Subhas C Biswas

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. ncbi request reprint Nerve growth factor (NGF) down-regulates the Bcl-2 homology 3 (BH3) domain-only protein Bim and suppresses its proapoptotic activity by phosphorylation
    Subhas 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
  2. doi request reprint Glucagon-like peptide-1 (GLP-1) diminishes neuronal degeneration and death caused by NGF deprivation by suppressing Bim induction
    Subhas 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
  3. ncbi request reprint Pro-apoptotic Bim induction in response to nerve growth factor deprivation requires simultaneous activation of three different death signaling pathways
    Subhas 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
  4. ncbi request reprint Bim is a direct target of a neuronal E2F-dependent apoptotic pathway
    Subhas 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
  5. ncbi request reprint Puma and p53 play required roles in death evoked in a cellular model of Parkinson disease
    Subhas 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
  6. ncbi request reprint Bim is elevated in Alzheimer's disease neurons and is required for beta-amyloid-induced neuronal apoptosis
    Subhas 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
  7. ncbi request reprint 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 inactivation
    Cristina Malagelada
    Department of Pathology and Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA
    J Neurosci 26:9996-10005. 2006
  8. ncbi request reprint B-myb and C-myb play required roles in neuronal apoptosis evoked by nerve growth factor deprivation and DNA damage
    David 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
  9. pmc Sertad1 plays an essential role in developmental and pathological neuron death
    Subhas 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
  10. pmc Cell cycle molecules define a pathway required for neuron death in development and disease
    Lloyd 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

Detail Information

Publications11

  1. ncbi request reprint Nerve growth factor (NGF) down-regulates the Bcl-2 homology 3 (BH3) domain-only protein Bim and suppresses its proapoptotic activity by phosphorylation
    Subhas 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...
  2. doi request reprint Glucagon-like peptide-1 (GLP-1) diminishes neuronal degeneration and death caused by NGF deprivation by suppressing Bim induction
    Subhas 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...
  3. ncbi request reprint Pro-apoptotic Bim induction in response to nerve growth factor deprivation requires simultaneous activation of three different death signaling pathways
    Subhas 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...
  4. ncbi request reprint Bim is a direct target of a neuronal E2F-dependent apoptotic pathway
    Subhas 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...
  5. ncbi request reprint Puma and p53 play required roles in death evoked in a cellular model of Parkinson disease
    Subhas 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...
  6. ncbi request reprint Bim is elevated in Alzheimer's disease neurons and is required for beta-amyloid-induced neuronal apoptosis
    Subhas 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...
  7. ncbi request reprint 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 inactivation
    Cristina Malagelada
    Department of Pathology and Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA
    J Neurosci 26:9996-10005. 2006
    ....
  8. ncbi request reprint B-myb and C-myb play required roles in neuronal apoptosis evoked by nerve growth factor deprivation and DNA damage
    David 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...
  9. pmc Sertad1 plays an essential role in developmental and pathological neuron death
    Subhas 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...
  10. pmc Cell cycle molecules define a pathway required for neuron death in development and disease
    Lloyd 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...
  11. ncbi request reprint Association of LAR-like receptor protein tyrosine phosphatases with an enabled homolog in Hirudo medicinalis
    Subhas C Biswas
    Department of Biological Sciences, Columbia University, New York, New York 10027, USA
    Mol Cell Neurosci 21:657-70. 2002
    ..Additionally, RNA interference (RNAi) of HmLAR1 in intact leech embryos leads to the hyperphosphorylation of Lena. We propose, therefore, that Lena is an in vivo substrate of HmLAR1 in neurons and perhaps of HmLAR2 in the Comb cells...