Paul, Surojit

selected publications

academic article
- Aging is associated with dimerization and inactivation of the brain-enriched tyrosine phosphatase STEP.. Neurobiology of aging. 41:25-38. 2016
- Zn2+-dependent activation of the Trk signaling pathway induces phosphorylation of the brain-enriched tyrosine phosphatase STEP: molecular basis for Zn2+-induced ERK MAPK activation. 2015
- Novel crosstalk between ERK MAPK and p38 MAPK leads to homocysteine-NMDA receptor-mediated neuronal cell death. 2013
- Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia. 2013
- Dephosphorylation of specific sites in the kinase-specificity sequence domain leads to ubiquitin-mediated degradation of the tyrosine phosphatase STEP.. The Biochemical journal. 440:115-125. 2011
- Oxidative stress-induced oligomerization inhibits the activity of the non-receptor tyrosine phosphatase STEP61. 2011
- NR2B-NMDA receptor mediated modulation of the tyrosine phosphatase STEP regulates glutamate induced neuronal cell death. 2010
- NR2B-NMDA receptor-mediated increases in intracellular Ca2+ concentration regulate the tyrosine phosphatase, STEP, and ERK MAP kinase signaling. 2010
- Knockout of striatal enriched protein tyrosine phosphatase in mice results in increased ERK1/2 phosphorylation.. Synapse (New York, N.Y.). 63:69-81. 2009
- The striatal-enriched protein tyrosine phosphatase gates long-term potentiation and fear memory in the lateral amygdala.. Biological psychiatry. 61:1049-1061. 2007
- Regulation of NMDA receptor trafficking by amyloid-beta.. Nature neuroscience. 8:1051-1058. 2005
- Regulation of a protein phosphatase cascade allows convergent dopamine and glutamate signals to activate ERK in the striatum.. Proceedings of the National Academy of Sciences of the United States of America. 102:491-496. 2005
- NMDA-mediated activation of the tyrosine phosphatase STEP regulates the duration of ERK signaling.. Nature neuroscience. 6:34-42. 2003
- The Dopamine/D1 receptor mediates the phosphorylation and inactivation of the protein tyrosine phosphatase STEP via a PKA-dependent pathway. 2000

research overview

Research Interests
- Glutamatergic signaling pathways in the CNS
- Protein tyrosine phosphatases and neurological disorders
- Oxidative stress and aging

Research Summary
Research in my laboratory focuses on understanding the cellular mechanisms of neuronal injury and development of strategies for intervention in neurological disorders related to excitotoxicity and oxidative stress.

Excitotoxicity refers to the deleterious effects of overstimulation of the neurotransmitter glutamate. Excessive neuronal Ca2+ entry and activation of series of Ca2+ dependent enzymes along with enhanced oxidative stress induce excitotoxic neuronal cell death. Excitotoxicity is known to be involved in several neurological diseases, including focal cerebral ischemia, traumatic brain injury, Huntington’s chorea and amyotrophic lateral sclerosis. To evaluate the role of the brain-specific tyrosine phosphatase STEP (STriatal Enriched Phosphatase) in neurological disorders related to excitotoxicity we use a broad range of interdisciplinary approaches, including neuronal cultures, rodent models of cerebral ischemia, mouse genetic models, biochemical, molecular, immunohistochemical, behavioral and magnetic resonance imaging strategies.

Our earlier work showed that the activity and stability of STEP is tightly regulated by several post-translational modifications that include phosphorylation, polyubiquitination and intermolecular dimerization. The neurotransmitters dopamine and glutamate play critical roles in regulating the activity of STEP. Additional studies using cell culture models of excitotoxicity and hypoxia-reoxygenation injury as well as an animal model of focal cerebral ischemia demonstrated a role of STEP in neuroprotection through down regulation of p38 mitogen activated protein kinase, a stress-activated kinase that is involved in neuroinflammation and death.

Our current focus is to elucidate additional signaling pathways that regulate the activity of STEP and identify novel target molecules that are modulated by STEP signaling. We are also evaluating whether a STEP-derived peptide could reduce the consequences of ischemic injury and impart long-term neuroprotection. The STEP KO mice are also being used to evaluate the molecular basis of exacerbated ischemic brain injury in the absence of STEP. Another interest of the laboratory is to evaluate the role of STEP in regulating the key pathways affected by oxidative stress during aging and age-associated increase in hypertension.

education and training

awards and honors

Young Investigator Award, conferred by National Association for Research on Schizophrenia and Depression, 2004

full name

Surojit Paul

mailing address

Department of Neurology, 1, University of New Mexico, MSC 116035

Albuquerque, New Mexico 87131

United States of America

VIVO

Paul, Surojit Associate Professor

Positions

Publications

selected publications

academic article

Research

research overview

Background

education and training

awards and honors

Contact

full name

mailing address