<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Forte TM</submitter><funding>NHLBI NIH HHS</funding><pagination>88-93</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4820885</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>30(2)</volume><pubmed_abstract>Apolipoprotein (apo) A-V is a novel member of the class of exchangeable apo's involved in triacylglycerol (TG) homeostasis. Whereas a portion of hepatic-derived apoA-V is secreted into plasma and functions to facilitate lipoprotein lipase-mediated TG hydrolysis, another portion is recovered intracellularly, in association with cytosolic lipid droplets. Loss of apoA-V function is positively correlated with elevated plasma TG and increased risk of cardiovascular disease. Single nucleotide polymorphisms (SNP) in the &lt;i>APOA5&lt;/i> locus can affect transcription efficiency or introduce deleterious amino acid substitutions. Likewise, rare mutations in &lt;i>APOA5&lt;/i> that compromise functionality are associated with increased plasma TG and premature myocardial infarction. Genetically engineered mous</pubmed_abstract><journal>Journal of biomedical research</journal><pubmed_title>Apolipoprotein A-V gene therapy for disease prevention / treatment: a critical analysis.</pubmed_title><pmcid>PMC4820885</pmcid><funding_grant_id>R37 HL064159</funding_grant_id><pubmed_authors>Forte TM</pubmed_authors><pubmed_authors>Sharma V</pubmed_authors><pubmed_authors>Ryan RO</pubmed_authors></additional><is_claimable>false</is_claimable><name>Apolipoprotein A-V gene therapy for disease prevention / treatment: a critical analysis.</name><description>Apolipoprotein (apo) A-V is a novel member of the class of exchangeable apo's involved in triacylglycerol (TG) homeostasis. Whereas a portion of hepatic-derived apoA-V is secreted into plasma and functions to facilitate lipoprotein lipase-mediated TG hydrolysis, another portion is recovered intracellularly, in association with cytosolic lipid droplets. Loss of apoA-V function is positively correlated with elevated plasma TG and increased risk of cardiovascular disease. Single nucleotide polymorphisms (SNP) in the &lt;i>APOA5&lt;/i> locus can affect transcription efficiency or introduce deleterious amino acid substitutions. Likewise, rare mutations in &lt;i>APOA5&lt;/i> that compromise functionality are associated with increased plasma TG and premature myocardial infarction. Genetically engineered mous</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Mar</publication><modification>2025-04-04T12:39:16.388Z</modification><creation>2019-03-27T03:11:13Z</creation></dates><accession>S-EPMC4820885</accession><cross_references><pubmed>26679785</pubmed><doi>10.7555/JBR.30.20150059</doi></cross_references></HashMap>