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Second anabolic steroids, a model of the GPR120S ligand binding site was tested using point mutagenesis of the receptor. This mutagenesis validated key features of the model, including the role of Arg99 in co ordinating the agonist carboxylate group, and interactions of the agonists with the conserved transmembrane VI Trp “toggle switch” involved in receptor activation. Another mutation (Asn215) provided evidence for ligand specific binding modes within the pocket.
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Inhibition of VEGF receptor 2 signaling in the spinal cord attenuated behavioral nociceptive responses to mechanical, heat and formalin stimuli, indicating that spinal VEGF receptor 2 activation has potent pro nociceptive actions. Furthermore, intrathecal VEGF A165a resulted in mechanical and heat hyperalgesia anabolic steroids, whereas the sister inhibitory isoform VEGF A165b resulted in anti nociception. These results support a role for myelinated fiber pathways, and alternative pre mRNA splicing of factors such as VEGF A in the spinal processing of neuropathic pain.
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