Cited by 130Metabolism, Diabetes, and CancerProtein Kinase Regulation and GTPase SignalingPI3K/AKT/mTOR signaling in cancer

Signalling through the insulin receptor

Whitehead, Jonathan P, Clark, Sharon F, Ursø, Birgitte, James, David E·2000·Current Opinion in Cell Biology

Abstract

The insulin receptor substrates function at the heart of the insulin signalling network. It has recently become apparent that the intracellular localisation of these molecules is regulated in a precise manner that is critical for both the generation and the termination of the insulin signal. Some insulin receptor substrate isoforms appear to be associated with an insoluble matrix that resembles the cytoskeleton. When inappropriately dissociated from this matrix the signalling network collapses concomitant with loss of insulin sensitivity.

Integrity signals

Registry

Crossref · 10.1016/s0955-0674(99)00079-4

Cites

72 of 72 references verified0 citation errors · 0 not checkable

Statistics

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

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • Insulin initiates its stimulatory effect on glucose metabolism by binding to specific receptors on the muscle cell surface.

    “The cellular events via which insulin initiates its stimulatory effect on glucose metabolism start with binding of the hormone to specific receptors that are present on the muscle cell surface [2, 138–140].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [140]

  • Phosphorylated tyrosine residues of IRS-1 mediate association with the 85-kDa regulatory subunit of PI3K, activating the enzyme.

    “The phosphorylated tyrosine residues of IRS-1 mediate an association with the 85-kDa regulatory subunit of phosphatidylinositol 3-kinase (PI3K), leading to activation of the enzyme [138–140, 143, 144].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [140]

  • PI3K inhibitors impair glucose transport and block activation of glycogen synthase and HK-II expression.

    “Inhibitors of PI3K impair glucose transport and block the activation of glycogen synthase and hexokinase- (HK-) II expression [138–146]”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [140]

Cites

Flagged first, then by citations

1 of the 73 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Whitehead, J. P., Clark, S. F., Ursø, B., & James, D. E.
Affiliations
  • The University of Queensland (AU)
  • University of Copenhagen (DK)
Corresponding author
  • Whitehead, Jonathan P
  • Clark, Sharon F
  • Ursø, Birgitte
  • James, David E
Venue
Current Opinion in Cell Biology
Publisher
Elsevier BV
Published
2000-04
Volume
12
Issue
2
Pages
222-228
ISSN
0955-0674 (ISSN-L)
OpenAlex
W2049761828
Cited by
130
References
73
Citations by year
2024: 2 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 9 · 2014: 4 · 2013: 2 · 2012: 3
FWCI
1.20
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
insulin receptor, insulin receptor substrate, insulin signaling, signal termination, insulin sensitivity, subcellular localization
MeSH terms
Animals, Insulin Resistance, Phosphoproteins, Receptor, Insulin, Signal Transduction, Insulin Receptor Substrate Proteins

About these checks

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.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review