Brett Langley

Summary

Affiliation: Weill Medical College of Cornell University
Country: USA

Publications

  1. ncbi request reprint Remodeling chromatin and stress resistance in the central nervous system: histone deacetylase inhibitors as novel and broadly effective neuroprotective agents
    Brett Langley
    Burke Medical Research Institute, White Plains, NY 10605, USA
    Curr Drug Targets CNS Neurol Disord 4:41-50. 2005
  2. pmc Sirtuin deacetylases as therapeutic targets in the nervous system
    Brett Langley
    The Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, 10605, USA
    Neurotherapeutics 10:605-20. 2013
  3. doi request reprint Specific acetylation of p53 by HDAC inhibition prevents DNA damage-induced apoptosis in neurons
    Camille Brochier
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 33:8621-32. 2013
  4. pmc HDAC6 is a target for protection and regeneration following injury in the nervous system
    Mark A Rivieccio
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Proc Natl Acad Sci U S A 106:19599-604. 2009
  5. pmc Small molecule activation of adaptive gene expression: tilorone or its analogs are novel potent activators of hypoxia inducible factor-1 that provide prophylaxis against stroke and spinal cord injury
    Rajiv R Ratan
    Burke Cornell Medical Research Institute, Weill Medical College of Cornell University, White Plains, NY 10605, USA
    Ann N Y Acad Sci 1147:383-94. 2008
  6. pmc Harnessing hypoxic adaptation to prevent, treat, and repair stroke
    Rajiv R Ratan
    Winifred Masterson Burke Medical Research Institute, White Plains, NY 10605, USA
    J Mol Med (Berl) 85:1331-8. 2007
  7. doi request reprint Targeting histone deacetylases as a multifaceted approach to treat the diverse outcomes of stroke
    Brett Langley
    Burke Cornell Medical Research Institute, 785 Mamaroneck Road, White Plains, NY 10605, USA
    Stroke 40:2899-905. 2009
  8. pmc Putting the 'HAT' back on survival signalling: the promises and challenges of HDAC inhibition in the treatment of neurological conditions
    Sama F Sleiman
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, 10605 NY, USA
    Expert Opin Investig Drugs 18:573-84. 2009
  9. pmc Histone deacetylase inhibitors de-repress tyrosine hydroxylase expression in the olfactory bulb and rostral migratory stream
    Yosuke Akiba
    Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    Biochem Biophys Res Commun 393:673-7. 2010
  10. pmc Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection
    Brett Langley
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 28:163-76. 2008

Collaborators

Detail Information

Publications22

  1. ncbi request reprint Remodeling chromatin and stress resistance in the central nervous system: histone deacetylase inhibitors as novel and broadly effective neuroprotective agents
    Brett Langley
    Burke Medical Research Institute, White Plains, NY 10605, USA
    Curr Drug Targets CNS Neurol Disord 4:41-50. 2005
    ..These studies demonstrate that pharmacological HDAC inhibition is a promising therapeutic approach for the treatment of a range of central nervous system disorders...
  2. pmc Sirtuin deacetylases as therapeutic targets in the nervous system
    Brett Langley
    The Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, 10605, USA
    Neurotherapeutics 10:605-20. 2013
    ..Lastly, we highlight the numerous studies suggesting that sirtuins are efficacious therapeutic targets in neurodegenerative disease and injury...
  3. doi request reprint Specific acetylation of p53 by HDAC inhibition prevents DNA damage-induced apoptosis in neurons
    Camille Brochier
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 33:8621-32. 2013
    ....
  4. pmc HDAC6 is a target for protection and regeneration following injury in the nervous system
    Mark A Rivieccio
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Proc Natl Acad Sci U S A 106:19599-604. 2009
    ..Together, these findings define HDAC6 as a potential nontoxic therapeutic target for ameliorating CNS injury characterized by oxidative stress-induced neurodegeneration and insufficient axonal regeneration...
  5. pmc Small molecule activation of adaptive gene expression: tilorone or its analogs are novel potent activators of hypoxia inducible factor-1 that provide prophylaxis against stroke and spinal cord injury
    Rajiv R Ratan
    Burke Cornell Medical Research Institute, Weill Medical College of Cornell University, White Plains, NY 10605, USA
    Ann N Y Acad Sci 1147:383-94. 2008
    ..Altogether these findings identify tilorone as a novel and potent modulator of HIF-mediated gene expression in neurons with neuroprotective properties...
  6. pmc Harnessing hypoxic adaptation to prevent, treat, and repair stroke
    Rajiv R Ratan
    Winifred Masterson Burke Medical Research Institute, White Plains, NY 10605, USA
    J Mol Med (Berl) 85:1331-8. 2007
    ..The breadth and depth of this homeostatic program offers a hopeful alternative to the current pessimism towards stroke therapeutics...
  7. doi request reprint Targeting histone deacetylases as a multifaceted approach to treat the diverse outcomes of stroke
    Brett Langley
    Burke Cornell Medical Research Institute, 785 Mamaroneck Road, White Plains, NY 10605, USA
    Stroke 40:2899-905. 2009
    ..Together, the findings suggest that HDAC inhibition is a strategy capable of targeting diverse pathophysiologies of stroke with a wide therapeutic window...
  8. pmc Putting the 'HAT' back on survival signalling: the promises and challenges of HDAC inhibition in the treatment of neurological conditions
    Sama F Sleiman
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, 10605 NY, USA
    Expert Opin Investig Drugs 18:573-84. 2009
    ..Despite the fact that HDAC inhibitors are in an advanced stage of development, we suggest other approaches to modulating HDAC function that may be less toxic and more efficacious than the canonical agents developed so far...
  9. pmc Histone deacetylase inhibitors de-repress tyrosine hydroxylase expression in the olfactory bulb and rostral migratory stream
    Yosuke Akiba
    Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    Biochem Biophys Res Commun 393:673-7. 2010
    ....
  10. pmc Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection
    Brett Langley
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 28:163-76. 2008
    ....
  11. pmc Controlled enzymatic production of astrocytic hydrogen peroxide protects neurons from oxidative stress via an Nrf2-independent pathway
    RENEE E HASKEW-LAYTON
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, The Burke Medical Research Institute, White Plains, NY 10605, USA
    Proc Natl Acad Sci U S A 107:17385-90. 2010
    ..These findings demonstrate the utility of rgDAAO for spatially and temporally controlling intracellular H(2)O(2) concentrations to uncover unique astrocyte-dependent neuroprotective mechanisms...
  12. pmc Chromatin modifications associated with DNA double-strand breaks repair as potential targets for neurological diseases
    Camille Brochier
    The Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, 10605, USA
    Neurotherapeutics 10:817-30. 2013
    ..Finally, we suggest that understanding the epigenetic modifications specific to neuronal DNA repair is crucial for the development of efficient neurotherapeutic strategies. ..
  13. ncbi request reprint Translation of ischemic preconditioning to the patient: prolyl hydroxylase inhibition and hypoxia inducible factor-1 as novel targets for stroke therapy
    Rajiv R Ratan
    Department of Neurology and Neuroscience, Burke Cornell Medical Research Institute, Weill Medical College of Cornell, White Plains, NY 10605, USA
    Stroke 35:2687-9. 2004
    ..Here, we review evidence suggesting that the HIF-1 prolyl hyroxylases are inhibited during ischemic preconditioning and that pharmacological inhibitors of these enzymes are viable targets for stroke therapy...
  14. ncbi request reprint Neuroprotective effects of phenylbutyrate in the N171-82Q transgenic mouse model of Huntington's disease
    Gabriella Gardian
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, New York 10021, USA
    J Biol Chem 280:556-63. 2005
    ....
  15. ncbi request reprint Proteolytic processing of myostatin is auto-regulated during myogenesis
    Craig McFarlane
    AgResearch, East Street, Hamilton, New Zealand
    Dev Biol 283:58-69. 2005
    ....
  16. ncbi request reprint Titin-cap associates with, and regulates secretion of, Myostatin
    Gina Nicholas
    Animal Genomics, AgResearch, East Street, Hamilton, New Zealand
    J Cell Physiol 193:120-31. 2002
    ..These results suggest that T-cap, by interacting with Myostatin, controls Myostatin secretion in myogenic precursor cells without affecting the processing step of precursor Myostatin...
  17. ncbi request reprint Myostatin inhibits myoblast differentiation by down-regulating MyoD expression
    Brett Langley
    Animal Genomics, AgResearch, Private Bag 3123, East Street, Hamilton, New Zealand
    J Biol Chem 277:49831-40. 2002
    ....
  18. ncbi request reprint Myostatin inhibits rhabdomyosarcoma cell proliferation through an Rb-independent pathway
    Brett Langley
    Animal Genomics, AgResearch, Private Bag 3123, East Street, Hamilton, New Zealand
    Oncogene 23:524-34. 2004
    ..These results suggest that myostatin could potentially be used as an inhibitor of RMS proliferation and define a previously uncharacterized, Rb-independent mechanism for the inhibition of muscle precursor cell proliferation by myostatin...
  19. ncbi request reprint Oxidative stress-induced death in the nervous system: cell cycle dependent or independent?
    Brett Langley
    Department of Neurology, Harvard Medical School and the Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    J Neurosci Res 77:621-9. 2004
    ..The determining factor for which or how many pathways are induced appears to be context dependent and determined by the level and duration of oxidative stress...
  20. ncbi request reprint Novel roles for arginase in cell survival, regeneration, and translation in the central nervous system
    Philipp S Lange
    Department of Neurology, Harvard Medical School and the Beth Israel Deaconess Medical Center, Boston MA 02115, USA
    J Nutr 134:2812S-2817S; discussion 2818S-2819S. 2004
    ..Beyond molecular mechanisms, this review will also include relevant clinical findings in patients with neurodegenerative diseases...
  21. ncbi request reprint Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis
    Sandra Camelo
    Laboratory of Transcriptional and Immune Regulation, Brigham and Women s Hospital, Department of Neurology, Harvard Medical School, Boston, MA 02139, USA
    J Neuroimmunol 164:10-21. 2005
    ..A transcriptional imbalance in MS may contribute to immune dysregulation and neurodegeneration, and we identify HDAC inhibition as a transcriptional intervention to ameliorate this imbalance...
  22. ncbi request reprint Single cysteine to tyrosine transition inactivates the growth inhibitory function of Piedmontese myostatin
    Carole Berry
    Animal Genomics, AgResearch, Hamilton, New Zealand
    Am J Physiol Cell Physiol 283:C135-41. 2002
    ..This mutation also appears to affect either processing or stability of mature myostatin without altering the secretion of myostatin...