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Mayadevi.M, PhD

Scientist C

+91-471-2529534

mmayadevi@rgcb.res.in

mayadevi
mayadevi

Mayadevi.M, PhD

Scientist C

+91-471-2529534

mmayadevi@rgcb.res.in

  • Profile

    • Ph.D Biotechnology (University of Kerala)
    • M. Sc (University of Kerala)
    • 2011-till date: Scientist C, Rajiv Gandhi Centre For Biotechnology
    • 2001-2011: Scientist B, Rajiv Gandhi Centre For Biotechnology
    • 1993-2001: Research Officer, Rajiv Gandhi Centre For Biotechnology
    • 1992-1993: Research Assistant, Rajiv Gandhi Centre For Development of Education, Science and Technology, Thiruvananthapuram
    • 1989-1990: Research Assistant, Baylor Research Institute, Baylor University Medical Centre, Dallas, USA
    • 1986-1989: Research Assistant, Case Western Reserve University, Cleveland, USA
    • Life Member, Society For Neurochemistry, India
    • Life Member, Indian Academy of Neurosciences
  • Research

    Mechanisms underlying Excitotoxicity

    The excitatory neurotransmitter glutamate is critical for brain functions such as learning and memory. In spite of this, an elevation in extracellular glutamate brings in an overload of calcium into the cell leading to excitotoxicity. Excitotoxic neuronal death is implicated in many neurodegenerative diseases. Prolonged exposure to glutamate can be a causative death signal for neurons in such cases. Although neuronal excitotoxicity is known to involve binding ofglutamate to NMDA receptor, resulting in successive events deleterious to neurons, there may be other extrinsic factors contributing or accelerating neuronal death which are being explored.

    Calcium/calmodulin dependent protein kinase II (CaMKII) is a downstream player in synaptic calcium signaling and is known to mediate molecular events leading to excitotoxicity. CaMKIINα is an endogenous protein inhibitor of CaMKII, the physiological functions of which are elusive. A peptide derived from CaMKIINα is widely used as an inhibitor of CaMKII. The binding of CaMKIINα to a noncatalytic site of CaMKII, may have additional functional consequences. As a collaborative project we are investigating the functions other than the inhibitory functions of the CaMKIINα inhibitor protein.

  • Publications

    1. Ramasarma, T., Rao, A. V. S., Maya Devi, M., Omkumar, R. V., Bhagyashree, K. S. and Bhat, S. V. (2015) New insights of superoxide dismutase inhibition of pyrogallol autoxidation Mol. Cell. Biochem. 400(1-2) 277-85.
    2. Prabhu Ramya. R, Suma Priya, S., Mayadevi, M. and Omkumar, R. V. (2012)  Regulation of phosphorylation at Ser-1303 of GluN2B receptor in the post synaptic density. Neurochem. Int. 61(7):981-5. 10.1016/j.neuint.2012.08.016.
    3. Mayadevi, M., Sherin, D.R, Keerthi, V.S., Rajasekharan, K.N. and Omkumar R.V. (2012). Curcumin is an inhibitor of Calcium/calmodulin dependent protein kinase II. Bioorg. Med. Chem. 20. 6040-6047
    4. Cheriyan, J., Archana, G. M., Pradeep, K. K., Mayadevi, M. and Omkumar, R.V. (2012) Effect of multimeric structure of CaMKII in the GluN2B-mediated modulation of kinetic parameters of ATP. PLoS One 7.9.e45064

    Book Chapters

    1. Mayadevi, M., Archana, G. M., Ramya R. Prabhu, and R. V. Omkumar (2012) Molecular Mechanisms in Synaptic Plasticity. Chapter in “Neuroscience – Dealing With Frontiers” Ed. Dr. Carlos M. Contreras, ISBN 979-953-307-363-6
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