<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gordon SM</submitter><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>National Mouse Metabolic Phenotyping Center</funding><funding>WSD</funding><funding>Great Rivers Affiliate of the American Heart Association</funding><funding>NIH</funding><pagination>184-94</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4987197</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>146</volume><pubmed_abstract>&lt;h4>Unlabelled&lt;/h4>Given their association with cardiovascular disease protection, there has been intense interest in understanding the biology of high density lipoproteins (HDL). HDL is actually a family of diverse particle types, each made up of discrete - but as yet undetermined - combinations of proteins drawn from up to 95 lipophilic plasma proteins. The abundant apolipoproteins (apo) of the A class (apoA-I, apoA-II and apoA-IV) have been proposed to act as organizing platforms for auxiliary proteins, but this concept has not been systematically evaluated. We assessed the impact of genetic knock down of each platform protein on the particle size distribution of auxiliary HDL proteins. Loss of apoA-I or apoA-II massively reduced HDL lipids and changed the plasma size pattern and/or abu</pubmed_abstract><journal>Journal of proteomics</journal><pubmed_title>Impact of genetic deletion of platform apolipoproteins on the size distribution of the murine lipoproteome.</pubmed_title><pmcid>PMC4987197</pmcid><funding_grant_id>R01 HL067093</funding_grant_id><funding_grant_id>R21 HL104136</funding_grant_id><funding_grant_id>R01 HL062542</funding_grant_id><funding_grant_id>R01 HL111829</funding_grant_id><funding_grant_id>HL67093</funding_grant_id><funding_grant_id>HL111829</funding_grant_id><funding_grant_id>UL1 TR001425</funding_grant_id><funding_grant_id>HL104136</funding_grant_id><funding_grant_id>K23 HL118132</funding_grant_id><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Lu LJ</pubmed_authors><pubmed_authors>Tso P</pubmed_authors><pubmed_authors>Shah AS</pubmed_authors><pubmed_authors>Gordon SM</pubmed_authors><pubmed_authors>Zhu X</pubmed_authors><pubmed_authors>Davidson WS</pubmed_authors><pubmed_authors>Reardon CA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of genetic deletion of platform apolipoproteins on the size distribution of the murine lipoproteome.</name><description>&lt;h4>Unlabelled&lt;/h4>Given their association with cardiovascular disease protection, there has been intense interest in understanding the biology of high density lipoproteins (HDL). HDL is actually a family of diverse particle types, each made up of discrete - but as yet undetermined - combinations of proteins drawn from up to 95 lipophilic plasma proteins. The abundant apolipoproteins (apo) of the A class (apoA-I, apoA-II and apoA-IV) have been proposed to act as organizing platforms for auxiliary proteins, but this concept has not been systematically evaluated. We assessed the impact of genetic knock down of each platform protein on the particle size distribution of auxiliary HDL proteins. Loss of apoA-I or apoA-II massively reduced HDL lipids and changed the plasma size pattern and/or abu</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Sep</publication><modification>2025-04-25T20:26:52.005Z</modification><creation>2019-03-27T02:20:47Z</creation></dates><accession>S-EPMC4987197</accession><cross_references><pubmed>27385375</pubmed><doi>10.1016/j.jprot.2016.06.035</doi></cross_references></HashMap>