Research Topics
Genomes and Genes
| Richard J YouleSummaryAffiliation: National Institutes of Health Country: USA Publications
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Detail Information
Publications
Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilizationDamien Arnoult
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
EMBO J 22:4385-99. 2003..Thus EndoG and AIF seem to define a 'caspase-dependent' mitochondria-initiated apoptotic DNA degradation pathway that is conserved between mammals and nematodes...
Mitochondrial fission, fusion, and stressRichard J Youle
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Science 337:1062-5. 2012..Disruptions in these processes affect normal development, and they have been implicated in neurodegenerative diseases, such as Parkinson's...
Cell biology. Cellular demolition and the rules of engagementRichard J Youle
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Science 315:776-7. 2007- 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... - Mitochondrial fission in apoptosisRichard J Youle
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Rev Mol Cell Biol 6:657-63. 2005..One of the steps in apoptosis is the fragmentation of mitochondria, and recent evidence indicates that the mitochondrial fission machinery actively participates in the process of programmed cell death... - Mechanisms of mitophagyRichard J Youle
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 2C 917, Bethesda, Maryland 20892, USA
Nat Rev Mol Cell Biol 12:9-14. 2011..Moreover, mitophagy is regulated in many metazoan cell types by parkin and PTEN-induced putative kinase protein 1 (PINK1), and mutations in the genes encoding these proteins have been linked to forms of Parkinson's disease... - Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by ParkinAtsushi Tanaka
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
J Cell Biol 191:1367-80. 2010..Inhibition of Drp1-mediated mitochondrial fission, the proteasome, or p97 prevents Parkin-induced mitophagy... - Novel structure of the N terminus in yeast Fis1 correlates with a specialized function in mitochondrial fissionMotoshi Suzuki
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 280:21444-52. 2005..Although the TPR-like helix bundle of Fis1 mediates the interaction with Dnm1 and Mdv1, the N terminus of Fis1 is a prerequisite to recruit Mdv1 to facilitate mitochondrial fission... - Roles of the mammalian mitochondrial fission and fusion mediators Fis1, Drp1, and Opa1 in apoptosisYang ja Lee
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Mol Biol Cell 15:5001-11. 2004..However, we provide further evidence that multiple components of the mitochondrial morphogenesis machinery can positively and negatively regulate apoptosis... - Parkin is recruited selectively to impaired mitochondria and promotes their autophagyDerek Narendra
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
J Cell Biol 183:795-803. 2008..These results show that Parkin promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondria in the pathogenesis of Parkinson's disease... - Bcl-x(L) retrotranslocates Bax from the mitochondria into the cytosolFrank Edlich
Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, MD 20892, USA
Cell 145:104-16. 2011..We propose that Bcl-x(L) inhibits and maintains Bax in the cytosol by constant retrotranslocation of mitochondrial Bax... - The mitochondrial E3 ubiquitin ligase MARCH5 is required for Drp1 dependent mitochondrial divisionMariusz Karbowski
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20852, USA
J Cell Biol 178:71-84. 2007..Collectively, our data suggest a model in which mitochondrial division is regulated by a MARCH5 ubiquitin-dependent switch... - Endophilin B1 is required for the maintenance of mitochondrial morphologyMariusz Karbowski
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bldg 35, Rm 917, MSC 3407, 35 Lincoln Drive, Bethesda, MD 20892 1414, USA
J Cell Biol 166:1027-39. 2004.... - Cytomegalovirus cell death suppressor vMIA blocks Bax- but not Bak-mediated apoptosis by binding and sequestering Bax at mitochondriaDamien Arnoult
National Institute of Neurological Disorders and Stroke Biochemistry Section, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 101:7988-93. 2004.... - Parkin overexpression selects against a deleterious mtDNA mutation in heteroplasmic cybrid cellsDer Fen Suen
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 107:11835-40. 2010..These data support the model that Parkin functions in a mitochondrial quality control pathway. Additionally, they suggest that transiently increasing levels of Parkin expression might ameliorate certain mitochondrial diseases... - Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase ParkinMichael Lazarou
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Dev Cell 22:320-33. 2012..We propose that the association of PINK1 with the TOM complex allows rapid reimport of PINK1 to rescue repolarized mitochondria from mitophagy, and discount mitochondrial-specific factors for Parkin translocation and activation... - Bcl-x(L) sequesters its C-terminal membrane anchor in soluble, cytosolic homodimersSeon Yong Jeong
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1414, USA
EMBO J 23:2146-55. 2004..The C-terminal tail of Bcl-x(L) is also required to mediate Bcl-x(L)/Bax heterodimer formation. Both mitochondrial import and antiapoptotic activity of different Bcl-x(L) mutants correlate with their ability to form homodimers... - Bax activates endophilin B1 oligomerization and lipid membrane vesiculationTatiana K Rostovtseva
Laboratory of Physical and Structural Biology, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 284:34390-9. 2009..This activity of purified Bax protein to induce cell-free assembly of Endo B1 may reflect its activity in cells that regulates apoptosis and/or mitochondrial fusion... - Quantitation of mitochondrial dynamics by photolabeling of individual organelles shows that mitochondrial fusion is blocked during the Bax activation phase of apoptosisMariusz Karbowski
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
J Cell Biol 164:493-9. 2004..The block in mitochondrial fusion occurs within the same time range as Bax coalescence on the mitochondria and outer mitochondrial membrane permeabilization, and it may be a consequence of Bax/Bak activation during apoptosis... - Control of mitochondrial permeability by Bcl-2 family membersJuanita C Sharpe
Biochemistry Section, Surgical Neurology Branch, NINDS, NIH, Bethesda, MD 20892, USA
Biochim Biophys Acta 1644:107-13. 2004..The molecular mechanisms of the different models for the permeabilization of membranes by the Bcl-2 family members and the regulation of Bcl-2 family member subcellular localizations are discussed... - The solution structure of human mitochondria fission protein Fis1 reveals a novel TPR-like helix bundleMotoshi Suzuki
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
J Mol Biol 334:445-58. 2003.... - A chimeric protein induces tumor cell apoptosis by delivering the human Bcl-2 family BH3-only protein BadAntonella Antignani
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892 3704, USA
Biochemistry 44:4074-82. 2005..The completely human sequence and the elevated selectivity for cancer cells could prevent immunogenicity and the nonspecific toxicity of targeted toxins in future clinical application of this fusion protein... - Mitochondrial dynamics and apoptosisDer Fen Suen
Biochemistry Section, Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, MD 20892, USA
Genes Dev 22:1577-90. 2008..This review will cover the recent advances and presents competing models on how the mitochondrial fission and fusion machinery may intersect apoptosis pathways... - Outer mitochondrial membrane protein degradation by the proteasomeAlbert Neutzner
Biochemistry Section, SNB, NINDS, NIH, Bethesda, MD 20892, USA
Novartis Found Symp 287:4-14; discussion 14-20. 2007..Some of these mitochondrial RING domain proteins also regulate mitochondrial morphology, indicating a critical role of ubiquitin signalling in the maintenance of mitochondrial homeostasis... - p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for bothDerek Narendra
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke National Institutes of Health, Bethesda, MD, USA
Autophagy 6:1090-106. 2010..They also suggest that proteins other than p62 are likely required for mitophagy downstream of Parkin substrates other than VDAC1... - Parkin-induced mitophagy in the pathogenesis of Parkinson diseaseDerek Narendra
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Autophagy 5:706-8. 2009..These findings suggest that Parkin promotes mitophagy of dysfunctional mitochondria following loss of mitochondrial membrane potential and implicates the targeted elimination of mitochondria in the pathogenesis of Parkinson disease... - A systematic search for endoplasmic reticulum (ER) membrane-associated RING finger proteins identifies Nixin/ZNRF4 as a regulator of calnexin stability and ER homeostasisAlbert Neutzner
Biochemistry Section, Surgical Neurological Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 286:8633-43. 2011..Importantly, Nixin physically interacts with calnexin in a glycosylation-independent manner, induces calnexin ubiquitination, and p97-dependent degradation, indicating an ER-associated degradation-like mechanism of calnexin turnover... - PINK1 is selectively stabilized on impaired mitochondria to activate ParkinDerek P Narendra
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA
PLoS Biol 8:e1000298. 2010..In addition, they support a novel model for the negative selection of damaged mitochondria, in which PINK1 signals mitochondrial dysfunction to Parkin, and Parkin promotes their elimination... - Instability of the mitofusin Fzo1 regulates mitochondrial morphology during the mating response of the yeast Saccharomyces cerevisiaeAlbert Neutzner
Biochemistry Section, Surgical Neurological Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 280:18598-603. 2005..Proteasomal degradation of Fzo1 in response to the mating pheromone is proposed to mediate the remodeling of the mitochondrial network during the process of mating... - Endosome fusion induced by diphtheria toxin translocation domainAntonella Antignani
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive MSC 3704, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 105:8020-5. 2008..These changes to endosomes may reflect activities of the T domain that mediate toxin entry to the cytosol. The nontoxic mutant DT, CRM197, yields a new tool to manipulate endosome dynamics in living cells... - Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARLSeok Min Jin
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
J Cell Biol 191:933-42. 2010..Thus, differential localization to the inner and outer mitochondrial membranes appears to regulate PINK1 stability and function... - 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... - Bid, but not Bax, regulates VDAC channelsTatiana K Rostovtseva
Laboratory of Physical and Structural Biology, NICHD, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 279:13575-83. 2004..We speculate that by decreasing the probability of VDAC opening, Bid reduces metabolite exchange between mitochondria and the cytosol, leading to mitochondrial dysfunction... - The role of mitochondria in apoptosis*Chunxin Wang
Biochemistry Section, Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892, USA
Annu Rev Genet 43:95-118. 2009..We also compare and contrast apoptosis pathways in Caenorhabditis elegans, Drosophila melanogaster, and mammals that indicate major mysteries remaining to be solved... - Pseudomonas exotoxin A-mediated apoptosis is Bak dependent and preceded by the degradation of Mcl-1Xing Du
Laboratory of Molecular Biology, National Cancer Institute, 37 Convent Drive, Bethesda, MD 20892 4264, USA
Mol Cell Biol 30:3444-52. 2010..Overexpression of Mcl-1 and Bcl-x(L) inhibited PE-induced MEF death. Our data suggest that Bak is the preferential mediator of PE-mediated apoptosis and that the rapid degradation of Mcl-1 unleashes Bak to activate apoptosis... - A chemical inhibitor of DRP1 uncouples mitochondrial fission and apoptosisAtsushi Tanaka
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20824, USA
Mol Cell 29:409-10. 2008..In a recent issue of Developmental Cell, Cassidy-Stone et al. (2008) identified mdivi-1, a new DRP1 inhibitor that prevents mitochondria division and Bax-mediated mitochondrial outer membrane permeabilization during apoptosis... - Role of Bax and Bak in mitochondrial morphogenesisMariusz Karbowski
Biochemistry Section, SNB, NINDS, NIH, Bethesda, Maryland 20892, USA
Nature 443:658-62. 2006..Our results show that Bax and Bak regulate mitochondrial dynamics in healthy cells and indicate that Bcl-2 family members may also regulate apoptosis through organelle morphogenesis machineries... - Mitochondrial fission and fusion and their roles in the heartLesley A Kane
National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
J Mol Med (Berl) 88:971-9. 2010..This review will provide an overview of mitochondrial fission and fusion as well as recent developments in the understanding of these processes in the heart... - How do Bax and Bak lead to permeabilization of the outer mitochondrial membrane?Antonella Antignani
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive MSC 3704, Bethesda, MD 20892, USA
Curr Opin Cell Biol 18:685-9. 2006..Work linking Bcl-2 family members to mitochondrial morphogenesis in worms and mammals suggests some common functions of Bcl-2 family proteins may exist... - Jak3-independent trafficking of the common gamma chain receptor subunit: chaperone function of Jaks revisitedSigrun R Hofmann
National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, 10 Center Dr, Bldg 10, Rm 9N256, Bethesda, MD 20892 1820, USA
Mol Cell Biol 24:5039-49. 2004..However, full-length Jak3 is required for normal trafficking of this cytokine receptor/Jak pair, a finding that has important structural and clinical implications... - Targeting mitochondrial dysfunction: role for PINK1 and Parkin in mitochondrial quality controlDerek P Narendra
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
Antioxid Redox Signal 14:1929-38. 2011..This recent work suggests that Parkin and PINK1 may be among the first mammalian proteins identified with a direct role in regulating mitophagy, and implicate a failure of mitophagy in the pathogenesis of Parkinson's disease... - Role of the ubiquitin conjugation system in the maintenance of mitochondrial homeostasisAlbert Neutzner
Surgical Neurology Branch National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA
Ann N Y Acad Sci 1147:242-53. 2008.... - The cytokine, granulocyte-macrophage colony-stimulating factor (GM-CSF), can deliver Bcl-XL as an extracellular fusion protein to protect cells from apoptosis and retain differentiation inductionAntonella Antignani
Biochemistry Section, Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 282:11246-54. 2007..This fully human fusion protein has potential to prevent monocytopenia and represents a new strategy for engineering anti-apoptotic therapeutics... - Cytomegalovirus proteins vMIA and m38.5 link mitochondrial morphogenesis to Bcl-2 family proteinsKristi L Norris
Biochemistry Section, Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892, USA
J Virol 82:6232-43. 2008..Thus, vMIA and m38.5 share some, but not all, features of apoptosis regulation through Bcl-2 family interaction and allow the dissection of Bax translocation into discrete steps... - Structural mechanism of Bax inhibition by cytomegalovirus protein vMIAJunhe Ma
Laboratory of Molecular Biophysics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 109:20901-6. 2012..The structure suggests that by stabilizing key elements in Bax needed to unravel for its MOM insertion and oligomerization, vMIA prevents these important steps in apoptosis... - Bcl-xL and caspase inhibition increase the survival of rat oxytocin and vasopressin magnocellular neurons in organotypic cultureShirley B House
Laboratory of Neurochemistry, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Exp Neurol 200:267-71. 2006..01) but not VP MCNs (P > 0.09). Unlike the Bcl-xL, Z-VAD-fmk's effectiveness in reducing MCN cell death was not sustained for the full 15 days in vitro... - Scission, spores, and apoptosis: a proposal for the evolutionary origin of mitochondria in cell death inductionStephan Frank
Biochemistry Section, SNB, NINDS/NIH, Building 10, Room 5D-37, Bethesda, MD 20892, USA
Biochem Biophys Res Commun 304:481-6. 2003..This hypothesis would explain why what is generally considered the "power house" of the cell came to integrate the cell death response and regulate apoptosis... - Morphology of mitochondria during apoptosis: worms-to-beetles in wormsRichard J Youle
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20815, USA
Dev Cell 8:298-9. 2005..elegans development inhibits programmed cell death bridges this gap and should advance a more detailed understanding of the role of mitochondria in caspase activation... - Ubiquitin ligase RNF167 regulates AMPA receptor-mediated synaptic transmissionMarc P Lussier
Receptor Biology Section and Biochemistry Section Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 109:19426-31. 2012..Therefore, our study identifies RNF167 as a selective regulator of AMPAR-mediated neurotransmission and expands our understanding of how ubiquitination dynamically regulates excitatory synapses... - Parkin is a lipid-responsive regulator of fat uptake in mice and mutant human cellsKye Young Kim
Center for Molecular Medicine, NHLBI, 10 Center Drive, Bethesda, Maryland, 20892 1454, USA
J Clin Invest 121:3701-12. 2011..Whether this metabolic regulation contributes to premature Parkinsonism warrants investigation... - Extracellular Bad fused to toxin transport domains induces apoptosisMakoto Ichinose
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
Cancer Res 62:1433-8. 2002..We conclude that extracellular Bad can be delivered into cells via the transport domain of a bacterial toxin and may be used to induce apoptosis... - PINK1 and Parkin Flag Miro to Direct Mitochondrial TrafficLesley A Kane
National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Cell 147:721-3. 2011..In this issue of Cell, Wang et al. (2011) now show that PINK1 and Parkin also regulate mitochondrial trafficking and quarantine damaged mitochondria by severing their connection to the microtubule network... - Mitochondrial fission and fusionIain Scott
National Heart, Lung and Blood Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
Essays Biochem 47:85-98. 2010..In the present chapter we discuss the mechanisms behind mitochondrial fission and fusion, and discuss the implications of changes in organelle morphology during the life of a cell... - Entry into cells and selective degradation of tRNAs by a cytotoxic member of the RNase A familyShailendra K Saxena
Biochemistry Section, Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892-1414, USA
J Biol Chem 277:15142-6. 2002..We conclude that the degradation of tRNAs may be a primary factor in the cytotoxic activity of onconase... - Mitochondrial fission and fusion mediators, hFis1 and OPA1, modulate cellular senescenceSeungmin Lee
Department of Biochemistry, Ajou University School of Medicine, Ajou University, 5 Wonchon dong, Yeongtong Gu, Suwon 443 721, Korea
J Biol Chem 282:22977-83. 2007..Thus, one of the key functions of mitochondrial fission might be prevention of the sustained extensive mitochondrial elongation that triggers cellular senescence... - The permeability transition pore signals apoptosis by directing Bax translocation and multimerizationFrancesaA De Giorgi
European Institute of Chemistry and Biology, and INSERM E.9929, Victor Segalen-Bordeaux 2 University, 33076 Bordeaux Cedex, France
FASEB J 16:607-9. 2002..We conclude that the PTP is not itself a component of the Cyt.c release machinery, but that it acts indirectly by signaling Bax translocation and multimerization... - Mitofusin-1 protein is a generally expressed mediator of mitochondrial fusion in mammalian cellsAnsgar Santel
Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
J Cell Sci 116:2763-74. 2003..Thus, Mfn1 appears to be a key player in mediating mitochondrial fusion and morphology in mammalian cells... - Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosisYoshinori Takahashi
Drug Discovery Program, H Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33612, USA
Mol Cell Biol 25:9369-82. 2005..Taken together, these findings support the notion that Bif-1 is an important component of the mitochondrial pathway for apoptosis as a novel Bax/Bak activator, and loss of this proapoptotic molecule may contribute to tumorigenesis... - JNK-mediated BIM phosphorylation potentiates BAX-dependent apoptosisGirish V Putcha
Department of Neurology and Department of Molecular Biology and Pharmacology, Washington University School of Medicine, Saint Louis, MO 63110, USA
Neuron 38:899-914. 2003..Thus, JNKs regulate the proapoptotic activity of BIM(EL) during TFD, both transcriptionally and posttranslationally... - Nitric oxide-induced mitochondrial fission is regulated by dynamin-related GTPases in neuronsMark J Barsoum
Apoptosis and Cell Death Program, Burnham Institute for Medical Research, La Jolla, CA, USA
EMBO J 25:3900-11. 2006..Importantly, NO-induced neuronal cell death was mitigated by Mfn1 and Drp1(K38A). Thus, persistent mitochondrial fission may play a causal role in NO-mediated neurotoxicity... - Role of mitochondrial remodeling in programmed cell death in Drosophila melanogasterGaurav Goyal
National Centre for Biological Sciences, Tata Institute of Fundamental Research, GKVK Campus, Bellary Road, Bangalore 560 065, India
Dev Cell 12:807-16. 2007..Thus, mitochondrial remodeling is capable of modifying the propensity of cells to undergo death in Drosophila... - Drp-1-dependent division of the mitochondrial network blocks intraorganellar Ca2+ waves and protects against Ca2+-mediated apoptosisGyorgy Szabadkai
Department of Experimental and Diagnostic Medicine, Section of General Pathology and Interdisciplinary Center for the Study of Inflammation, University of Ferrara, 44100 Ferrara, Italy
Mol Cell 16:59-68. 2004.... - OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusionClaudia Zanna
Dipartimento di Biologia Evoluzionistica Sperimentale, Universita di Bologna, Via Irnerio 42, 40126 Bologna, Italy
Brain 131:352-67. 2008..The results disclose a novel link between OPA1, apoptosis inducing factor and the respiratory complexes that may shed some light on the pathogenic mechanism of DOA...