<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Neess D</submitter><funding>Lundbeck Foundation</funding><pagination>3460-72</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3030352</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>286(5)</volume><pubmed_abstract>The acyl-CoA-binding protein (ACBP)/diazepam binding inhibitor is an intracellular protein that binds C(14)-C(22) acyl-CoA esters and is thought to act as an acyl-CoA transporter. In vitro analyses have indicated that ACBP can transport acyl-CoA esters between different enzymatic systems; however, little is known about the in vivo function in mammalian cells. We have generated mice with targeted disruption of ACBP (ACBP(-/-)). These mice are viable and fertile and develop normally. However, around weaning, the ACBP(-/-) mice go through a crisis with overall weakness and a slightly decreased growth rate. Using microarray analysis, we show that the liver of ACBP(-/-) mice displays a significantly delayed adaptation to weaning with late induction of target genes of the sterol regulatory eleme</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.</pubmed_title><pmcid>PMC3030352</pmcid><funding_grant_id>R7-2006-648</funding_grant_id><pubmed_authors>Mandrup S</pubmed_authors><pubmed_authors>Elle IC</pubmed_authors><pubmed_authors>Pagmantidis V</pubmed_authors><pubmed_authors>Færgeman N</pubmed_authors><pubmed_authors>Bek S</pubmed_authors><pubmed_authors>Finsen B</pubmed_authors><pubmed_authors>Kruhoffer M</pubmed_authors><pubmed_authors>Bloksgaard M</pubmed_authors><pubmed_authors>Due M</pubmed_authors><pubmed_authors>Neess D</pubmed_authors><pubmed_authors>Wilbertz J</pubmed_authors><pubmed_authors>Marcher AB</pubmed_authors><pubmed_authors>Helledie T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.</name><description>The acyl-CoA-binding protein (ACBP)/diazepam binding inhibitor is an intracellular protein that binds C(14)-C(22) acyl-CoA esters and is thought to act as an acyl-CoA transporter. In vitro analyses have indicated that ACBP can transport acyl-CoA esters between different enzymatic systems; however, little is known about the in vivo function in mammalian cells. We have generated mice with targeted disruption of ACBP (ACBP(-/-)). These mice are viable and fertile and develop normally. However, around weaning, the ACBP(-/-) mice go through a crisis with overall weakness and a slightly decreased growth rate. Using microarray analysis, we show that the liver of ACBP(-/-) mice displays a significantly delayed adaptation to weaning with late induction of target genes of the sterol regulatory eleme</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Feb</publication><modification>2025-04-05T10:56:26.484Z</modification><creation>2019-06-06T22:37:41Z</creation></dates><accession>S-EPMC3030352</accession><cross_references><pubmed>21106527</pubmed><doi>10.1074/jbc.M110.161109</doi><doi>10.1074/jbc.m110.161109</doi></cross_references></HashMap>