Casitas B-lineage lymphoma b (Cbl-b) is one of the E3 ubiquitin ligases that ubiquitinate Tropomyosin-related kinase A (TrkA), a key nerve growth factor receptor involved in the pathological pain. Here we found that Cbl-b was abundant in dorsal root ganglion (DRG) neurons of mice and co-localized with TrkA. Ubiquitination of TrkA by Cbl-b exerted a tonic negative control over the protein level of TrkA.
View Article and Find Full Text PDFThe calcium/calmodulin-dependent protein phosphase calcineurin (CaN) regulates synaptic plasticity by controlling the phosphorylation of synaptic proteins including AMPA type glutamate receptors. The regulator of calcineurin 1 (RCAN1) is characterized as an endogenous inhibitor of CaN and its dysregulation is implicated in multiple neurological disorders. However, whether RCAN1 is engaged in nociceptive processing in the spinal dorsal horn remains unrevealed.
View Article and Find Full Text PDFThe A-kinase anchoring protein 150 (AKAP150) organizes kinases and phosphatases to regulate AMPA receptors (AMPARs) that are pivotal for synaptic plasticity. AKAP150 itself undergoes S-palmitoylation. However, the roles of AKAP150 and its palmitoylation in spinal nociceptive processing remain unknown.
View Article and Find Full Text PDFMaterials (Basel)
April 2021
In order to improve the tribological properties of epoxy (EP), EP composites were prepared by filling different proportions of silicon carbide (SiC) particles and molybdenum disulfide (MoS) powder. SiC and MoS particle surfaces were modified by the silane coupling agent KH560 to improve dispersion and avoid agglomeration of the inorganic particles in the EP resin matrix. The effect of different proportions of modified MoS content on the tribological properties of SiC/EP composites, and the wear mechanism of the worn surface, were investigated when the filler content was fixed at 55 wt.
View Article and Find Full Text PDF-methyl-d-aspartate (NMDA) glutamate receptors (NMDARs) containing GluN2B subunits are prevalent early after birth in most brain regions in rodents. Upon synapse maturation, GluN2B is progressively removed from synapses, which affects NMDAR function and synaptic plasticity. Aberrant recruitment of GluN2B into mature synapses has been implicated in several neuropathologies that afflict adults.
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