Discover Community Create You

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

Article

Correction of apolipoprotein A-I-mediated lipid efflux and high density lipoprotein particle formation in human Niemann-Pick type C disease fibroblasts.

The Journal of biological chemistry - 1 Dec 2006

Boadu Emmanuel, Choi Hong Y, Lee Diana W K, Waddington Emma I, Chan Teddy, Asztalos Bela, Vance Jean E, Chan Alicia, Castro Graciela, Francis Gordon A

Abstract excerpt

Impaired cell cholesterol trafficking in Niemann-Pick type C (NPC) disease results in the first known instance of impaired regulation of the ATP-binding cassette transporter A1 (ABCA1), a lipid transporter mediating the rate-limiting step in high density lipoprotein (HDL) formation, as a cause of low plasma HDL-cholesterol in humans. We show here that treatment of human NPC1(-/-) fibroblasts with the liver X...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apolipoprotein A-I
Share to ATP Binding Cassette Transporter 1

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to ATP Binding Cassette Transporter, Subfamily G, Member 1

Share to Lipoproteins

Share to Lipoproteins, HDL

Share to Niemann-Pick C1 Protein

Share to Niemann-Pick Diseases

Share to Phosphatidylcholines

Source

Identifiers

PMID: 17020879
DOI: 10.1074/jbc.M606890200

Genes

NPC1
ABCA1
ABCG1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Correction of apolipoprotein A-I-mediated lipid efflux and high density lipoprotein particle formation in human Niemann-Pick type C disease fibroblasts.PMID 17020879Read ↗

Impaired ABCA1-dependent lipid efflux and hypoalphalipoproteinemia in human Niemann-Pick type C disease.Semantic proximity Read ↗

Lysosomal acid lipase deficiency impairs regulation of ABCA1 gene and formation of high density lipoproteins in cholesteryl ester storage disease.Semantic proximity Read ↗

Niemann-Pick type C disease: molecular mechanisms and potential therapeutic approaches.Semantic proximity Read ↗

NPC1 and NPC2 regulate cellular cholesterol homeostasis through generation of low density lipoprotein cholesterol-derived oxysterols.Semantic proximity Read ↗

The role of vesicular transport in ABCA1-dependent lipid efflux and its connection with NPC pathways.Semantic proximity Read ↗

NPC1L1 (Niemann-Pick C1-like 1) mediates sterol-specific unidirectional transport of non-esterified cholesterol in McArdle-RH7777 hepatoma cells.Semantic proximity Read ↗

Trafficking defects in endogenously synthesized cholesterol in fibroblasts, macrophages, hepatocytes, and glial cells from Niemann-Pick type C1 mice.Semantic proximity Read ↗

Autophagy in Niemann–Pick C disease is dependent upon Beclin-1 and responsive to lipid trafficking defectsSemantic proximity Read ↗

Niemann-Pick Type C disease: characterizing lipid levels in patients with variant lysosomal cholesterol storage.Semantic proximity Read ↗

Reduction of TMEM97 increases NPC1 protein levels and restores cholesterol trafficking in Niemann-pick type C1 disease cells.Semantic proximity Read ↗

Histone deacetylase inhibitor treatment dramatically reduces cholesterol accumulation in Niemann-Pick type C1 mutant human fibroblasts.Semantic proximity Read ↗

Differential Trafficking Phenotypes of NPC1 Mutant Proteins Reveal Distinct Cholesterol Accumulation Profiles.Semantic proximity Read ↗

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