A trimeric Rab7 GEF controls NPC1-dependent lysosomal cholesterol export

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 2041-1723

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: A trimeric Rab7 GEF controls NPC1-dependent lysosomal cholesterol export ; volume:11 ; number:1 ; day:3 ; month:11 ; year:2020 ; pages:1-18 ; date:12.2020
Nature Communications ; 11, Heft 1 (3.11.2020), 1-18, 12.2020

Creator: Boomen, Dick J. H. van den
Sienkiewicz, Agata
Berlin, Ilana
Jongsma, Marlieke L. M.
Elsland, Daphne M. van
Luzio, J. Paul
Neefjes, Jacques J. C.
Lehner, Paul J.

Contributor: SpringerLink (Online service)

DOI: 10.1038/s41467-020-19032-0

URN: urn:nbn:de:101:1-2020121208240840951005

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:31 AM CEST

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Associated

Boomen, Dick J. H. van den
Sienkiewicz, Agata
Berlin, Ilana
Jongsma, Marlieke L. M.
Elsland, Daphne M. van
Luzio, J. Paul
Neefjes, Jacques J. C.
Lehner, Paul J.
SpringerLink (Online service)

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A trimeric Rab7 GEF controls NPC1-dependent lysosomal cholesterol export

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Other Objects (12)

USP15-dependent lysosomal pathway controls p53-R175H turnover in ovarian cancer cells

Fine‐Tuning of Cholesterol Homeostasis Controls Erythroid Differentiation

The FTLD risk factor TMEM106B controls lysosomal trafficking and dendrite outgrowth

Presenilin deficiency leads to altered protein N-glycosylation and endo-lysosomal cholesterol accumulation

The Role of Oxidized Cholesterol in Diabetes-Induced Lysosomal Dysfunction in the Brain

Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

Fasting‐sensitive SUMO‐switch on Prox1 controls hepatic cholesterol metabolism

Amyloid precursor protein controls cholesterol turnover needed for neuronal activity

Cholesterol alters mitophagy by impairing optineurin recruitment and lysosomal clearance in Alzheimer’s disease

Lysosomal alpha-galactosidase A controls the generation of self lipid antigens for NKT cells

Cholesterol-dependent cytolysins impair pro-inflammatory macrophage responses

USP15-dependent lysosomal pathway controls p53-R175H turnover in ovarian cancer cells

Fine‐Tuning of Cholesterol Homeostasis Controls Erythroid Differentiation

The FTLD risk factor TMEM106B controls lysosomal trafficking and dendrite outgrowth

Presenilin deficiency leads to altered protein N-glycosylation and endo-lysosomal cholesterol accumulation

The Role of Oxidized Cholesterol in Diabetes-Induced Lysosomal Dysfunction in the Brain

Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

Fasting‐sensitive SUMO‐switch on Prox1 controls hepatic cholesterol metabolism

Amyloid precursor protein controls cholesterol turnover needed for neuronal activity

Cholesterol alters mitophagy by impairing optineurin recruitment and lysosomal clearance in Alzheimer’s disease

Lysosomal alpha-galactosidase A controls the generation of self lipid antigens for NKT cells

Cholesterol-dependent cytolysins impair pro-inflammatory macrophage responses

USP15-dependent lysosomal pathway controls p53-R175H turnover in ovarian cancer cells

Fine‐Tuning of Cholesterol Homeostasis Controls Erythroid Differentiation

The FTLD risk factor TMEM106B controls lysosomal trafficking and dendrite outgrowth

Presenilin deficiency leads to altered protein N-glycosylation and endo-lysosomal cholesterol accumulation

The Role of Oxidized Cholesterol in Diabetes-Induced Lysosomal Dysfunction in the Brain

Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

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Fasting‐sensitive SUMO‐switch on Prox1 controls hepatic cholesterol metabolism

Amyloid precursor protein controls cholesterol turnover needed for neuronal activity

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Lysosomal alpha-galactosidase A controls the generation of self lipid antigens for NKT cells

Cholesterol-dependent cytolysins impair pro-inflammatory macrophage responses

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