S Finkbeiner

Summary

Affiliation: University of California
Country: USA

Publications

  1. doi request reprint Bridging the Valley of Death of therapeutics for neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease, Taube Koret Center for Huntington s Disease Research, Consortium for Fronto temporal Dementia Research, and Department of Neurology, University of California, San Francisco, California, USA
    Nat Med 16:1227-32. 2010
  2. ncbi request reprint Calcium regulation of the brain-derived neurotrophic factor gene
    S Finkbeiner
    Department of Neurology, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cell Mol Life Sci 57:394-401. 2000
  3. ncbi request reprint New roles for introns: sites of combinatorial regulation of Ca2+- and cyclic AMP-dependent gene transcription
    S Finkbeiner
    the Gladstone Institute of Neurological Disease, Departments of Neurology and Physiology, University of California, San Francisco, San Francisco, CA 94143, USA
    Sci STKE 2001:pe1. 2001
  4. ncbi request reprint An evaluation of specificity in activity-dependent gene expression in neurons
    John Bradley
    Departments of Neurology and Physiology, Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94103, USA
    Prog Neurobiol 67:469-77. 2002
  5. pmc Tau reduction prevents Abeta-induced defects in axonal transport
    Keith A Vossel
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Science 330:198. 2010
  6. ncbi request reprint Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease
    Jorge J Palop
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 55:697-711. 2007
  7. ncbi request reprint Disease-modifying pathways in neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease and Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 26:10349-57. 2006
  8. ncbi request reprint Splice variants of the NR1 subunit differentially induce NMDA receptor-dependent gene expression
    John Bradley
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141, USA
    J Neurosci 26:1065-76. 2006
  9. ncbi request reprint To fear or not to fear: what was the question? A potential role for Ras-GRF in memory
    S Finkbeiner
    Department of Neurology, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Bioessays 20:691-5. 1998
  10. ncbi request reprint AMPA receptors regulate transcription of the plasticity-related immediate-early gene Arc
    Vikram R Rao
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Nat Neurosci 9:887-95. 2006

Research Grants

  1. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven M Finkbeiner; Fiscal Year: 2010
  2. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2009
  3. Mechanisms of Huntingtin Induced Neurodegeneration
    Steven Finkbeiner; Fiscal Year: 2009
  4. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2007
  5. Mechanisms of Huntingtin Induced Neurodegeneration
    Steven Finkbeiner; Fiscal Year: 2007
  6. Zeiss LSM510 Confocal Multiphoton/META Microscope
    Steven Finkbeiner; Fiscal Year: 2004
  7. MECHANISMS OF HUNTINGTIN-INDUCED NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2003
  8. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2009

Collaborators

Detail Information

Publications23

  1. doi request reprint Bridging the Valley of Death of therapeutics for neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease, Taube Koret Center for Huntington s Disease Research, Consortium for Fronto temporal Dementia Research, and Department of Neurology, University of California, San Francisco, California, USA
    Nat Med 16:1227-32. 2010
    ..Here we consider the many obstacles to the development of therapeutics for neurodegenerative disease within academia, with a special focus on organizational issues...
  2. ncbi request reprint Calcium regulation of the brain-derived neurotrophic factor gene
    S Finkbeiner
    Department of Neurology, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cell Mol Life Sci 57:394-401. 2000
    ..This review focuses on the mechanisms by which calcium influx regulates brain-derived neurotrophic factor expression and the implications that these results have for potential roles of neurotrophins in synaptic function...
  3. ncbi request reprint New roles for introns: sites of combinatorial regulation of Ca2+- and cyclic AMP-dependent gene transcription
    S Finkbeiner
    the Gladstone Institute of Neurological Disease, Departments of Neurology and Physiology, University of California, San Francisco, San Francisco, CA 94143, USA
    Sci STKE 2001:pe1. 2001
    ..Finkbeiner examines recent work by Schlegel and colleagues demonstrating that sequences within the first intron of the c-fos gene help to regulate Fos expression under different conditions...
  4. ncbi request reprint An evaluation of specificity in activity-dependent gene expression in neurons
    John Bradley
    Departments of Neurology and Physiology, Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94103, USA
    Prog Neurobiol 67:469-77. 2002
    ..In particular, we describe data which suggests that Ca2+ channels may function in signal complexes at the synapse to propagate signals that contribute to distinct nuclear responses...
  5. pmc Tau reduction prevents Abeta-induced defects in axonal transport
    Keith A Vossel
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Science 330:198. 2010
    ..Lowering tau levels prevented these defects without affecting baseline axonal transport. Thus, Aβ requires tau to impair axonal transport, and tau reduction protects against Aβ-induced axonal transport defects...
  6. ncbi request reprint Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease
    Jorge J Palop
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 55:697-711. 2007
    ..Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD...
  7. ncbi request reprint Disease-modifying pathways in neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease and Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 26:10349-57. 2006
  8. ncbi request reprint Splice variants of the NR1 subunit differentially induce NMDA receptor-dependent gene expression
    John Bradley
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141, USA
    J Neurosci 26:1065-76. 2006
    ..Thus, the NR1 C terminus couples to multiple downstream signaling pathways that can be modulated selectively by RNA splicing...
  9. ncbi request reprint To fear or not to fear: what was the question? A potential role for Ras-GRF in memory
    S Finkbeiner
    Department of Neurology, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Bioessays 20:691-5. 1998
    ..This paper suggests that Ras-GRF couples synaptic activity to the molecular mechanisms that consolidate changes in synaptic strength within specific neuronal circuits...
  10. ncbi request reprint AMPA receptors regulate transcription of the plasticity-related immediate-early gene Arc
    Vikram R Rao
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Nat Neurosci 9:887-95. 2006
    ..These results provide insights into the activity-dependent mechanisms of Arc expression and suggest that, in addition to effecting short-term plasticity, AMPA receptors regulate genes involved in long-term plasticity...
  11. pmc Arc regulates spine morphology and maintains network stability in vivo
    Carol L Peebles
    Gladstone Institute of Neurological Disease and the Keck Program in Striatal Physiology, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 107:18173-8. 2010
    ..Supporting this, loss of Arc in vivo leads to a significant decrease in the proportion of thin spines and an epileptic-like network hyperexcitability...
  12. ncbi request reprint NMDA and AMPA receptors: old channels, new tricks
    Vikram R Rao
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Trends Neurosci 30:284-91. 2007
    ..We discuss evidence that signals from NMDA receptors and AMPA receptors are integrated to specify transcriptional responses for particular plasticity related genes...
  13. pmc The serum response factor and a putative novel transcription factor regulate expression of the immediate-early gene Arc/Arg3.1 in neurons
    Sean A Pintchovski
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 29:1525-37. 2009
    ..This element binds serum response factor, which is recruited by synaptic activity to regulate Arc. Thus, Arc is the first target of serum response factor that functions at synapses to mediate plasticity...
  14. ncbi request reprint Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions
    F Saudou
    Department of Neurology, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cell 95:55-66. 1998
    ..These findings suggest that mutant huntingtin acts within the nucleus to induce neurodegeneration. However, intranuclear inclusions may reflect a cellular mechanism to protect against huntingtin-induced cell death...
  15. pmc Quantitative relationships between huntingtin levels, polyglutamine length, inclusion body formation, and neuronal death provide novel insight into huntington's disease molecular pathogenesis
    Jason Miller
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Neurosci 30:10541-50. 2010
    ..Finally, the model that emerges from our quantitative measurements places critical limits on the potential mechanisms by which mutant htt might induce neurodegeneration, which should help direct future research...
  16. pmc Single neuron ubiquitin-proteasome dynamics accompanying inclusion body formation in huntington disease
    Siddhartha Mitra
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Biol Chem 284:4398-403. 2009
    ..After forming IBs, impairment is lower in neurons with IBs than in those without. These findings suggest IBs are a protective cellular response to mutant protein mediated in part by improving intracellular protein degradation...
  17. pmc The ubiquitin-proteasome pathway in Huntington's disease
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease, 1650 Owens St, San Francisco, CA94158, USA
    ScientificWorldJournal 8:421-33. 2008
    ..A number of potential mechanisms that link compromised ubiquitin-proteasome pathway function and neurodegeneration have been proposed and may offer opportunities for therapeutic intervention...
  18. pmc High-content screening of primary neurons: ready for prime time
    Aaron Daub
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, United States
    Curr Opin Neurobiol 19:537-43. 2009
    ..HCS with live-cell imaging therefore provides an unprecedented capability to detect spatiotemporal changes in cells and is particularly suited for time-dependent, stochastic processes such as neurodegenerative disorders...
  19. pmc Cytoplasmic mislocalization of TDP-43 is toxic to neurons and enhanced by a mutation associated with familial amyotrophic lateral sclerosis
    Sami J Barmada
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 30:639-49. 2010
    ..These results suggest that mutant TDP-43 is mislocalized to the cytoplasm, where it exhibits a toxic gain-of-function and induces cell death...
  20. ncbi request reprint Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death
    Montserrat Arrasate
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141, USA
    Nature 431:805-10. 2004
    ..Surprisingly, inclusion body formation predicts improved survival and leads to decreased levels of mutant huntingtin elsewhere in a neuron. Thus, inclusion body formation can function as a coping response to toxic mutant huntingtin...
  21. pmc A small-molecule scaffold induces autophagy in primary neurons and protects against toxicity in a Huntington disease model
    Andrey S Tsvetkov
    Gladstone Institute of Neurological Disease and Taube Koret Center for Huntington s Disease Research and Consortium for Fronto temporal Dementia Research, University of California, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 107:16982-7. 2010
    ..This pharmacophore should prove useful in studying autophagy in neurons and in developing therapies for neurodegenerative proteinopathies...
  22. pmc Automated microscope system for determining factors that predict neuronal fate
    Montserrat Arrasate
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 102:3840-5. 2005
    ..The ability to monitor complex processes at single-cell resolution quickly, quantitatively, and over long intervals should have wide applications for biology...
  23. pmc Protein turnover and inclusion body formation
    Siddhartha Mitra
    Gladstone Institute of Neurological Disease, San Francisco, CA 945158, USA
    Autophagy 5:1037-8. 2009
    ..These findings suggest that IB formation is a protective cellular response mediated in part by increased degradation of intracellular protein...

Research Grants17

  1. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven M Finkbeiner; Fiscal Year: 2010
    ..This project is significant because it will elucidate pathogenic mechanisms and therapeutic targets for HD, as it did during the previous period;the findings should also be relevant to Alzheimer's and Parkinson's disease. ..
  2. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2009
    ..This project is significant because it will elucidate pathogenic mechanisms and therapeutic targets for HD, as it did during the previous period; the findings should also be relevant to Alzheimer's and Parkinson's disease. ..
  3. Mechanisms of Huntingtin Induced Neurodegeneration
    Steven Finkbeiner; Fiscal Year: 2009
    ..To determine if IB formation provides a measure of protection against the deleterious effects of polyQ-expanded htt on neuronal function and survival. Specific Aim 3. To elucidate neurotoxic species of polyQ-expanded htt. ..
  4. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2007
    ..Aim 3. To determine whether htt must oligomerize or contain a contiguous stretch of pure glutamine residues to form a disease-associated conformation. ..
  5. Mechanisms of Huntingtin Induced Neurodegeneration
    Steven Finkbeiner; Fiscal Year: 2007
    ..To determine if IB formation provides a measure of protection against the deleterious effects of polyQ-expanded htt on neuronal function and survival. Specific Aim 3. To elucidate neurotoxic species of polyQ-expanded htt. ..
  6. Zeiss LSM510 Confocal Multiphoton/META Microscope
    Steven Finkbeiner; Fiscal Year: 2004
    ..The NIH will benefit because the microscope will significantly expand the abilities of the major users, enabling them to achieve funded aims and to perform previously unfeasible experiments. ..
  7. MECHANISMS OF HUNTINGTIN-INDUCED NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2003
    ..Completion of these aims should reveal new insights into general mechanisms of neurodgeneration and to the identification of potential molecular targets for new HD therapies. ..
  8. POLYGLUTAMINE CONFORMATION AND NEURODEGENERATION
    Steven Finkbeiner; Fiscal Year: 2009
    ..This project is significant because it will elucidate pathogenic mechanisms and therapeutic targets for HD, as it did during the previous period; the findings should also be relevant to Alzheimer's and Parkinson's disease. ..