying its role in cancer development, revealing how conventional therapy works and stimulating the search for "BH3 mimetics" as a novel class of anticancer drugs...
- The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralizedMark F van Delft
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia
Cancer Cell 10:389-99. 2006..Hence, ABT-737 should prove efficacious in tumors with low Mcl-1 levels, or when combined with agents that inactivate Mcl-1, even to treat those tumors that overexpress Bcl-2...
- Bcl-2 inhibitors: targeting mitochondrial apoptotic pathways in cancer therapyMin H Kang
Cancer Center and the Department of Cell Biology and Biochemistry, School of Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas 79430, USA
Clin Cancer Res 15:1126-32. 2009..Here, we review the role of the Bcl-2 family in apoptotic pathways and those agents that are known and/or designed to inhibit the anti-apoptotic Bcl-2 family of proteins...
- 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...
- Molecular characterization of mitochondrial apoptosis-inducing factorS A Susin
Centre National de la Recherche Scientifique, UPR 420, Villejuif, France
Nature 397:441-6. 1999..These results indicate that AIF is a mitochondrial effector of apoptotic cell death...
- BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectlyTomomi Kuwana
La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA
Mol Cell 17:525-35. 2005..In this model, the simple inhibition of antiapoptotic functions is insufficient to induce apoptosis unless a direct activator of Bax or Bak is present...
- Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunityP Bouillet
The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia
Science 286:1735-8. 1999..Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity. Moreover, particular death stimuli appear to activate apoptosis through distinct BH3-only proteins...
- The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissuesT Lindsten
Department of Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
Mol Cell 6:1389-99. 2000..Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis...
- Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell deathE Yang
Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110
Cell 80:285-91. 1995..The susceptibility of a cell to a death signal is determined by these competing dimerizations in which levels of Bad influence the effectiveness of Bcl-2 versus Bcl-xL in repressing death...
- How do BCL-2 proteins induce mitochondrial outer membrane permeabilization?Jerry E Chipuk
St Jude Children s Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA
Trends Cell Biol 18:157-64. 2008....
- BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosisE H Cheng
Howard Hughes Medical Institute, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
Mol Cell 8:705-11. 2001..Thus, in mammals, BH3 domain-only molecules activate multidomain proapoptotic members to trigger a mitochondrial pathway, which both releases cytochrome c to activate caspases and initiates caspase-independent mitochondrial dysfunction...
- Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blockedJ Yang
Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA
Science 275:1129-32. 1997..Overexpression of Bcl-2 prevented the efflux of cytochrome c from the mitochondria and the initiation of apoptosis. Thus, one possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria...
- Bim: a novel member of the Bcl-2 family that promotes apoptosisL O'Connor
The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Victoria, Australia
EMBO J 17:384-95. 1998..Hence, Bim appears to act as a 'death ligand' which can only neutralize certain members of the pro-survival Bcl-2 sub-family...
- Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivoT Miyashita
La Jolla Cancer Research Foundation, Cancer Research Center, CA 92037
Oncogene 9:1799-805. 1994..The findings suggest a potential mechanism by which p53 regulates apoptosis, as well as responses to radiation and chemotherapeutic drugs in cancer...
- Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosisM Sattler
Pharmaceutical Discovery Division, Abbott Laboratories, Abbott Park, IL 60064, USA
Science 275:983-6. 1997..Mutations in full-length Bak that disrupt either type of interaction inhibit the ability of Bak to heterodimerize with Bcl-xL...
- Mitochondria as the central control point of apoptosisS Desagher
UPR CNRS 9023, CCIPE, 141 rue de la Cardonille, F 34094 Montpellier Cedex 5, France
Trends Cell Biol 10:369-77. 2000..Here, we attempt to summarize our current view of the mechanisms that lead to the efflux of many proteins from mitochondria during apoptosis and the role played by Bcl-2 family proteins in the control of this event...
- Bcl-2 family members: dual regulators of apoptosis and autophagyBeth Levine
Howard Hughes Medical Institute, Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390 9113, USA
Autophagy 4:600-6. 2008..This hitherto neglected crosstalk between the core machineries regulating autophagy and apoptosis may redefine the role of Bcl-2 family proteins in oncogenesis and tumor progression...
- The Bcl-2 family: roles in cell survival and oncogenesisSuzanne Cory
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville 3050, Victoria, Australia
Oncogene 22:8590-607. 2003..Finally, it discusses the promise of novel anticancer therapeutics that target these vital regulators...
- Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDACS Shimizu
Osaka University Medical School, Biomedical Research Center, Department of Medical Genetics, Suita, Japan
Nature 399:483-7. 1999..Our results indicate that the Bcl-2 family of proteins bind to the VDAC in order to regulate the mitochondrial membrane potential and the release of cytochrome c during apoptosis...
- Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathwayC Tournier
Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
Science 288:870-4. 2000..These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway...
- Mule/ARF-BP1, a BH3-only E3 ubiquitin ligase, catalyzes the polyubiquitination of Mcl-1 and regulates apoptosisQing Zhong
Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 75390, USA
Cell 121:1085-95. 2005..Thus, Mule is a unique BH3-containing E3 ubiquitin ligase apical to Bcl-2 family proteins during DNA damage-induced apoptosis...
- The pathophysiology of mitochondrial cell deathDouglas R Green
Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA
Science 305:626-9. 2004..The general rules governing the pathophysiology of MOMP and controversial issues regarding its regulation are discussed...
- Interleukin-3-induced phosphorylation of BAD through the protein kinase AktL del Peso
Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Science 278:687-9. 1997..Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway...
- Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membraneR Eskes
Serono Pharmaceutical Research Institute, Ares Serono International S A, CH 1228 Plan les Ouates, Geneva, Switzerland
Mol Cell Biol 20:929-35. 2000..Bax mitochondrial membrane insertion triggered by Bid may represent a key step in pathways leading to apoptosis...
- Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)J Zha
Department of Medicine, Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, Missouri 63110, USA
Cell 87:619-28. 1996..The rapid phosphorylation of BAD following IL-3 connects a proximal survival signal with the BCL-2 family, modulating this checkpoint for apoptosis...
- PUMA, a novel proapoptotic gene, is induced by p53K Nakano
Regulation of Cell Growth Laboratory, National Cancer Institute at Frederick, Maryland 21702, USA
Mol Cell 7:683-94. 2001..Antisense inhibition of PUMA expression reduced the apoptotic response to p53, and PUMA is likely to play a role in mediating p53-induced cell death through the cytochrome c/Apaf-1-dependent pathway...
- 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...
- BCL-2 family members and the mitochondria in apoptosisA Gross
Department of Pathology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Genes Dev 13:1899-911. 1999
- BCL-2 is phosphorylated and inactivated by an ASK1/Jun N-terminal protein kinase pathway normally activated at G(2)/MK Yamamoto
Departments of Pathology and Medicine, Harvard Medical School and Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Mol Cell Biol 19:8469-78. 1999..Thus, stress response kinases phosphorylate BCL-2 during cell cycle progression as a normal physiologic process to inactivate BCL-2 at G(2)/M...
- 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...
- Promoting apoptosis as a strategy for cancer drug discoveryStephen W Fesik
Cancer Research, Abbott Laboratories, Department R460, Building AP10 LL, 100 Abbott Park Road, Abbott Park, Illinois 60064, USA
Nat Rev Cancer 5:876-85. 2005....
- Bax-deficient mice with lymphoid hyperplasia and male germ cell deathC M Knudson
Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, MO 63110, USA
Science 270:96-9. 1995..Multinucleated giant cells and dysplastic cells accompanied massive cell death. Thus, the loss of Bax results in hyperplasia or hypoplasia, depending on the cellular context...
- BH3 profiling identifies three distinct classes of apoptotic blocks to predict response to ABT-737 and conventional chemotherapeutic agentsJing Deng
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 12:171-85. 2007..BCL-2 dependence correlates with high levels of proapoptotic BIM sequestered by BCL-2. Strikingly, BH3 profiling can also predict sensitivity to conventional chemotherapeutic agents like etoposide, vincristine, and adriamycin...
- Bax directly induces release of cytochrome c from isolated mitochondriaJ M Jurgensmeier
Program on Apoptosis and Cell Death Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
Proc Natl Acad Sci U S A 95:4997-5002. 1998....
- The BCL-2 protein family: opposing activities that mediate cell deathRichard J Youle
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, The National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Rev Mol Cell Biol 9:47-59. 2008..Although these insights into interactions among BCL-2 family proteins reveal how these proteins are regulated, a unifying hypothesis for the mechanisms they use to activate caspases remains elusive...
- 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...
- Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemiaMarina Konopleva
Section of Molecular Hematology and Therapy, Department of Blood and Marrow Transplantation, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
Cancer Cell 10:375-88. 2006..These data suggest that ABT-737 could be a highly effective antileukemia agent when the mechanisms of resistance identified here are considered...
- Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic functionLin Chen
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville Victoria 3050, Australia
Mol Cell 17:393-403. 2005..The results suggest that apoptosis relies on selective interactions between particular subsets of these proteins and that it should be feasible to discover BH3-mimetic drugs that inactivate specific prosurvival targets...
- Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosisMariusz Karbowski
Biochemistry Section, SNB, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
J Cell Biol 159:931-8. 2002..Surprisingly, Drp1 and Mfn2, but not other proteins implicated in the regulation of mitochondrial morphology, colocalize with Bax in these foci. We suggest that Bax participates in apoptotic fragmentation of mitochondria...
- Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell deathD Hockenbery
Department of Medicine, Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, Missouri 63110
Nature 348:334-6. 1990..Thus, Bcl-2 is unique among proto-oncogenes, being localized to mitochondria and interfering with programmed cell death independent of promoting cell division...
- Caspase-2 induces apoptosis by releasing proapoptotic proteins from mitochondriaYin Guo
Center for Apoptosis Research and the Department of Microbiology and Immunology, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
J Biol Chem 277:13430-7. 2002..The caspase-2-released Cyt c is sufficient to activate the Apaf-caspase-9 apoptosome in vitro. In combination, our data suggest that caspase-2 is a direct effector of the mitochondrial apoptotic pathway...
- Preclinical studies of TW-37, a new nonpeptidic small-molecule inhibitor of Bcl-2, in diffuse large cell lymphoma xenograft model reveal drug action on both Bcl-2 and Mcl-1Ramzi M Mohammad
Division of Hematology and Oncology, Department of Internal Medicine, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan, USA
Clin Cancer Res 13:2226-35. 2007..We have previously employed the natural product (-)-gossypol to test its therapeutic potential as a small-molecule inhibitor of Bcl-2 for the treatment of B-cell lymphomas...
- Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosisI Marzo
CNRS, UPR 420, 19 rue Guy Moquet, F 94801 Villejuif, France
Science 281:2027-31. 1998..Hence, the proapoptotic molecule Bax and the constitutive mitochondrial protein ANT cooperate within the PTPC to increase mitochondrial membrane permeability and to trigger cell death...
- Targeting the Bcl-2-regulated apoptosis pathway by BH3 mimetics: a breakthrough in anticancer therapy?V Labi
Division of Developmental Immunology, Department of Biocenter, Innsbruck Medical University, Innsbruck, Austria
Cell Death Differ 15:977-87. 2008....
- Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3Bingzhen Lin
The Burnham Institute, Cancer Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
Cell 116:527-40. 2004....
- Tumor suppressor p53 is a direct transcriptional activator of the human bax geneT Miyashita
La Jolla Cancer Research Foundation, California 92037
Cell 80:293-9. 1995..Taken together, the results suggest that bax is a p53 primary-response gene, presumably involved in a p53-regulated pathway for induction of apoptosis...
- Bcl-2 and the regulation of programmed cell deathJ C Reed
La Jolla Cancer Research Foundation, Cancer Research Center, California 92037
J Cell Biol 124:1-6. 1994
- Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiationDeepak Nijhawan
Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA
Genes Dev 17:1475-86. 2003..The disappearance of Mcl-1 is also required for other mitochondrial apoptotic events including Bax translocation, cytochrome c release, and caspase activation...
- Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosisT Nakagawa
Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
J Cell Biol 150:887-94. 2000..These data suggest a novel apoptotic pathway involving calcium-mediated calpain activation and cross-talks between calpain and caspase families...
- Novel primitive lymphoid tumours induced in transgenic mice by cooperation between myc and bcl-2A Strasser
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia
Nature 348:331-3. 1990..Suprisingly, the tumours derive from a cell with the hallmarks of a primitive haemopoietic cell, perhaps a lymphoid-committed stem cell...
- Autophagy delays apoptotic death in breast cancer cells following DNA damageM J Abedin
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455, USA
Cell Death Differ 14:500-10. 2007..These studies underscore a potential role for autophagy inhibitors in combination with conventional chemotherapeutic drugs in early breast cancer therapy...
- 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...
- Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membraneTomomi Kuwana
La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA
Cell 111:331-42. 2002..We conclude that mitochondrial protein release in apoptosis can be mediated by supramolecular openings in the outer mitochondrial membrane, promoted by BH3/Bax/lipid interaction and directly inhibited by Bcl-x(L)...
- Mcl-1 overexpression in hepatocellular carcinoma: a potential target for antisense therapyWolfgang Sieghart
Section of Experimental Oncology Molecular Pharmacology, Department of Clinical Pharmacology, Medical University Vienna, Waehringer Guertel 18 20, 1090 Vienna, Austria
J Hepatol 44:151-7. 2006..Here we investigated the presence of Mcl-1 protein in hepatocellular carcinoma (HCC) tissues and its potential role as a molecular drug target for HCC therapy...
- 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..
- Mitochondrial p53 activates Bak and causes disruption of a Bak-Mcl1 complexJ I Ju Leu
Department of Genetics, University of Pennsylvania School of Medicine, 422 Curie Boulevard, Philadelphia, PA 19104, USA
Nat Cell Biol 6:443-50. 2004..These results are consistent with a model in which p53 and Mcl1 have opposing effects on mitochondrial apoptosis by interacting with, and modulating the activity of, the death effector Bak...
- The mitochondrion in apoptosis: how Pandora's box opensN Zamzami
Centre National de la Recherche Scientifique, UMR1599, Institut Gustave Roussy, 39 rue Camille-Desmoulins, F-94805 Villejuif, France
Nat Rev Mol Cell Biol 2:67-71. 2001..Here we suggest that opening of a multiprotein complex called the mitochondrial permeability transition pore complex is sufficient (and, usually, necessary) for triggering apoptosis...
- Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteinsSimon N Willis
The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia
Genes Dev 19:1294-305. 2005..The finding that different prosurvival proteins have selective roles has notable implications for the design of anti-cancer drugs that target the Bcl-2 family...
- Inhibition of TRAIL-induced apoptosis by Bcl-2 overexpressionSimone Fulda
University Children s Hospital, Prittwitzstr 43, D 89075 Ulm, Germany
Oncogene 21:2283-94. 2002..g. by Bcl-2 and by XIAP, these findings may have important clinical implication. Thus, strategies targeting the molecular basis of resistance towards TRAIL may be necessary in some tumors for cancer therapy with TRAIL...
- Free fatty acids promote hepatic lipotoxicity by stimulating TNF-alpha expression via a lysosomal pathwayAriel E Feldstein
Department of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
Hepatology 40:185-94. 2004..quot; In conclusion, these data support a lipotoxic model of FFA-mediated lysosomal destabilization...
- Escaping cell death: survival proteins in cancerM Jaattela
Institute of Cancer Biology, Danish Cancer Society, Strandboulevarden 49, Copenhagen, DK 2100, Denmark
Exp Cell Res 248:30-43. 1999..Understanding the molecular mechanisms of action of these proteins may offer novel modes of rationally and selectively manipulating the sensitivity of cancer cells to therapy...
- The Bax subfamily of Bcl2-related proteins is essential for apoptotic signal transduction by c-Jun NH(2)-terminal kinaseKui Lei
Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Mol Cell Biol 22:4929-42. 2002..These data demonstrate that proapoptotic members of the Bax protein subfamily are essential for JNK-dependent apoptosis...
- Structural biology of the Bcl-2 family of proteinsAndrew M Petros
Global Pharmaceutical Research and Development, Abbott Laboratories, Department 460, Bldg AP10 LL, 100 Abbott Park Road, Abbott Park, IL 60064 6048, USA
Biochim Biophys Acta 1644:83-94. 2004....
- Structural insights into the degradation of Mcl-1 induced by BH3 domainsPeter E Czabotar
The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia
Proc Natl Acad Sci U S A 104:6217-22. 2007..We compared the three-dimensional structures of the complexes formed between BH3 peptides of both Bim and Noxa, and we show that a discrete C-terminal sequence of the Noxa BH3 is necessary to instigate Mcl-1 degradation...
- Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737Victoria Del Gaizo Moore
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
J Clin Invest 117:112-21. 2007..Indeed, activator BH3-only occupation of BCL2 may prime cancer cells for death, offering a potential explanation for the marked chemosensitivity of certain cancers that express abundant BCL2, such as CLL and follicular lymphoma...
- MCL1 provides a window on the role of the BCL2 family in cell proliferation, differentiation and tumorigenesisR W Craig
Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH, USA
Leukemia 16:444-54. 2002..Targeting this family may thus provide a means of inhibiting cancer development and inducing apoptosis in tumor cells...
- Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1Ulrich Maurer
Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, California 92121, USA
Mol Cell 21:749-60. 2006..The results demonstrate that the control of MCL-1 stability by GSK-3 is an important mechanism for the regulation of apoptosis by growth factors, PI3K, and AKT...
- MCL1, a gene expressed in programmed myeloid cell differentiation, has sequence similarity to BCL2K M Kozopas
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205
Proc Natl Acad Sci U S A 90:3516-20. 1993..The discovery of MCL1 broadens our perspective on an emerging MCL1/BCL2 gene family and will allow further comparison with oncogene families...
- Initiation of apoptosis by granzyme B requires direct cleavage of bid, but not direct granzyme B-mediated caspase activationV R Sutton
Cancer Immunology Laboratory, Peter MacCallum Cancer Institute, Melbourne 8006, Australia
J Exp Med 192:1403-14. 2000..Overall, our results indicate that mitochondrial perturbation by Bid is necessary to achieve a lethal threshold of caspase activity and cell death due to granzyme B...
- p53 has a direct apoptogenic role at the mitochondriaMotohiro Mihara
Department of Pathology, Stony Brook University, Stony Brook, NY 11794, USA
Mol Cell 11:577-90. 2003..This opens the possibility that mutations might represent "double-hits" by abrogating the transcriptional and mitochondrial apoptotic activity of p53...
- 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...
- Ways of dying: multiple pathways to apoptosisJerry M Adams
The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia
Genes Dev 17:2481-95. 2003
- The Bcl-2 protein familyB Antonsson
Serono Pharmaceutical Research Institute, 14 Chemin des Aulx, Plan les Ouates Geneva, CH 1228, Switzerland
Exp Cell Res 256:50-7. 2000
- Apoptotic pathways: paper wraps stone blunts scissorsD R Green
La Jolla Institute for Allergy and Immunology, San Diego, California 92121, USA
Cell 102:1-4. 2000
- In vivo ablation of surface immunoglobulin on mature B cells by inducible gene targeting results in rapid cell deathK P Lam
Institute for Genetics, University of Cologne, Federal Republic of Germany
Cell 90:1073-83. 1997..Ablation leads to rapid death of mature B lymphocytes, which is preceded by down-regulation of MHC antigens and up-regulation of CD95 (Fas) and can be delayed by constitutive bcl-2 expression...
- Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosisE Oda
Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo 113 0033, Japan
Science 288:1053-8. 2000..We also demonstrate that blocking the endogenous Noxa induction results in the suppression of apoptosis. Noxa may thus represent a mediator of p53-dependent apoptosis...
- The role of dynamin-related protein 1, a mediator of mitochondrial fission, in apoptosisS Frank
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Behesda, Maryland 20892, USA
Dev Cell 1:515-25. 2001..Remarkably, inhibition of Drp1 blocks cell death, implicating mitochondrial fission as an important step in apoptosis...
- The role of apoptosis in response to photodynamic therapy: what, where, why, and howNancy L Oleinick
Department of Radiation Oncology and the CWRU UHC Ireland Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA
Photochem Photobiol Sci 1:1-21. 2002..necrotic pathway and for producing tumor ablation in conjunction with tissue-level mechanisms operating in vivo...
- VDAC-dependent permeabilization of the outer mitochondrial membrane by superoxide induces rapid and massive cytochrome c releaseM Madesh
Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
J Cell Biol 155:1003-15. 2001..Thus, O2*- triggers apoptosis via VDAC-dependent permeabilization of the mitochondrial outer membrane without apparent contribution of proapoptotic Bcl-2 family proteins...
- X-linked IAP is a direct inhibitor of cell-death proteasesQ L Deveraux
The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA
Nature 388:300-4. 1997....
- Comparison of chemical inhibitors of antiapoptotic Bcl-2-family proteinsD Zhai
Cell Death Differ 13:1419-21. 2006
- Interleukin-7 mediates the homeostasis of naïve and memory CD8 T cells in vivoK S Schluns
Department of Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA
Nat Immunol 1:426-32. 2000..Homeostatic proliferation of memory cells was also partially dependent on IL-7. These results point to IL-7 as a pivotal cytokine in T cell homeostasis...
- Tumor necrosis factor induces Bcl-2 and Bcl-x expression through NFkappaB activation in primary hippocampal neuronsM Tamatani
Department of Anatomy and Neuroscience, Osaka University Medical School, 2 2 Yamadaoka, Suita, Osaka 565 0872, Japan
J Biol Chem 274:8531-8. 1999..These findings indicate that induction of Bcl-2 and Bcl-x expression through NFkappaB activation is involved in the neuroprotective action of TNF against hypoxia- or nitric oxide-induced injury...
- PUMA mediates the apoptotic response to p53 in colorectal cancer cellsJian Yu
The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD 21231, USA
Proc Natl Acad Sci U S A 100:1931-6. 2003..These results suggest that the balance between PUMA and p21 is pivotal in determining the responses to p53 activation and provide a model for understanding the basis of p53 mutations in human cancer...
- Mitochondria: releasing power for life and unleashing the machineries of deathDonald D Newmeyer
La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA
Cell 112:481-90. 2003..In this review, we examine a few promising mechanisms that have been gaining attention recently...
- Induction of apoptosis by the Bcl-2 homologue BakT Chittenden
Apoptosis Technology Inc, Cambridge, Massachusetts 02139, USA
Nature 374:733-6. 1995..Moreover, enforced expression of Bak induces rapid and extensive apoptosis of serum-deprived fibroblasts. This raises the possibility that Bak is directly involved in activating the cell death machinery...
- Bax activation and mitochondrial insertion during apoptosisLisenn Lalier
INSERM U601, F 44000 Nantes, France
Apoptosis 12:887-96. 2007..The mechanism by which Bax triggers the MOM permeabilization once activated will be discussed in some other reviews in this special issue...
- Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cellsB Antonsson
Serono Pharmaceutical Research Institute, Serono International S A, 14 Chemin des Aulx, CH 1228 Plan les Ouates, Geneva, Switzerland
J Biol Chem 276:11615-23. 2001..Bax oligomerization appears to be required for its proapoptotic activity, and the Bax oligomer/complex might constitute the structural entirety of the cytochrome c-conducting channel in the outer mitochondrial membrane...
- Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1P F Dijkers
Department of Pulmonary Diseases, University Medical Center Utrecht, G03 550, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
Curr Biol 10:1201-4. 2000..We propose a mechanism by which cytokines promote lymphocyte survival by inhibition of FKHR-L1, preventing Bim expression...
- Interleukin 6 upregulates myeloid cell leukemia-1 expression through a STAT3 pathway in cholangiocarcinoma cellsHajime Isomoto
Mayo Clinic College of Medicine, Rochester, MN 55905, USA
Hepatology 42:1329-38. 2005..In conclusion, we have directly demonstrated a STAT3 regulatory element in the Mcl-1 promoter. Downregulation of Mcl-1 transcription by inhibiting this cascade is a potential strategy for the treatment of this cancer...
- JNK suppresses apoptosis via phosphorylation of the proapoptotic Bcl-2 family protein BADChenfei Yu
Ben May Institute for Cancer Research, The University of Chicago, 5841 South Maryland Avenue, MC 60627, Chicago, IL 60637 USA
Mol Cell 13:329-40. 2004..Thus, our results provide a molecular mechanism by which JNK contributes to cell survival...
- Degradation of the proapoptotic proteins Bik, Puma, and Bim with Bcl-2 domain 3 homology in Chlamydia trachomatis-infected cellsFeng Dong
Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229, USA
Infect Immun 73:1861-4. 2005..This observation has provided new information on the chlamydial antiapoptosis mechanisms...
- Life-or-death decisions by the Bcl-2 protein familyJ M Adams
The Walter and Eliza Hall Institute of Medical Research, P O Royal Melbourne Hospital, 3050, Melbourne, Australia
Trends Biochem Sci 26:61-6. 2001..Pro-apoptotic family members act as sentinels for cellular damage: cytotoxic signals induce their translocation to the organelles where they bind to their pro-survival relatives, promote organelle damage and trigger apoptosis...
- Bcl-2-family proteins and hematologic malignancies: history and future prospectsJohn C Reed
Burnham Institute for Medical Research, La Jolla, CA 92037, USA
Blood 111:3322-30. 2008..Experimental therapies targeting Bcl-2 family mRNAs or proteins are currently in clinical testing, raising hopes that a new class of anticancer drugs may be near...
- Promotion of PDT Induced phototoxicity by bile acidsDavid Kessel; Fiscal Year: 2003..If the results of preliminary studies are borne out by further investigation, UDCA could offer a safe and effective means for promoting clinical PDT efficacy. ..
- Epigallocatechin gallate, Prostate cancer & AngiogenesisMyoung Kim; Fiscal Year: 2004..abstract_text> ..
- Conference on Photodynamic TherapyDavid Kessel; Fiscal Year: 2002..The most recent PDT meeting, sponsored by the International Photodynamic Assn, has more than 600 participants. ..
- 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. ..
- Dissecting the Death Pathway in the Islet beta-cellNika Danial; Fiscal Year: 2005..abstract_text> ..
- MECHANISM OF ACTION OF CRYTOPHYCINSSusan Mooberry; Fiscal Year: 2002..The differences in the biological responses of the congeners will determine the relationships between biological events and the ultimate ability to initiate apoptosis. ..
- INTEGRATED STUDY OF MUSCULOSKELETAL LOSS AND RESTORATIONEsther E Dupont Versteegden; Fiscal Year: 2010..Identifying these common pathways influencing muscle and bone integrity could lead to putative targets for pharmacologic or therapeutic interventions. ..
- Impaired Regulation of Muscle size with AgingESTHER DUPONT VERSTEEGDEN; Fiscal Year: 2002..Also, potential regulatory pathways and molecules involved in control of muscle size will be determined. ..
- MECHANISMS IN THE REGULATION OF APOPTOSISJerry Adams; Fiscal Year: 2006..Justification: As the proposal addresses central issues about the regulation of apoptosis, builds onproductive research, and exploits novel findings, it should significantly advance the molecular dissection of apoptosis. ..
- Orthogonal Strategies for Specific Knockout ProductionCY STEIN; Fiscal Year: 2005..Finally, in Specific Aim 4, we will evaluate the molecular consequences of the down regulation of bcl-2 and bcl-xL by employing the 12,000 gene-containing Affymetrix oligonucleotide microarray technology. ..
- NO-MEDIATED MODIFICATION OF NMDA RECEPTOR DURING HYPOXIAOm Mishra; Fiscal Year: 2008..abstract_text> ..
- JNK exacerbates ischemia/reperfusion injury in hyperglycemic subjects.Keith A Webster; Fiscal Year: 2010..Experiments are proposed to test this hypothesis in mouse models. If our hypothesis is correct we will described the molecular basis for this an begin to develop new approaches for treatment. ..
- Controlling the BCL-2 Pathway of Mitochondrial ApoptosisAnthony Letai; Fiscal Year: 2007..Finally, we will use the mitochondrial, cellular and mouse assays developed above to test the efficacy and specificity of BH3 mimetics of both small molecule and peptidomimetic origin. [unreadable] [unreadable]..
- Mechanism of Action of G3139CY STEIN; Fiscal Year: 2007..unreadable] [unreadable] [unreadable]..
- MOLECULAR STUDIES OF GENE TARGETED OLIGONUCLEOTIDESCY STEIN; Fiscal Year: 2002..Finally, in Specific Aim 3, we will amplify the delivery of alt-OMPs and chi-OMPs to cells by condensing them with a novel delivery agent, tetra (N-methylpyridyl) porphine. ..
- NO-MEDIATED MODIFICATION OF NMDA RECEPTOR DURING HYPOXIAOm Mishra; Fiscal Year: 2006..abstract_text> ..
- TNF-Induced Apoptosis of Lymphocytes in Aged HumansSudhir Gupta; Fiscal Year: 2004..These studied should mechanism (s) for increased TNF-a-induced apoptosis during aging. ..
- Bc1-2 Family Proteins in the Ischemic Neuronal InjuryXiao Ming Yin; Fiscal Year: 2006..To characterize the molecular interactions of Bid and Bax in inducing dysfunction of mitochondria isolated from the brain. ..
- BCL2 AND BECLIN AND ALPHAVIRUS PATHOGENESISBeth Levine; Fiscal Year: 2003..The proposed studies will provide novel insights into host cellular mechanisms that regulate whether neurons live or die in responses to viral infection. ..
- RETINOIC ACID RESPONSE IN HUMAN LUNG CANCERXiao Kun Zhang; Fiscal Year: 2002....
- MECHANISMS OF STRESS-INDUCED APOPTOSIS IN T CELLSDouglas Green; Fiscal Year: 2001..His focus on T lymphocytes is important in the context of understanding how the immune system responds to DNA damage and related stress to remove potentially damaged cells, that could otherwise pose a threat to immune integrity. ..
- ANTICANCER DRUG RESISTANCE BY BCL-2 ONCOGENE EXPRESSIONRaymond Meyn; Fiscal Year: 2007..abstract_text> ..
- Regulation of auditory neuron neurite growth by activityMarlan Hansen; Fiscal Year: 2008..The results of these studies will provide critical data on the consequences of electrical activity on SGN neurite growth and cochlear innervation. ..
- TRANSGENIC/KNOCKOUT ANIMALS IN MYOCARDIAL PRESERVATIONDIPAK DAS; Fiscal Year: 2008..The results of this proposed research will hopefully increase our understanding of redox regulation by Trx/Grx in the ischemic myocardium. [unreadable] [unreadable]..
- Evolution of Primary and Resistant Solid TumorsRonald DePinho; Fiscal Year: 2008..Finally, nanosensors will be developed that are capable to detecting telomerase activity and quantifying telomere reserves. ..
- MATERNAL ALCOHOLISM AND CNS DEVELOPMENT IN OFFSPRINGMARY DRUSE MANTEUFFEL; Fiscal Year: 2007..Analyses will include western blot analyses, real-time quantitative RT-PCR, fluorescence and light microscopy, immunohistochemistry, and enzyme assays. ..
- High-Content Cell-Based Screening for Modulators of AutophagyXiao Ming Yin; Fiscal Year: 2007..Our long term hope is that the knowledge and the materials developed through this study will be valuable for future clinical applications. [unreadable] [unreadable] [unreadable]..
- Chemoprevention of Prostate Cancer by CurcuminSharmila Shankar; Fiscal Year: 2008..We expect the proposed studies to yield data in support of our hypothesis and to serve as a critical step in developing new approaches to prostate cancer prevention. [unreadable] [unreadable] [unreadable]..
- Role of Redox Dependent Signaling in LeukemiaJoya Chandra; Fiscal Year: 2010..Tactics that quelch ROS production, or block downstream signaling through Fyn in BCR/ABL containing cells may provide promising therapeutic modalities. ..
- OVARIAN STEROID REGULATION OF SEROTONIN IN PRIMATESCYNTHIA LOUISE BETHEA; Fiscal Year: 2010..Altogether, we will show that ovarian steroids support serotonin neuron survival and we will provide pivotal underlying genomic mechanisms. ..
- Non-Canonical NF-kappaB Signaling In Endothelial CellsMichael J May; Fiscal Year: 2010..This proposal will investigate the signals that control blood vessel activation and will therefore identify novel drug targets for preventing or treating chronic inflammation. ..
- Aberrant Crypt Foci as a Biomarker for ChemopreventionFrank Sinicrope; Fiscal Year: 2009....
- The impact of growth modulation of liver carcinogenesisXiao Ming Yin; Fiscal Year: 2009....
- BI-1, A Regulator of ER-Stress Pathways Linked to ApoptosisJohn Reed; Fiscal Year: 2009..Altogether, these studies will improve understanding of how damage to the ER is linked to apoptosis, and will potentially reveal strategies for neuronal preservation in stroke and neurodegenerative diseases. ..
- NUTRIENT EFFECTS ON INSULIN ACTIONMichael Pagliassotti; Fiscal Year: 2009..abstract_text> ..
- High Throughput Screening Assays for NOD1 and NOD2 InhibitorsJohn Reed; Fiscal Year: 2008..unreadable] [unreadable] [unreadable]..
- Arsenite Effects on CD40 Signaling and B-Cell ApoptosisDONNA MUSCARELLA; Fiscal Year: 2008..abstract_text> ..
- ANALYSIS OF BECLIN 1 IN AUTOPHAGY AND TUMOR SUPPRESSIONBeth Levine; Fiscal Year: 2009..abstract_text> ..
- K7 regulates KSHV G protein-coupled receptor turnoverPinghui Feng; Fiscal Year: 2007..unreadable] [unreadable] [unreadable]..
- High throughput screening for inhibitors of Akt plasma mHongbo Luo; Fiscal Year: 2006..Discovery of these inhibitors will greatly facilitate our research on Ptdlns(3,4,5)P3/Akt signaling. Moreover, the identified inhibitors can be directly utilized as starting chemical compounds for novel anti- cancer drug development. ..
- SJOGRENS SYNDROME SALIVARY GLAND AND APOPTOSISHoward Dang; Fiscal Year: 2001..Caspase inhibitors will be used to identify specific proteases during apoptosis. Biopsy material from patents with Sjogren's syndrome will be immunostained for bcl-2 family member expression. ..
- Becton Dickinson Flow Cytometry SystemBellur Prabhakar; Fiscal Year: 2002..Careful evaluation of the three available systems prompted our users group to recommend the BD FACS Vantage SE since it would satisfy the needs of our institution's NIH-funded investigators. ..
- MYOCARDIAL PRESERVATION DURING ISCHEMIC ARRESTDIPAK DAS; Fiscal Year: 2009..Ischemic heart disease represent the major cardiovascular related problems. Straitegies to reduce ischemic injury should improve the heart health leading to the reduction of death due to heart diseases. ..
- Angiogenic Enhancement of Dopamine Neuron GraftsCaryl Sortwell; Fiscal Year: 2003..This strategy will be evaluated using primary mesencephalic tissue. However, results from these studies will be applicable to alternative sources of DA neurons, including stem- and progenitor-derived cells. ..
- Poly (ADP-Ribose) synthetase in expression of endotheliaBasilia Zingarelli; Fiscal Year: 2003..abstract_text> ..
- Conference on Mouse Models of CancerRonald DePinho; Fiscal Year: 2003..Such systems hold significant promise in accelerating and making more accurate the evaluation of these compounds prior to entry into the clinic. ..
- Lipotrope stimulates breast cancer cell deathChung Park; Fiscal Year: 2003..abstract_text> ..
- American Society for Neural Transplantation and RepairCaryl Sortwell; Fiscal Year: 2004..This application requests $15,000 in total direct costs to support travel awards for the top 15 graduate students/postdocs from US institutions that apply (awards of $1000 per student/postdoc). ..
- Induced hypothermic arrest in traumatic shockHasan Alam; Fiscal Year: 2005..Sub aim 2: Develop and test methods and techniques that can facilitate the induction of hypothermic arrest in the setting of traumatic shock. ..
- Human B cell homeostasis in a new transgenic xenochimeraRobert Woodland; Fiscal Year: 2005..Furthermore, These transgenic mice will form the basis of a new test system to study the efficacy of adjuvants and vaccines currently being developed against agents of bioterrorism. ..
- Mapping RGC susceptibility alleles Robert Nickells; Fiscal Year: 2007..unreadable] [unreadable] [unreadable]..
- Bcl-2 Family Protein and Apoptosis in SchizophreniaLARS JARSKOG; Fiscal Year: 2005..Stereological neuronal cell counting and measurement of somal size will also be assessed. Finally, young adult rats will receive typical and atypical antipsychotics to assess their effect on the apoptotic regulatory proteins. ..
- American Society for Neural Transplantation and RepairCaryl Sortwell; Fiscal Year: 2005..This application requests $15,000 in total direct costs to support travel awards for the top 15 graduate students/postdocs from US institutions that apply (awards of $1000 per student/postdoc). ..
- TR3/nur77 in Survival and Death of Cancer CellsXiao Kun Zhang; Fiscal Year: 2005....
- Regulation of substrate-linked mitochondrial ROS generationDavid Hockenbery; Fiscal Year: 2007..unreadable] [unreadable]..
- Anti-Leukemic Activity of the Novel Triterpeniod CDDOMichael Andreeff; Fiscal Year: 2004..The long-term goal of our proposed mechanistic and efficacy studies is to determine the potential of CDDO as a novel anti-leukemia and anti-tumor agent. ..
- CANCER AND LEUKEMIA GROUP BStephen Graziano; Fiscal Year: 2002..Through our established outreach efforts, new advances in cancer therapy will be rapidly disseminated to large groups of patients in Central New York. ..
- Cell Metabolism and Myc induced growth, death, and neoplasiaDavid Hockenbery; Fiscal Year: 2009....
- Small Molecule Inhibitors of BcI xL Survival ProteinDavid Hockenbery; Fiscal Year: 2004..3. Determine the role of endogenous pro-apoptotic dimer partners of Eel-if in the cytotoxic mechanism of antimycin A. ..
- DELTAVISION RESTORATION MICROSCOPY SYSTEM MODEL 483Conly Rieder; Fiscal Year: 2001..This Core will maintain the instrument and provide technical support to those Principal Investigators/Program Directors who are in need of low-light high- resolution 3-D fluorescent imaging. ..
- Nicotine/NNK Signaling in Human Lung Cancer CellsXingming Deng; Fiscal Year: 2008..abstract_text> ..