{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Neess D"],"funding":["Lundbeck Foundation"],"pagination":["3460-72"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3030352"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["286(5)"],"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"],"journal":["The Journal of biological chemistry"],"pubmed_title":["Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning."],"pmcid":["PMC3030352"],"funding_grant_id":["R7-2006-648"],"pubmed_authors":["Mandrup S","Elle IC","Pagmantidis V","Færgeman N","Bek S","Finsen B","Kruhoffer M","Bloksgaard M","Due M","Neess D","Wilbertz J","Marcher AB","Helledie T"],"additional_accession":[]},"is_claimable":false,"name":"Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.","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","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Feb","modification":"2025-04-05T10:56:26.484Z","creation":"2019-06-06T22:37:41Z"},"accession":"S-EPMC3030352","cross_references":{"pubmed":["21106527"],"doi":["10.1074/jbc.M110.161109","10.1074/jbc.m110.161109"]}}