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Cited by 553

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

THE LDL RECEPTOR LOCUS IN FAMILIAL HYPERCHOLESTEROLEMIA: Mutational Analysis of a Membrane Protein

Hobbs, Helen H., Russell, David W., Brown, Michael S., Goldstein, Joseph L.·1990·Annual Review of Genetics
DOI 10.1146/annurev.ge.24.120190.001025
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Abstract

Orthologs and paralogs are two fundamentally different types of homologous genes that evolved, respectively, by vertical descent from a single ancestral gene and by duplication. Orthology and paralogy are key concepts of evolutionary genomics. A ...Read More

Overview

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Crossref · 10.1146/annurev.ge.24.120190.001025

Cites

2 of 2 references verified0 citation errors · 0 not checkable

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Recomputing p-values needs the paper’s full text.

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Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • USP2 regulates the LDLR pathway by counteracting the E3-ubiquitin ligase IDOL.

    “It has been reported that USP2 can regulate the deubiquitination of LDLR.13)”

    From USP16 Regulates the Stability and Function of LDL receptor by Deubiquitination (2020) · cites this paper as [14]

  • Complete absence or defective LDLRs due to mutations in the LDLR gene cause familial hypercholesterolemia, characterized by autosomal dominant inheritance of hypercholesterolemia and premature atherosclerotic cardiovascular disease.

    “Complete absence or defective LDLRs due to mutations in the LDLR gene cause FH, characterized by an autosomal dominant inheritance of hypercholesterolemia and premature ASCVD (a list of mutations can be found in Table 1)1–4.”

    From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [4]

  • The strongest negative regulator of SQLE-mNeon found in the screen was the E3 ubiquitin ligase MARCH6 and its cognate E2 partner UBE2J2.

    “Conversely, the strongest negative regulator of SQLE-mNeon found in our screen was the E3 ubiquitin ligase MARCH6, and its cognate E2 partner UBE2J2, which we have recently reported to be critical determinants of cholesterol-dependent degradation of SQLE25–27.”

    From Haploid genetic screens identify SPRING/C12ORF49 as a determinant of SREBP signaling and cholesterol metabolism (2020) · cites this paper as [25]

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Metadata

Authors
Hobbs, H. H., Russell, D. W., Brown, M. S., & Goldstein, J. L.
Venue
Annual Review of Genetics
Publisher
Annual Reviews
Published
1990-12
Volume
24
Issue
1
Pages
133-170
ISSN
  • 0066-4197
  • 1545-2948
DOI
10.1146/annurev.ge.24.120190.001025
Cited by
553
References
2
Language
en

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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