<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fu Q</submitter><funding>the Natural Science Foundation of Hubei Provincial Department of Education</funding><pagination>17448069221076460</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8891909</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>18</volume><pubmed_abstract>Bone cancer pain (BCP) seriously affects the quality of life; however, due to its complex mechanism, the clinical treatment was unsatisfactory. Recent studies have showed several Rac-specific guanine nucleotide exchange factors (GEFs) that affect development and structure of neuronal processes play a vital role in the regulation of chronic pain. P-Rex2 is one of GEFs that regulate spine density, and the present study was performed to examine the effect of P-Rex2 on the development of BCP. Tumor cells implantation induced the mechanical hyperalgesia, which was accompanied by an increase in spinal protein P-Rex2, phosphorylated Rac1 (p-Rac1) and phosphorylated GluR1 (p-GluR1), and number of spines. Intrathecal injection a P-Rex2-targeting RNAi lentivirus relieved BCP and reduced the expressi</pubmed_abstract><journal>Molecular pain</journal><pubmed_title>P-Rex2 mediation of synaptic plasticity contributes to bone cancer pain.</pubmed_title><pmcid>PMC8891909</pmcid><funding_grant_id>B2020109</funding_grant_id><pubmed_authors>Wan S</pubmed_authors><pubmed_authors>Fu Q</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Su S</pubmed_authors><pubmed_authors>Huang X</pubmed_authors><pubmed_authors>Xu X</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>P-Rex2 mediation of synaptic plasticity contributes to bone cancer pain.</name><description>Bone cancer pain (BCP) seriously affects the quality of life; however, due to its complex mechanism, the clinical treatment was unsatisfactory. Recent studies have showed several Rac-specific guanine nucleotide exchange factors (GEFs) that affect development and structure of neuronal processes play a vital role in the regulation of chronic pain. P-Rex2 is one of GEFs that regulate spine density, and the present study was performed to examine the effect of P-Rex2 on the development of BCP. Tumor cells implantation induced the mechanical hyperalgesia, which was accompanied by an increase in spinal protein P-Rex2, phosphorylated Rac1 (p-Rac1) and phosphorylated GluR1 (p-GluR1), and number of spines. Intrathecal injection a P-Rex2-targeting RNAi lentivirus relieved BCP and reduced the expressi</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan-Dec</publication><modification>2025-04-04T07:50:49.043Z</modification><creation>2025-04-04T07:50:49.043Z</creation></dates><accession>S-EPMC8891909</accession><cross_references><pubmed>35083941</pubmed><doi>10.1177/17448069221076460</doi></cross_references></HashMap>