Research Topics
Genomes and Genes | Lloyd GreeneSummaryAffiliation: Columbia University Country: USA Publications
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Publications
Direct interaction of the molecular scaffolds POSH and JIP is required for apoptotic activation of JNKsNickolay V Kukekov
Department of Pathology and Center for Neurobiology and Behavior College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
J Biol Chem 281:15517-24. 2006..Our observations indicate that this complex is required for JNK activation and cell death in response to apoptotic stimuli...- Nerve growth factor selectively regulates expression of transcripts encoding ribosomal proteinsJames M Angelastro
Department of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, 630 W, 168th Street, New York, NY 10032, USA
BMC Neurosci 3:3. 2002..Here, we used database information to identify transcripts in our SAGE libraries that encode ribosomal proteins and have compared the effect of NGF on their relative levels of expression... - Early events in neurotrophin signalling via Trk and p75 receptorsL A Greene
Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
Curr Opin Neurobiol 5:579-87. 1995..Recent studies indicate that p75 dramatically influences Trk activity and ligand interactions, and may mediate signals through the ceramide second-messenger pathway... - The transcription factor ATF5: role in neurodevelopment and neural tumorsLloyd A Greene
Department of Pathology and Cell Biology Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurochem 108:11-22. 2009..Further studies are needed to identify the transcriptional targets of ATF5 and the mechanisms by which its expression is regulated in neuroprogenitors and tumors... - Cell cycle molecules define a pathway required for neuron death in development and diseaseLloyd A Greene
Department of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, 630 W 168th Street, New York, NY 10032, USA
Biochim Biophys Acta 1772:392-401. 2007..The components of this pathway appear to represent potential therapeutic targets for prevention of disease-associated neuron death... - Akt as a victim, villain and potential hero in Parkinson's disease pathophysiology and treatmentLloyd A Greene
Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, 630W 168th Street, New York, NY 10032, USA
Cell Mol Neurobiol 31:969-78. 2011.... - Cell cycle molecules and vertebrate neuron death: E2F at the hubL A Greene
Department of Pathology, Columbia University College of Physicians and Surgeons, New York 10032, USA
Cell Death Differ 11:49-60. 2004..The discovery and elaboration of the neuronal apoptotic E2F pathway provides abundant targets as well as small molecule candidates for potential therapeutic intervention in nervous system trauma and degenerative disease... - Nerve growth factor (NGF) down-regulates the Bcl-2 homology 3 (BH3) domain-only protein Bim and suppresses its proapoptotic activity by phosphorylationSubhas C Biswas
Department of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, 630 W 168th Street, New York, NY 10032, USA
J Biol Chem 277:49511-6. 2002..Thus, NGF protects neurons from the proapoptotic effects of Bim both by acute phosphorylation and the longer term repression of expression... - Analysis of gene expression changes in a cellular model of Parkinson diseaseElizabeth J Ryu
Institute of Human Nutrition, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Neurobiol Dis 18:54-74. 2005..Such intervention may include both inhibiting the induction/activity of death-promoting genes and enhancing those with neuroprotective activity... - Downregulation of activating transcription factor 5 is required for differentiation of neural progenitor cells into astrocytesJames M Angelastro
Department of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 25:3889-99. 2005..These findings identify ATF5 as a key regulator of astrocyte formation and potentially of the VZ to SVZ transition... - POSH acts as a scaffold for a multiprotein complex that mediates JNK activation in apoptosisZhiheng Xu
Department of Pathology and Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
EMBO J 22:252-61. 2003..Thus, POSH appears to function as a scaffold in a multiprotein complex that links activated Rac1 and downstream elements of the JNK apoptotic cascade... - The basic region and leucine zipper transcription factor MafK is a new nerve growth factor-responsive immediate early gene that regulates neurite outgrowthBeata Torocsik
Department of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 22:8971-80. 2002..Our findings support a role for MafK as a novel regulator of neuronal differentiation... - Endoplasmic reticulum stress and the unfolded protein response in cellular models of Parkinson's diseaseElizabeth J Ryu
Department of Pathology, Center for Neurobiology and Behavior, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 22:10690-8. 2002..Our findings, coupled with evidence from familial forms of Parkinson's disease, raise the possibility of widespread involvement of endoplasmic reticulum stress and the unfolded protein response in the pathophysiology of this disease... - Cbl negatively regulates JNK activation and cell deathAndrew A Sproul
Department of Biological Sciences, Columbia University, New York, New York, USA
Cell Res 19:950-61. 2009..Apoptotic stimuli lead to loss of Cbl protein/activity, thereby removing a critical brake on JNK activation and on cell death... - Sertad1 plays an essential role in developmental and pathological neuron deathSubhas C Biswas
Department of Pathology and Cell Biology and Taub Center for Alzheimer s Disease Research, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 30:3973-82. 2010..Sertad1 thus appears to be essential for neuron death in trophic support deprivation in vitro and in vivo and in models of DNA damage and Alzheimer's disease. It may therefore be a suitable target for therapeutic intervention... - Siah1 interacts with the scaffold protein POSH to promote JNK activation and apoptosisZhiheng Xu
Department of Pathology and Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
J Biol Chem 281:303-12. 2006..These findings thus reveal a "loop" mechanism in which the JNK pathway promotes SIAH1 stabilization and in which SIAH1 in turn activates the JNK pathway and, ultimately, contributes to cell death... - Highly efficient small interfering RNA delivery to primary mammalian neurons induces MicroRNA-like effects before mRNA degradationThomas J Davidson
Department of Pathology, Taub Institute for the Study of Alzheimer's Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 24:10040-6. 2004..Using this technique, we found that protein knock-down (evident after 6 hr) precedes any decrease in targeted message (evident after 24 hr), suggesting an early, translational repression by perfectly targeted siRNAs... - Glucagon-like peptide-1 (GLP-1) diminishes neuronal degeneration and death caused by NGF deprivation by suppressing Bim inductionSubhas C Biswas
Department of Pathology, Center for Neurobiology and Behavior and Taub Center for Alzheimer s Disease Research, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Neurochem Res 33:1845-51. 2008..Thus, GLP-1 may protect neurons, at least in part, by suppressing Bim induction. Our findings support the idea that drugs that mimic or elevate GLP-1 represent potential therapeutics for neurodegenerative diseases... - Identification of POSH2, a novel homologue of the c-Jun N-terminal kinase scaffold protein POSHMichael Wilhelm
Department of Pediatrics, Columbia University Health Sciences, New York, NY 10032, USA
Dev Neurosci 29:355-62. 2007..These results indicate that POSH2 may regulate JNK activation and consequent apoptosis under conditions of increased expression... - RTP801 is induced in Parkinson's disease and mediates neuron death by inhibiting Akt phosphorylation/activationCristina Malagelada
Department of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA
J Neurosci 28:14363-71. 2008..These observations support a sequential mechanism in which PD-associated stresses induce RTP801, suppress mTOR signaling, deplete phosphorylated/activated Akt and permit neuron degeneration and death... - Pro-apoptotic Bim induction in response to nerve growth factor deprivation requires simultaneous activation of three different death signaling pathwaysSubhas C Biswas
Department of Pathology, Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Biol Chem 282:29368-74. 2007..It also permits neurons to utilize individual pathways such as JNK signaling for other purposes without risk of demise... - Bim is elevated in Alzheimer's disease neurons and is required for beta-amyloid-induced neuronal apoptosisSubhas C Biswas
Department of Pathology, Center for Neurobiology and Behavior and Taub Institute for Research on Alzheimer s Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 27:893-900. 2007..Our observations indicate that Bim is a proapoptotic effector of Abeta and of dysregulated cell cycle proteins in AD and identify both Bim and cell cycle elements as potential therapeutic targets... - Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson's diseaseCristina Malagelada
Department of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA
J Neurosci 30:1166-75. 2010.... - Proapoptotic Nix activates the JNK pathway by interacting with POSH and mediates death in a Parkinson disease modelMichael Wilhelm
Department of Pediatrics, Columbia University Health Sciences, New York, New York 10032, USA
J Biol Chem 282:1288-95. 2007..These results indicate that Nix promotes cell death via interaction with POSH and activation of the JNK/c-Jun pathway and that Nix protein is induced and contributes to cell death in a cellular model of Parkinson disease... - RTP801 is elevated in Parkinson brain substantia nigral neurons and mediates death in cellular models of Parkinson's disease by a mechanism involving mammalian target of rapamycin inactivationCristina Malagelada
Department of Pathology and Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA
J Neurosci 26:9996-10005. 2006.... - B-myb and C-myb play required roles in neuronal apoptosis evoked by nerve growth factor deprivation and DNA damageDavid X Liu
Department of Pathology, Center for Neurobiology and Behavior and Taub Center for Alzheimer s Disease Research, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 24:8720-5. 2004..There is also significant protection from death induced by direct E2F-dependent gene de-repression. Our findings thus establish required roles for B- and C-myb in neuronal apoptosis... - Regulation of neuron survival and death by p130 and associated chromatin modifiersDavid X Liu
Department of Pathology, Columbia University Medical Center, New York, New York 10032, USA
Genes Dev 19:719-32. 2005..Thus, neuron survival and death are dependent on the integrity of E2F4-p130-HDAC/Suv39H1 complexes... - CHOP/GADD153 is a mediator of apoptotic death in substantia nigra dopamine neurons in an in vivo neurotoxin model of parkinsonismRobert M Silva
Department of Neurology, The College of Physicians and Surgeons, Columbia University, New York 10032, USA
J Neurochem 95:974-86. 2005..We conclude that the role of CHOP depends on the nature of the toxic stimulus. For 6OHDA, an oxidative metabolite of dopamine, it is a mediator of apoptotic death... - Bim is a direct target of a neuronal E2F-dependent apoptotic pathwaySubhas C Biswas
Department of Pathology, Center for Neurobiology and Behavior, Taub Center for Alzheimer s Disease Research, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 25:8349-58. 2005..These findings support a model in which apoptotic stimuli lead to cdk4 activation, consequent de-repression of E2F-regulated mybs, and induction of pro-apoptotic Bim... - Puma and p53 play required roles in death evoked in a cellular model of Parkinson diseaseSubhas C Biswas
Department of Pathology, Center for Neurobiology and Behavior and Taub Center for Alzheimer s Disease Research, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Neurochem Res 30:839-45. 2005..Involvement of p53 in 6-OHDA evoked death was confirmed by the protective actions of a DN p53 and pifithrin alpha, inhibitors of p53 signaling. Our findings thus indicate that p53 and PUMA play required roles in a cellular model of PD... - You can't go home again: transcriptionally driven alteration of cell signaling by NGFLloyd A Greene
Department of Pathology, Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Neurochem Res 30:1347-52. 2005..We discuss specific examples based on reports in the literature as well as on data derived from a serial analysis of gene expression (SAGE) study of NGF-promoted transcriptional changes in PC12 pheochromocytoma cells... - Regulated expression of ATF5 is required for the progression of neural progenitor cells to neuronsJames M Angelastro
Department of Pathology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
J Neurosci 23:4590-600. 2003..These findings indicate that ATF5 blocks the differentiation of neuroprogenitor cells into neurons and must be downregulated to permit this process to occur... - Regulation of apoptotic c-Jun N-terminal kinase signaling by a stabilization-based feed-forward loopZhiheng Xu
Department of Pathology and Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, 630 W 168th Street, New York, New York 10032, USA
Mol Cell Biol 25:9949-59. 2005..Our findings suggest a self-amplifying, feed-forward loop mechanism by which apoptotic stimuli promote the stabilization of JNK pathway components, thereby contributing to cell death... - Cell death pathways in Parkinson's disease: proximal triggers, distal effectors, and final stepsOren A Levy
Department of Neurology, Columbia University School of Medicine, New York, NY, USA
Apoptosis 14:478-500. 2009..In this review, we will discuss cell death triggers and effectors that are relevant to PD, highlighting important unresolved issues and implications for the development of neuroprotective therapies... - The transcription factor ATF5 is widely expressed in carcinomas, and interference with its function selectively kills neoplastic, but not nontransformed, breast cell linesSara E Monaco
Department of Pathology, Columbia University College of Physicians and Surgeons, New York, NY, USA
Int J Cancer 120:1883-90. 2007..Our data demonstrate elevated ATF5 expression in a wide variety of neoplasms and that interference with ATF5 function selectively triggers death of breast carcinoma cells. Such findings may have potential therapeutic application... - ATF5 regulates the proliferation and differentiation of oligodendrocytesJeffrey L Mason
Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA
Mol Cell Neurosci 29:372-80. 2005..Regulation of oligodendrocyte, astrocyte, and neuronal differentiation indicates that ATF5 operates as a general regulator of the timing of differentiation, independent of cell lineage... - Activation of the apoptotic JNK pathway through the Rac1-binding scaffold protein POSHZhiheng Xu
Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China
Methods Enzymol 406:479-89. 2006..Use of these techniques may lead to a better understanding of the components of this pathway and of how it is suppressed in viable cells and rapidly activated in response to apoptotic stimuli... - Malignant pheochromocytoma: current status and initiatives for future progressGraeme Eisenhofer
National Institutes of Health, Bethesda, Maryland 20892 1620, USA
Endocr Relat Cancer 11:423-36. 2004..Again the success of this will require well-designed and coordinated multi-center studies...
Research Grants
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd Greene; Fiscal Year: 2002..The hypothesis will be evaluated that neuronal apoptosis evoked by different causes is mediated by distinct caspase family members. ..
- NEUROCHEMICAL STUDIES ON CULTURED NEURONSLloyd Greene; Fiscal Year: 2002..work will provide insight into a wide variety of key brain functions and has the potential to lead to design of pharmaceutical agents for the treatment and prevention of a number of maladies affecting the nervous system ..
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd Greene; Fiscal Year: 2003..Studies will focus on characterizing the role of the scaffold protein POSH in this pathway and on using gene profiling technology to identify those death associated genes that this pathway regulates. ..
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd Greene; Fiscal Year: 2006..Studies will focus on characterizing the role of the scaffold protein POSH in this pathway and on using gene profiling technology to identify those death associated genes that this pathway regulates. ..
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd Greene; Fiscal Year: 2007..Studies will focus on characterizing the role of the scaffold protein POSH in this pathway and on using gene profiling technology to identify those death associated genes that this pathway regulates. ..
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd Greene; Fiscal Year: 2009..The components of these pathways thus represent targets that can be used to block neuron death and ameliorate diseases such as neurodegenerative disorders, stroke and trauma. ..
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd A Greene; Fiscal Year: 2010..The components of these pathways thus represent targets that can be used to block neuron death and ameliorate diseases such as neurodegenerative disorders, stroke and trauma. ..
- NEUROCHEMICAL STUDIES ON CULTURED NEURONSLloyd Greene; Fiscal Year: 1999..5) Particular intracellular domains of trk that endow it with signalling properties responsible for the specificity of NGF actions. 6) Intracellular domains of trk responsible for high affinity NGF binding and internalization. ..
- NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHLloyd Greene; Fiscal Year: 2009..The components of these pathways thus represent targets that can be used to block neuron death and ameliorate diseases such as neurodegenerative disorders, stroke and trauma. ..