Molecular mechanisms of type III hyperlipoproteinemia: The contribution of the carboxy-terminal domain of ApoE can account for the dyslipidemia that is associated with the E2/E2 phenotype.

doi:10.1021/bi0271796

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Back to search

Article

Molecular mechanisms of type III hyperlipoproteinemia: The contribution of the carboxy-terminal domain of ApoE can account for the dyslipidemia that is associated with the E2/E2 phenotype.

Biochemistry - 26 Aug 2003

Kypreos Kyriakos E, Li Xiaoping, van Dijk Ko Willems, Havekes Louis M, Zannis Vassilis I

Abstract excerpt

Apolipoprotein E2, which has an R158 for C substitution, has reduced affinity for the LDL receptor and is associated with type III hyperlipoproteinemia in humans. Consistent with these observations, we have found that following adenovirus-mediated gene transfer, full-length apoE2 aggravates the hypercholesterolemia and induces hypertriglyceridemia in E-deficient mice and induces combined hyperlipidemia in C57BL/6...

Topics

Adenoviridae
Animals
Apolipoprotein E2
Apolipoproteins E
Biological Transport, Active
CHO Cells
Cholesterol
Cricetinae
Female
Genes, Dominant
Humans

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Hyperlipidemias

Hyperlipoproteinemia Type III

Lipolysis

Lipoprotein Lipase

Lipoproteins, VLDL

Liver

Mice

Source

Open in PubMed

Identifiers

PMID: 12924933
DOI: 10.1021/bi0271796

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Molecular mechanisms of type III hyperlipoproteinemia: The contribution of the carboxy-terminal domain of ApoE can account for the dyslipidemia that is associated with the E2/E2 phenotype.PMID 12924933Read ↗

Molecular etiology of a dominant form of type III hyperlipoproteinemia caused by R142C substitution in apoE4.Semantic proximity Read ↗

Genetic factors precipitating type III hyperlipoproteinemia in hypolipidemic transgenic mice expressing human apolipoprotein E2.Semantic proximity Read ↗

Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia): questions, quandaries, and paradoxesSemantic proximity Read ↗

Hypolipidemic and hyperlipidemic phenotypes in transgenic mice expressing human apolipoprotein E2.Semantic proximity Read ↗

Type III hyperlipoproteinemia and spontaneous atherosclerosis in mice resulting from gene replacement of mouse Apoe with human Apoe*2.Semantic proximity Read ↗

ApoB-48 and apoB-100 differentially influence the expression of type-III hyperlipoproteinemia in APOE*2 mice.Semantic proximity Read ↗

A rare gain of function variant of hepatic lipase attenuates hypercholesterolaemia and atherosclerosis in mice via an LDL receptor-independent mechanism.Semantic proximity Read ↗

Defective VLDL metabolism and severe atherosclerosis in mice expressing human apolipoprotein E isoforms but lacking the LDL receptor.Semantic proximity Read ↗

Apolipoprotein E2 (Lys146-->Gln) causes hypertriglyceridemia due to an apolipoprotein E variant-specific inhibition of lipolysis of very low density lipoproteins-triglycerides.Semantic proximity Read ↗

Familial dysbetalipoproteinemia: a genetically heterogenous disease caused by mutations of the ligand apolipoprotein E.Semantic proximity Read ↗

Liver-directed gene transfer and prolonged expression of three major human ApoE isoforms in ApoE-deficient mice.Semantic proximity Read ↗

LDL receptor deficiency or apoE mutations prevent remnant clearance and induce hypertriglyceridemia in mice.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.