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The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Intracellular cholesterol mobilization involved in the ABCA1/apolipoprotein-mediated assembly of high density lipoprotein in fibroblasts

Yamauchi, Yoshio, Chang, Catherine C.Y., Hayashi, Michi, Abe-Dohmae, Sumiko, Reid, Patrick C., Chang, Ta-Yuan, Yokoyama, Shinji·2004·Journal of Lipid Research
DOI 10.1194/jlr.m400264-jlr200
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Crossref · 10.1194/jlr.m400264-jlr200

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  • Inhibiting ACAT increases the free cholesterol pool and facilitates lipid secretion to extracellular apoE-containing lipoproteins.

    “Thus, inhibiting ACAT increases the FC pool and facilitates lipid secretion to extracellular apoE-containing lipoproteins.”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [62]

    The section ‘Effect of ACAT enzyme activity on apoA-I-mediated cholesterol release’ reports that ACAT inhibition increased cholesterol and phospholipid release mediated by apoA-I, not apoE. Table 1 in ‘Measurement of the free cholesterol pool available for ACAT’ does not establish the claimed increase in free cholesterol: the ACAT-deficient cells had less measured free cholesterol than their parental cells. The paper therefore supports increased lipid release under its tested conditions, but not the specified apoE-containing recipients or the asserted increase in the free-cholesterol pool. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The decrease in endothelial cell disruption and atherosclerotic plaque development was dependent on apoA1 as the plasma cholesterol acceptor.

    “This decrease in endothelial cell disruption and atherosclerotic plaque development was dependent on apoA1 as the plasma cholesterol acceptor [57–63].”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [62]

    The section on the ACAT-accessible cholesterol pool reports that apoA-I mediates cholesterol release in cells expressing ABCA1. That supports apoA-I’s role in cellular cholesterol removal, but the paper does not report decreased endothelial cell disruption or atherosclerotic plaque development, or show that either outcome depends on apoA-I acting as a plasma cholesterol acceptor. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 42

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Metadata

Authors
Yamauchi, Y., Chang, C. C. Y., Hayashi, M., Abe-Dohmae, S., Reid, P. C., Chang, T.-Y., & Yokoyama, S.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2004-10
Volume
45
Issue
10
Pages
1943-1951
ISSN
0022-2275
DOI
10.1194/jlr.m400264-jlr200
Cited by
62
References
1
Language
en
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