Department of Pharmacology,
Feinberg School of Medicine,
Department of Pharmacology, Feinberg School of Medicine
Antonio Sanz-Clemente is an Assistant Professor of Pharmacology, at Feinberg School of Medicine, Northwestern University in Chicago, Illinois. He received his Ph.D. in biochemistry from the University of Zaragoza (Spain).
During Dr. Sanz-Clemente’s training, he developed a keen focus on research that encompasses regulation of synaptic proteins trafficking by post-translational modifications and its consequences for synaptic function. As a post-doctoral fellow in Katherine Roche’s lab at the National Institute of Neurological Disorders and Stroke (NINDS) he studied the molecular mechanisms underlying the regulation of glutamate receptors. In particular, Dr. Sanz-Clemente identified the molecular events that control the NMDA-type of glutamate receptors during development and contribute to synaptic maturation.
Dr. Sanz-Clemente received a K99 Pathway to Independence Award from the NIH, and in 2014 he was recruited as faculty at Northwestern University. The Sanz-Clemente Lab utilizes a multidisciplinary approach including biochemistry, cellular and molecular biology, pharmacology as well as a variety of imaging techniques for elucidating how synaptic receptors are controlled during development, in response to experience or other stimuli and what is their impact on synaptic function. Similarly, his research program investigates how the dysregulation of these mechanisms lead to synaptic alterations and, eventually, to neurological disorders.
Abeta oligomer-induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer's disease.
The Journal of neuroscience : the official journal of the Society for Neuroscience Jan, 2007 | Pubmed ID: 17251419
Dynamic Regulation of N-Methyl-d-aspartate (NMDA) and α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors by Posttranslational Modifications.
The Journal of biological chemistry Nov, 2015 | Pubmed ID: 26453298
Loss of M1 Receptor Dependent Cholinergic Excitation Contributes to mPFC Deactivation in Neuropathic Pain.
The Journal of neuroscience : the official journal of the Society for Neuroscience 03, 2017 | Pubmed ID: 28137966
A Rare Variant Identified Within the GluN2B C-Terminus in a Patient with Autism Affects NMDA Receptor Surface Expression and Spine Density.
The Journal of neuroscience : the official journal of the Society for Neuroscience 04, 2017 | Pubmed ID: 28283559
NMDAR-Activated PP1 Dephosphorylates GluN2B to Modulate NMDAR Synaptic Content.
Cell reports Jul, 2019 | Pubmed ID: 31291571
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