Results 151 to 160 of about 2,009 (183)

Intranasal CRMP2-Ubc9 inhibitor regulates Na V 1.7 to alleviate trigeminal neuropathic pain. [PDF]

open access: yesPain
Loya-Lopez SI   +11 more
europepmc   +1 more source

Quercetin attenuated ischemic stroke induced neurodegeneration by modulating glutamatergic and synaptic signaling pathways.

open access: yesHeliyon
Shah FA   +8 more
europepmc   +1 more source

Chemical shift perturbation mapping of the Ubc9-CRMP2 interface identifies a pocket in CRMP2 amenable for allosteric modulation of Nav1.7 channels [PDF]

open access: yesChannels, 2018
Drug discovery campaigns directly targeting the voltage-gated sodium channel NaV1.7, a highly prized target in chronic pain, have not yet been clinically successful. In a differentiated approach, we demonstrated allosteric control of trafficking and activity of NaV1.7 by prevention of SUMOylation of collapsin response mediator protein 2 (CRMP2). Spinal
Liberty Francois-Moutal   +2 more
exaly   +4 more sources

Phosphorylated CRMP2 Regulates Spinal Nociceptive Neurotransmission [PDF]

open access: yesMolecular Neurobiology, 2018
The collapsin response mediator protein 2 (CRMP2) has emerged as a central node in assembling nociceptive signaling complexes involving voltage-gated ion channels. Concerted actions of post-translational modifications, phosphorylation and SUMOylation, of CRMP2 contribute to regulation of pathological pain states.
Aubin Moutal   +2 more
exaly   +3 more sources

CRMP2 Protein SUMOylation Modulates NaV1.7 Channel Trafficking [PDF]

open access: yesJournal of Biological Chemistry, 2013
Voltage-gated sodium channel (NaV) trafficking is incompletely understood. Post-translational modifications of NaVs and/or auxiliary subunits and protein-protein interactions have been posited as NaV-trafficking mechanisms. Here, we tested if modification of the axonal collapsin response mediator protein 2 (CRMP2) by a small ubiquitin-like modifier ...
Erik T Dustrude   +2 more
exaly   +3 more sources

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