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

Endocytosis of beta-cyclodextrins is responsible for cholesterol reduction in Niemann-Pick type C mutant cells.

Proceedings of the National Academy of Sciences of the United States of America - 23 Mar 2010

Rosenbaum Anton I, Zhang Guangtao, Warren J David, Maxfield Frederick R

Abstract excerpt

Niemann-Pick type C disease (NPC) is a lysosomal storage disorder causing accumulation of unesterified cholesterol in lysosomal storage organelles. Recent studies have shown that hydroxypropyl-beta-cyclodextrin injections in npc1(-/-) mice are partially effective in treating this disease. Using cultured fibroblasts, we have investigated the cellular mechanisms responsible for reduction of cholesterol...

Read the complete abstract on PubMed

Topics

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

Share to Androstenes
Share to Biological Transport, Active

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cholesterol Esters

Share to Endocytosis

Share to Glycoproteins

Share to Niemann-Pick C1 Protein

Share to Niemann-Pick Disease, Type C

Share to Vesicular Transport Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 20212119
DOI: 10.1073/pnas.0914309107
PMCID: PMC2851804

Genes

NPC1
NPC2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Endocytosis of beta-cyclodextrins is responsible for cholesterol reduction in Niemann-Pick type C mutant cells.PMID 20212119Read ↗

Cyclodextrin Induces Calcium-Dependent Lysosomal ExocytosisSemantic proximity Read ↗

Function of the Niemann-Pick type C proteins and their bypass by cyclodextrin.Semantic proximity Read ↗

Cyclodextrin triggers MCOLN1-dependent endo-lysosome secretion in Niemann-Pick type C cellsSemantic proximity Read ↗

Weekly cyclodextrin administration normalizes cholesterol metabolism in nearly every organ of the Niemann-Pick type C1 mouse and markedly prolongs life.Semantic proximity Read ↗

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

Accumulation of glycosphingolipids in Niemann-Pick C disease disrupts endosomal transport.Semantic proximity Read ↗

Quantitative comparison of the efficacy of various compounds in lowering intracellular cholesterol levels in Niemann-Pick type C fibroblasts.Semantic proximity Read ↗

Glial contribution to cyclodextrin-mediated reversal of cholesterol accumulation in murine NPC1-deficient neurons <i>in vivo</i>Semantic proximity Read ↗

Cholesterol accumulation sequesters Rab9 and disrupts late endosome function in NPC1-deficient cells.Semantic proximity Read ↗

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

Distinct endosomal compartments in early trafficking of low density lipoprotein-derived cholesterol.Semantic proximity Read ↗

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