Conrad C Alano

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Differences among cell types in NAD(+) compartmentalization: a comparison of neurons, astrocytes, and cardiac myocytes
    Conrad C Alano
    Neurology Service, Veterans Affairs Medical Center, 127 Neurology, San Francisco, CA 94121, USA
    J Neurosci Res 85:3378-85. 2007
  2. pmc NAD+ depletion is necessary and sufficient for poly(ADP-ribose) polymerase-1-mediated neuronal death
    Conrad C Alano
    Department of Neurology, University of California, San Francisco, San Francisco Veterans Affairs Medical Center, San Francisco, California 94121, USA mail
    J Neurosci 30:2967-78. 2010
  3. pmc Vincristine attenuates N-methyl-N'-nitro-N-nitrosoguanidine-induced poly-(ADP) ribose polymerase activity in cardiomyocytes
    Jianqing Zhang
    Cardiology Section, VA Medical Center, San Francisco, CA 94121, USA
    J Cardiovasc Pharmacol 55:219-26. 2010
  4. pmc High-density lipoprotein determines adult mouse cardiomyocyte fate after hypoxia-reoxygenation through lipoprotein-associated sphingosine 1-phosphate
    Rong Tao
    Veterans Affairs Medical Center and Department of Medicine, University of California, San Francisco, USA
    Am J Physiol Heart Circ Physiol 298:H1022-8. 2010
  5. pmc Neuronal Sirt3 protects against excitotoxic injury in mouse cortical neuron culture
    Sun Hee Kim
    Department of Neurology, Veterans Affairs Medical Center, San Francisco, California, United States of America
    PLoS ONE 6:e14731. 2011
  6. pmc Cardiomyocyte S1P1 receptor-mediated extracellular signal-related kinase signaling and desensitization
    Rong Tao
    Department of Medicine, Veterans Affairs Medical Center, University of California, San Francisco, CA 94121, USA
    J Cardiovasc Pharmacol 53:486-94. 2009
  7. ncbi request reprint Tricarboxylic acid cycle substrates prevent PARP-mediated death of neurons and astrocytes
    Weihai Ying
    Department of Neurology, University of California at San Francisco and Veterans Affairs Medical Center, USA
    J Cereb Blood Flow Metab 22:774-9. 2002
  8. ncbi request reprint NAD+ as a metabolic link between DNA damage and cell death
    Weihai Ying
    Department of Neurology, University of California and the Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA
    J Neurosci Res 79:216-23. 2005
  9. ncbi request reprint Poly(ADP-ribose) polymerase-1-mediated cell death in astrocytes requires NAD+ depletion and mitochondrial permeability transition
    Conrad C Alano
    Department of Neurology, University of California, San Francisco and the Veterans Affairs Medical Center, San Francisco, California 94121, USA
    J Biol Chem 279:18895-902. 2004
  10. pmc Minocycline protects cardiac myocytes against simulated ischemia–reperfusion injury by inhibiting poly(ADP-ribose) polymerase-1
    Rong Tao
    Cardiology Section, San Francisco VA Medical Center and UCSF, San Francisco, CA, USA
    J Cardiovasc Pharmacol 56:659-68. 2010

Collaborators

Detail Information

Publications16

  1. ncbi request reprint Differences among cell types in NAD(+) compartmentalization: a comparison of neurons, astrocytes, and cardiac myocytes
    Conrad C Alano
    Neurology Service, Veterans Affairs Medical Center, 127 Neurology, San Francisco, CA 94121, USA
    J Neurosci Res 85:3378-85. 2007
    ..These results also suggest large differences in the mitochondrial and cytosolic compartmentalization of NAD(+) in these cell types...
  2. pmc NAD+ depletion is necessary and sufficient for poly(ADP-ribose) polymerase-1-mediated neuronal death
    Conrad C Alano
    Department of Neurology, University of California, San Francisco, San Francisco Veterans Affairs Medical Center, San Francisco, California 94121, USA mail
    J Neurosci 30:2967-78. 2010
    ..These results establish NAD(+) depletion as a causal event in PARP-1-mediated cell death and place NAD(+) depletion and glycolytic failure upstream of mitochondrial AIF release...
  3. pmc Vincristine attenuates N-methyl-N'-nitro-N-nitrosoguanidine-induced poly-(ADP) ribose polymerase activity in cardiomyocytes
    Jianqing Zhang
    Cardiology Section, VA Medical Center, San Francisco, CA 94121, USA
    J Cardiovasc Pharmacol 55:219-26. 2010
    ..We conclude that VCR protects cardiomyocytes from MNNG toxicity by regulating PARP-1 activation, intracellular energy metabolism, and prosurvival signaling...
  4. pmc High-density lipoprotein determines adult mouse cardiomyocyte fate after hypoxia-reoxygenation through lipoprotein-associated sphingosine 1-phosphate
    Rong Tao
    Veterans Affairs Medical Center and Department of Medicine, University of California, San Francisco, USA
    Am J Physiol Heart Circ Physiol 298:H1022-8. 2010
    ....
  5. pmc Neuronal Sirt3 protects against excitotoxic injury in mouse cortical neuron culture
    Sun Hee Kim
    Department of Neurology, Veterans Affairs Medical Center, San Francisco, California, United States of America
    PLoS ONE 6:e14731. 2011
    ..Here, we demonstrated the presence of Sirt3 in neurons, and characterized the role of Sirt3 in neuron survival under NMDA-induced excitotoxicity...
  6. pmc Cardiomyocyte S1P1 receptor-mediated extracellular signal-related kinase signaling and desensitization
    Rong Tao
    Department of Medicine, Veterans Affairs Medical Center, University of California, San Francisco, CA 94121, USA
    J Cardiovasc Pharmacol 53:486-94. 2009
    ..Thus, exogenous S1P induces rapid and reversible S1P1-mediated ERK phosphorylation. S1P-induced adult mouse cardiomyocyte survival requires ERK activation mediated via an S1P1-Gi pathway...
  7. ncbi request reprint Tricarboxylic acid cycle substrates prevent PARP-mediated death of neurons and astrocytes
    Weihai Ying
    Department of Neurology, University of California at San Francisco and Veterans Affairs Medical Center, USA
    J Cereb Blood Flow Metab 22:774-9. 2002
    ..Delivery of alternative substrates may be a promising strategy for delayed treatment of PARP1-mediated cell death in ischemia and other disorders...
  8. ncbi request reprint NAD+ as a metabolic link between DNA damage and cell death
    Weihai Ying
    Department of Neurology, University of California and the Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA
    J Neurosci Res 79:216-23. 2005
    ..This cell death pathway is particularly germane to brain because glucose is normally the only metabolic substrate that is transported rapidly across the blood-brain barrier...
  9. ncbi request reprint Poly(ADP-ribose) polymerase-1-mediated cell death in astrocytes requires NAD+ depletion and mitochondrial permeability transition
    Conrad C Alano
    Department of Neurology, University of California, San Francisco and the Veterans Affairs Medical Center, San Francisco, California 94121, USA
    J Biol Chem 279:18895-902. 2004
    ..These results suggest that NAD(+) depletion and MPT are necessary intermediary steps linking PARP-1 activation to AIF translocation and cell death...
  10. pmc Minocycline protects cardiac myocytes against simulated ischemia–reperfusion injury by inhibiting poly(ADP-ribose) polymerase-1
    Rong Tao
    Cardiology Section, San Francisco VA Medical Center and UCSF, San Francisco, CA, USA
    J Cardiovasc Pharmacol 56:659-68. 2010
    ..Therefore, we propose that the protective effect of minocycline on cardiac myocyte survival is the result of inhibition of PARP-1 activity...
  11. ncbi request reprint Expression and activity of poly(ADP-ribose) glycohydrolase in cultured astrocytes, neurons, and C6 glioma cells
    Mary B Sevigny
    Department of Neurology, University of California at San Francisco and Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA
    Brain Res Mol Brain Res 117:213-20. 2003
    ..Western blotting revealed full-length PARG as well as lower molecular weight PARG species in all four cell types...
  12. ncbi request reprint Players in the PARP-1 cell-death pathway: JNK1 joins the cast
    Conrad C Alano
    Department of Neurology, University of California and Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA
    Trends Biochem Sci 31:309-11. 2006
    ..A recent report by Xu and colleagues suggests that Jun kinase-1, a member of the mitogen-activated protein kinase family, might have a crucial role in this signaling pathway...
  13. pmc Minocycline inhibits poly(ADP-ribose) polymerase-1 at nanomolar concentrations
    Conrad C Alano
    Department of Neurology, University of California San Francisco and Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA
    Proc Natl Acad Sci U S A 103:9685-90. 2006
    ..The neuroprotective and antiinflammatory effects of minocycline and other tetracycline derivatives may be attributable to PARP-1 inhibition in some settings...
  14. pmc Pyrroloquinoline quinone preserves mitochondrial function and prevents oxidative injury in adult rat cardiac myocytes
    Rong Tao
    Cardiology Section, San Francisco VA Medical Center and UCSF, San Francisco, CA, USA
    Biochem Biophys Res Commun 363:257-62. 2007
    ..Our results provide direct evidence that PQQ reduces oxidative stress, mitochondrial dysfunction, and cell death in isolated adult rat cardiomyocytes. These findings provide new insight into the mechanisms of PQQ action in the heart...
  15. pmc Zinc inhibits astrocyte glutamate uptake by activation of poly(ADP-ribose) polymerase-1
    Sang Won Suh
    Department of Neurology, University of California, San Francisco, California, USA
    Mol Med 13:344-9. 2007
    ..These findings suggest that release of Zn2+ from neurons during brain insults could induce PARP-1 activation in astrocytes, leading to impaired glutamate uptake and exacerbation of neuronal injury...
  16. ncbi request reprint Mitochondrial permeability transition and calcium dynamics in striatal neurons upon intense NMDA receptor activation
    Conrad C Alano
    Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, New York 14642, USA
    J Neurochem 80:531-8. 2002
    ..The presented results indicate that MPT can be detected in living neurons using fluorescent Ca2+ indicators, which would allow the study of the physiological role of MPT in cell death...