Evidence map›Paper›PMID 27758770›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

Small GTPase ARF6 Regulates Endocytic Pathway Leading to Degradation of ATP-Binding Cassette Transporter A1.

Nigora Mukhamedova, Anh Hoang, Huanhuan L Cui, Irena Carmichael, Ying Fu, Michael Bukrinsky, Dmitri Sviridov

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 32 citations in OpenAlex.

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  13. ApoE4 Alters ABCA1 Membrane Trafficking in Astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  14. Article
  15. Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  16. Article
  17. Review
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Nigora MukhamedovaFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.).
Anh HoangFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.).
Huanhuan L CuiFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.).
Irena CarmichaelFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.).
Ying FuFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.).
Michael BukrinskyFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.).
Dmitri SviridovFrom the Department of Lipoproteins and Atherosclerosis, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia (N.M., A.H., H.L.C., I.C., Y.F., D.S.); Department of Medicine, Karolinska Institute, Stockholm, Sweden (H.L.C.); and Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC (M.B.). Dmitri.Sviridov@bakeridi.edu.au.
Karolinska Institutet · SE

Funding

SWG 2: Cure Research Scientific Working GroupP30AI117970 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI Italo Mocchetti · 2015 to 2026
$29.6M
HIV Disease and Impairement of High Density Lipoprotein MetabolismR01HL101274 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI BUKRINSKY, MICHAEL ILYA, FITZGERALD, MICHAEL LEO · 2010 to 2015
$4.0M
Metabolic complications of HIV disease caused by Nef released from HIV-infected cellsR01HL131473 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI BUKRINSKY, MICHAEL ILYA, SVIRIDOV, DMITRI · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL101274NHLBI NIH HHS R01 HL131473NIAID NIH HHS P30 AI117970
6 · The paper itself

Abstract

objectiveABCA1 (ATP-binding cassette transporter A1) is the principal protein responsible for cellular cholesterol efflux. Abundance and functionality of ABCA1 is regulated both transcriptionally and post-translationally, with endocytosis of ABCA1 being an important element of post-translational regulation. Functional ABCA1 resides on the plasma membrane but can be internalized and either degraded or recycled back to the plasma membrane. The interaction between the degradative and recycling pathways determines the abundance of ABCA1 and may contribute to the efflux of intracellular cholesterol. APPROACH AND

resultsHere, we show that the principal pathway responsible for the internalization of ABCA1 leading to its degradation in macrophages is ARF6-dependent endocytic pathway. This pathway was predominant in the regulation of ABCA1 abundance and efflux of plasma membrane cholesterol. Conversely, the efflux of intracellular cholesterol was predominantly controlled by ARF6-independent pathways, and inhibition of ARF6 shifted ABCA1 into recycling endosomes enhancing efflux of intracellular cholesterol.

conclusionsWe conclude that ARF6-dependent pathway is the predominant route responsible for the ABCA1 internalization and degradation, whereas ARF6-independent endocytic pathways may contribute to ABCA1 recycling and efflux of intracellular cholesterol.

Indexed as

EndocytosisADP-Ribosylation Factor 6ADP-Ribosylation FactorsAnimalsATP Binding Cassette Transporter 1Cell MembraneCholesterolDynamin IIMacrophagesMaleMiceMice, Inbred C57BLProteolysisRAW 264.7 CellsRNA InterferenceTransfectionAbca1 protein, mouseADP-Ribosylation Factor 6ADP-Ribosylation FactorsArf6 protein, mouseATP Binding Cassette Transporter 1CholesterolDNM2 protein, mouseDynamin IIcholesterolclathrinendocytosisendosomesmacrophages

Identifiers

PMID27758770
PMCPMC5123748
OpenAlexW2529122601

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.