Title : Spinal RyR2 pathway regulated by the RNA-binding protein HuD induces pain hypersensitivity in antiretroviral neuropathy.

Pub. Date : 2015 May

PMID : 25765490






6 Functional Relationships(s)
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1 Administration of ddC induced mechanical and cold allodynia, which were abolished by intrathecal administration of TMB-8, a blocker of Ca(2+) release from intracellular stores, and by ryanodine, a RyR antagonist. Zalcitabine ryanodine receptor 2 Homo sapiens
2 HuD binding to the RyR2 mRNA, the most abundant RyR isoform in the spinal cord, was demonstrated and RyR2 silencing prevented the ddC-induced neuropathic pain. Zalcitabine ryanodine receptor 2 Homo sapiens
3 HuD binding to the RyR2 mRNA, the most abundant RyR isoform in the spinal cord, was demonstrated and RyR2 silencing prevented the ddC-induced neuropathic pain. Zalcitabine ryanodine receptor 2 Homo sapiens
4 HuD binding to the RyR2 mRNA, the most abundant RyR isoform in the spinal cord, was demonstrated and RyR2 silencing prevented the ddC-induced neuropathic pain. Zalcitabine ryanodine receptor 2 Homo sapiens
5 The present findings identify a spinal RyR2 pathway activated in response to ddC administration, involving the binding activity on RyR2 mRNA by HuD. Zalcitabine ryanodine receptor 2 Homo sapiens
6 The present findings identify a spinal RyR2 pathway activated in response to ddC administration, involving the binding activity on RyR2 mRNA by HuD. Zalcitabine ryanodine receptor 2 Homo sapiens