<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lu H</submitter><funding>NEI NIH HHS</funding><funding>NIDA NIH HHS</funding><funding>NIAAA NIH HHS</funding><pagination>4132-42</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3175941</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>52(7)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>To use a systematic genetics approach to investigate the regulation of Gpnmb, a gene that contributes to pigmentary dispersion syndrome (PDS) and pigmentary glaucoma (PG) in the DBA/2J (D2) mouse.&lt;h4>Methods&lt;/h4>Global patterns of gene expression were studied in whole eyes of a large family of BXD mouse strains (n = 67) generated by crossing the PDS- and PG-prone parent (DBA/2J) with a resistant strain (C57BL/6J). Quantitative trait locus (eQTL) mapping methods and gene set analysis were used to evaluate Gpnmb coexpression networks in wild-type and mutant cohorts.&lt;h4>Results&lt;/h4>The level of Gpnmb expression was associated with a highly significant cis-eQTL at the location of the gene itself. This autocontrol of Gpnmb is likely to be a direct consequence of the known premat</pubmed_abstract><journal>Investigative ophthalmology &amp; visual science</journal><pubmed_title>Genetic dissection of the Gpnmb network in the eye.</pubmed_title><pmcid>PMC3175941</pmcid><funding_grant_id>AA017590</funding_grant_id><funding_grant_id>U01 AA014425</funding_grant_id><funding_grant_id>EY017841</funding_grant_id><funding_grant_id>R01 EY021200</funding_grant_id><funding_grant_id>P30 EY013080</funding_grant_id><funding_grant_id>P20 DA021131</funding_grant_id><funding_grant_id>R01 EY017841-04</funding_grant_id><funding_grant_id>P30EY013080</funding_grant_id><funding_grant_id>EY021200</funding_grant_id><funding_grant_id>AA014425</funding_grant_id><funding_grant_id>U01 AA017590</funding_grant_id><funding_grant_id>R01 EY017841</funding_grant_id><funding_grant_id>DA021131</funding_grant_id><pubmed_authors>Lu L</pubmed_authors><pubmed_authors>Jablonski MM</pubmed_authors><pubmed_authors>Sahu S</pubmed_authors><pubmed_authors>Lu H</pubmed_authors><pubmed_authors>Guan H</pubmed_authors><pubmed_authors>Pullen M</pubmed_authors><pubmed_authors>Williams RW</pubmed_authors><pubmed_authors>Geisert EE</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic dissection of the Gpnmb network in the eye.</name><description>&lt;h4>Purpose&lt;/h4>To use a systematic genetics approach to investigate the regulation of Gpnmb, a gene that contributes to pigmentary dispersion syndrome (PDS) and pigmentary glaucoma (PG) in the DBA/2J (D2) mouse.&lt;h4>Methods&lt;/h4>Global patterns of gene expression were studied in whole eyes of a large family of BXD mouse strains (n = 67) generated by crossing the PDS- and PG-prone parent (DBA/2J) with a resistant strain (C57BL/6J). Quantitative trait locus (eQTL) mapping methods and gene set analysis were used to evaluate Gpnmb coexpression networks in wild-type and mutant cohorts.&lt;h4>Results&lt;/h4>The level of Gpnmb expression was associated with a highly significant cis-eQTL at the location of the gene itself. This autocontrol of Gpnmb is likely to be a direct consequence of the known premat</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jun</publication><modification>2025-04-05T09:13:57.456Z</modification><creation>2019-03-27T00:44:05Z</creation></dates><accession>S-EPMC3175941</accession><cross_references><pubmed>21398278</pubmed><doi>10.1167/iovs.10-6493</doi></cross_references></HashMap>