<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lu R</submitter><funding>Natural Science Foundation of Shaanxi Province</funding><funding>Priority Academic Program Development of Jiangsu Higher Education Institutions</funding><funding>Ministry of Education, Culture, Sports, Science and Technology</funding><funding>National Natural Science Foundation of China</funding><funding>National Key Research and Development Program of China</funding><pagination>29-38</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6197696</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36</volume><pubmed_abstract>Rabbits (Oryctolagus cuniculus) have been the very frequently used as animal models in the study of human lipid metabolism and atherosclerosis, because they have similar lipoprotein metabolism to humans. Most of hyperlipidemia and atherosclerosis rabbit models are produced by feeding rabbits a high-cholesterol diet. Gene editing or knockout (KO) offered another means of producing rabbit models for study of the metabolism of lipids and lipoproteins. Even so, apolipoprotein (Apo)E KO rabbits must be fed a high-cholesterol diet to induce hyperlipidemia. In this study, we used the CRISPR/Cas9 system anchored exon 7 of low-density lipoprotein receptor (LDLR) in an attempt to generate KO rabbits. We designed two sgRNA sequences located in E7:g.7055-7074 and E7:g.7102-7124 of rabbit LDLR gene, re</pubmed_abstract><journal>EBioMedicine</journal><pubmed_title>Spontaneous severe hypercholesterolemia and atherosclerosis lesions in rabbits with deficiency of low-density lipoprotein receptor (LDLR) on exon 7.</pubmed_title><pmcid>PMC6197696</pmcid><funding_grant_id>81770457</funding_grant_id><funding_grant_id>2016YFE0126000</funding_grant_id><funding_grant_id>81570392</funding_grant_id><funding_grant_id>15H04718</funding_grant_id><funding_grant_id>2017JZ028</funding_grant_id><pubmed_authors>Yuan T</pubmed_authors><pubmed_authors>Zhou M</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Wu D</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors><pubmed_authors>Zhang T</pubmed_authors><pubmed_authors>He Z</pubmed_authors><pubmed_authors>Fan J</pubmed_authors><pubmed_authors>Liang J</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Lu R</pubmed_authors><pubmed_authors>Yuan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Spontaneous severe hypercholesterolemia and atherosclerosis lesions in rabbits with deficiency of low-density lipoprotein receptor (LDLR) on exon 7.</name><description>Rabbits (Oryctolagus cuniculus) have been the very frequently used as animal models in the study of human lipid metabolism and atherosclerosis, because they have similar lipoprotein metabolism to humans. Most of hyperlipidemia and atherosclerosis rabbit models are produced by feeding rabbits a high-cholesterol diet. Gene editing or knockout (KO) offered another means of producing rabbit models for study of the metabolism of lipids and lipoproteins. Even so, apolipoprotein (Apo)E KO rabbits must be fed a high-cholesterol diet to induce hyperlipidemia. In this study, we used the CRISPR/Cas9 system anchored exon 7 of low-density lipoprotein receptor (LDLR) in an attempt to generate KO rabbits. We designed two sgRNA sequences located in E7:g.7055-7074 and E7:g.7102-7124 of rabbit LDLR gene, re</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Oct</publication><modification>2025-04-18T12:07:58.807Z</modification><creation>2019-03-27T00:04:14Z</creation></dates><accession>S-EPMC6197696</accession><cross_references><pubmed>30243490</pubmed><doi>10.1016/j.ebiom.2018.09.020</doi></cross_references></HashMap>