<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Linnstaedt SD</submitter><funding>NHGRI NIH HHS</funding><funding>NIAMS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>8407-8420</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6158694</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>38(39)</volume><pubmed_abstract>Previous studies have shown that common variants of the gene coding for FK506-binding protein 51 (&lt;i>FKBP5&lt;/i>), a critical regulator of glucocorticoid sensitivity, affect vulnerability to stress-related disorders. In a previous report, &lt;i>FKBP5&lt;/i> rs1360780 was identified as a functional variant because of its effect on gene methylation. Here we report evidence for a novel functional &lt;i>FKBP5&lt;/i> allele, rs3800373. This study assessed the association between rs3800373 and post-traumatic chronic pain in 1607 women and men from two ethnically diverse human cohorts. The molecular mechanism through which rs3800373 affects adverse outcomes was established via &lt;i>in silico&lt;/i>, &lt;i>in vivo&lt;/i>, and &lt;i>in vitro&lt;/i> analyses. The rs3800373 minor allele predicted worse adverse outcomes after traum</pubmed_abstract><journal>The Journal of neuroscience : the official journal of the Society for Neuroscience</journal><pubmed_title>A Functional riboSNitch in the 3' Untranslated Region of &lt;i>FKBP5&lt;/i> Alters MicroRNA-320a Binding Efficiency and Mediates Vulnerability to Chronic Post-Traumatic Pain.</pubmed_title><pmcid>PMC6158694</pmcid><funding_grant_id>R01 AR060852</funding_grant_id><funding_grant_id>R01 GM101237</funding_grant_id><funding_grant_id>R01 HG008133</funding_grant_id><pubmed_authors>Domeier R</pubmed_authors><pubmed_authors>Lackey L</pubmed_authors><pubmed_authors>Kutchko KM</pubmed_authors><pubmed_authors>Tsai YH</pubmed_authors><pubmed_authors>Parker JS</pubmed_authors><pubmed_authors>Hendry PL</pubmed_authors><pubmed_authors>Pearson C</pubmed_authors><pubmed_authors>Rueckeis CA</pubmed_authors><pubmed_authors>Riker KD</pubmed_authors><pubmed_authors>Lewandowski C</pubmed_authors><pubmed_authors>McLean SA</pubmed_authors><pubmed_authors>McCarthy KR</pubmed_authors><pubmed_authors>Datner E</pubmed_authors><pubmed_authors>Kaushik S</pubmed_authors><pubmed_authors>Linnstaedt SD</pubmed_authors><pubmed_authors>Laederach A</pubmed_authors><pubmed_authors>Kurz MC</pubmed_authors><pubmed_authors>O'Neil B</pubmed_authors></additional><is_claimable>false</is_claimable><name>A Functional riboSNitch in the 3' Untranslated Region of &lt;i>FKBP5&lt;/i> Alters MicroRNA-320a Binding Efficiency and Mediates Vulnerability to Chronic Post-Traumatic Pain.</name><description>Previous studies have shown that common variants of the gene coding for FK506-binding protein 51 (&lt;i>FKBP5&lt;/i>), a critical regulator of glucocorticoid sensitivity, affect vulnerability to stress-related disorders. In a previous report, &lt;i>FKBP5&lt;/i> rs1360780 was identified as a functional variant because of its effect on gene methylation. Here we report evidence for a novel functional &lt;i>FKBP5&lt;/i> allele, rs3800373. This study assessed the association between rs3800373 and post-traumatic chronic pain in 1607 women and men from two ethnically diverse human cohorts. The molecular mechanism through which rs3800373 affects adverse outcomes was established via &lt;i>in silico&lt;/i>, &lt;i>in vivo&lt;/i>, and &lt;i>in vitro&lt;/i> analyses. The rs3800373 minor allele predicted worse adverse outcomes after traum</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Sep</publication><modification>2025-04-25T17:12:14.035Z</modification><creation>2019-06-06T20:13:05Z</creation></dates><accession>S-EPMC6158694</accession><cross_references><pubmed>30150364</pubmed><doi>10.1523/JNEUROSCI.3458-17.2018</doi><doi>10.1523/jneurosci.3458-17.2018</doi></cross_references></HashMap>