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Genomes and Genes | J M HardwickSummaryAffiliation: Johns Hopkins University Country: USA Publications
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Publications
Multipolar functions of BCL-2 proteins link energetics to apoptosisJ Marie Hardwick
W Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA
Trends Cell Biol 22:318-28. 2012..Even their sub-mitochondrial localizations remain controversial. Here we attempt to integrate seemingly conflicting information with the prospect that BCL-2 proteins themselves may be the critical crosstalk between life and death...- Seizure tests distinguish intermittent fasting from the ketogenic dietAdam L Hartman
Department of Neurology, Johns Hopkins Medicine, Baltimore, Maryland 21205, USA
Epilepsia 51:1395-402. 2010..We challenged this assumption by profiling the effects of these dietary regimens in mice subjected to a battery of acute seizure tests... 
Viral versus cellular BCL-2 proteinsJ M Hardwick
Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Public Health, Baltimore, Maryland 21205, USA
Cell Death Differ 10:S68-76. 2003..Thus, exploring the biochemical and biological functions of the viral BCL-2 family proteins will increase our understanding of their role in virus infections and will undoubtedly teach us something about their cellular kin...- Aven, a novel inhibitor of caspase activation, binds Bcl-xL and Apaf-1B N Chau
Department of Pharmacology and Molecular Sciences, Johns Hopkins University, Schools of Medicine and Public Health, Baltimore, Maryland 21205, USA
Mol Cell 6:31-40. 2000..Consistent with this idea, Aven inhibited the proteolytic activation of caspases in a cell-free extract and suppressed apoptosis induced by Apaf-1 plus caspase-9. Thus, Aven represents a new class of cell death regulator... - c-IAP1 is cleaved by caspases to produce a proapoptotic C-terminal fragmentR J Clem
Department of Molecular Microbiology and Immunology, Johns Hopkins Schools of Public Health and Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 276:7602-8. 2001..To the contrary, deletion of the caspase recruitment domain increased proapoptotic activity, apparently by stabilizing the C-terminal fragment... - Modulation of cell death by Bcl-XL through caspase interactionR J Clem
Department of Molecular Microbiology and Immunology, Johns Hopkins University Schools of Public Health and Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 95:554-9. 1998.... - Survival motor neuron protein modulates neuron-specific apoptosisD A Kerr
Departments of Neurology, Molecular Microbiology and Immunology, Anesthesiology and Critical Care Medicine, and Pharmacology and Molecular Sciences, The Johns Hopkins Schools of Medicine and Public Health, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 97:13312-7. 2000..g., Y272C), produce a proapoptotic form of SMN that may contribute to neuronal death in SMA and perhaps other neurodegenerative disorders... - Caspase-3-dependent cleavage of Bcl-2 promotes release of cytochrome cD G Kirsch
Oncology Center, Pharmacology and Molecular Sciences, and Neurology, Johns Hopkins Schools of Public Health and Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 274:21155-61. 1999..Therefore, caspase-3-dependent cleavage of Bcl-2 appears to promote further caspase activation as part of a positive feedback loop for executing the cell... - Inhibition of virus-induced neuronal apoptosis by BaxJ Lewis
Department of Pharmacology and Molecular Sciences, Johns Hopkins University Schools of Medicine and Public Health, Baltimore, Maryland 21205, USA
Nat Med 5:832-5. 1999..These findings indicate that cell-specific factors determine the anti-apoptotic versus pro-apoptotic function of Bax... - Gene-dependent cell death in yeastX Teng
Department of Pharmacology and Molecular Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA
Cell Death Dis 2:e188. 2011..Although these death mechanisms are yet uncharacterized, this study facilitates further exploration... - Pro-B-cell-specific transcription and proapoptotic function of protein kinase CetaT A Morrow
Graduate Program in Immunology, The Johns Hopkins University School of Public Health, Baltimore, Maryland 21205, USA
Mol Cell Biol 19:5608-18. 1999..These results suggest that the expression and proteolytic activation of PKCeta play an important role in the regulation of cell division and cell death during early B-cell development... - Bcl-2-mediated drug resistance: inhibition of apoptosis by blocking nuclear factor of activated T lymphocytes (NFAT)-induced Fas ligand transcriptionR K Srivastava
Laboratory of Immunology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224 6825, USA
J Exp Med 190:253-65. 1999..The effects of Bcl-2 can be overcome, at least partially, through phosphorylation of Bcl-2. Phosphorylated Bcl-2 cannot bind calcineurin, and NFAT activation, FasL expression, and apoptosis can occur after Bcl-2 phosphorylation... - Perspective: virus infections and the death of neuronsD E Griffin
Dept of Molecular Microbiology and Immunology, Johns Hopkins University School of Hygiene and Public Health, 615 N Wolfe St, Baltimore, MD 21205
Trends Microbiol 7:155-60. 1999..Infected neurons develop cytoplasmic blebbing characteristic of apoptosis, but a paucity of apoptotic nuclear changes potentially indicates unique aspects of virus-induced neuronal apoptosis that remain to be discovered... - Comparison of Bcl-2 to a Bcl-2 deletion mutant for mammalian cells exposed to culture insultsB Figueroa
Department of Chemical Engineering, The Johns Hopkins University, 3400 North Charles St, Baltimore, Maryland 21218, USA
Biotechnol Bioeng 73:211-22. 2001..These studies indicate that the cells regulate anti-apoptosis protein levels and these processing events can limit the effectiveness of cell death inhibition strategies in mammalian cell culture systems... - Fis1 deficiency selects for compensatory mutations responsible for cell death and growth control defectsW C Cheng
W Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA
Cell Death Differ 15:1838-46. 2008.... - Antibody-mediated clearance of alphavirus infection from neuronsB Levine
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205
Science 254:856-60. 1991..Thus, antibody can mediate clearance of alphavirus infection from neurons by restricting viral gene expression... - Enhancement of suicidal DNA vaccine potency by delaying suicidal DNA-induced cell deathT W Kim
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
Gene Ther 11:336-42. 2004..These results suggest that strategies to delay suicidal DNA-induced cell death using antiapoptotic proteins may greatly enhance the potency of suicidal DNA... - Alternate functions of viral regulators of cell deathY-B Chen
Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell Death Differ 13:1318-24. 2006 - Mitochondrial factors with dual roles in death and survivalW-C Cheng
Department of Molecular Microbiology and Immunology, Johns Hopkins School of Public Health, Baltimore, MD 21205, USA
Oncogene 25:4697-705. 2006..Here, we review some of the supporting evidence and stretch beyond the evidence to seek an understanding of the remaining questions... - Conversion of Bcl-2 to a Bax-like death effector by caspasesE H Cheng
Department of Molecular Microbiology and Immunology, Johns Hopkins School of Public Health, Baltimore, MD 21205, USA
Science 278:1966-8. 1997..Cleavage-resistant mutants of Bcl-2 had increased protection from interleukin-3 withdrawal and Sindbis virus-induced apoptosis. Thus, cleavage of Bcl-2 by caspases may ensure the inevitability of cell death... - Bax-independent inhibition of apoptosis by Bcl-XLE H Cheng
Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21287 7681, USA
Nature 379:554-6. 1996..Specific mutations that disrupt the ability of Bcl-XL to interact with Bax or Bak still preserve 70-80% of the anti-death activity of wild-type Bcl-XL... - Inhibition of drug-induced Fas ligand transcription and apoptosis by Bcl-XLR S Biswas
Department of Pharmaceutical Sciences, University of Maryland, School of Pharmacy, Baltimore 21201, USA
Mol Cell Biochem 225:7-20. 2001..Thus, paclitaxel and other drugs that disturb microtubule function kill cells, at least in part, through the induction of FasL, and Bcl-XL-mediated resistance to these agents is related to failure to induce FasL expression... - A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitorsC S Duckett
Howard Hughes Medical Institute, The University of Chicago, Chicago, IL 60637, USA
EMBO J 15:2685-94. 1996..Together these data suggest that iap and related cellular genes play an evolutionarily conserved role in the regulation of apoptosis...