Evidence map›Paper›PMID 15467833›Full record

ArticleThe Journal of clinical investigation2004

CEACAM1 modulates epidermal growth factor receptor--mediated cell proliferation.

George A Abou-Rjaily, Sang Jun Lee, Denisa May, Qusai Y Al-Share, Anthony M Deangelis, Randall J Ruch, Michael Neumaier, Holger Kalthoff, Sue-Hwa Lin, Sonia M Najjar

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.4field-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

42 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Structural aspects of CEACAM1 interactions.European journal of clinical investigation · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. CEACAM1: Shielding the liver against fibrosis.European journal of clinical investigation · 2024
    Article
  8. Loss of CEACAM1 in hepatocytes causes hepatic fibrosis.European journal of clinical investigation · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

10 authors at 5 institutions in 3 countries.

George A Abou-RjailyDepartment of Pharmacology and Therapeutics, Medical College of Ohio, Toledo, Ohio 43614, USA.
Sang Jun Lee
Denisa May
Qusai Y Al-Share
Anthony M Deangelis
Randall J Ruch
Michael Neumaier
Holger Kalthoff
Sue-Hwa Lin
Sonia M Najjar
University of Toledo · USCenter for Translational Molecular Medicine · NLChristian-Albrechts-Universität zu Kiel · DEHeidelberg University · DEUniversity of Toledo Medical Center · US

Funding

SUBSTRATES AND INSULIN RECEPTOR ENDOCYTOSISR01DK054254 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2000 to 2021
$5.8M
Regulation of Angiogenesis by C CAM1R01CA086342 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI LIN, SUE-HWA · 2001 to 2004
$675k
FUNCTION OF C-CAM IN PROSTATE CANCERR01CA064856 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI LIN, SUE-HWA · 1997 to 2000
$191k
INSULIN RECEPTOR SUBSTRATES AND LIPOGENESISR21DK057497 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA MICHAEL · 1999 to 2000
$101k
NCI NIH HHS CA-64856NCI NIH HHS CA-86342NCI NIH HHS R01 CA086342NIDDK NIH HHS DK-54254NIDDK NIH HHS DK-57497NIDDK NIH HHS R01 DK054254
6 · The paper itself

Abstract

Phosphorylation of the cell adhesion protein CEACAM1 increases insulin sensitivity and decreases insulin-dependent mitogenesis in vivo. Here we show that CEACAM1 is a substrate of the EGFR and that upon being phosphorylated, CEACAM1 reduces EGFR-mediated growth of transfected Cos-7 and MCF-7 cells in response to EGF. Using transgenic mice overexpressing a phosphorylation-defective CEACAM1 mutant in liver (L-SACC1), we show that the effect of CEACAM1 on EGF-dependent cell proliferation is mediated by its ability to bind to and sequester Shc, thus uncoupling EGFR signaling from the ras/MAPK pathway. In L-SACC1 mice, we also show that impaired CEACAM1 phosphorylation leads to ligand-independent increase of EGFR-mediated cell proliferation. This appears to be secondary to visceral obesity and the metabolic syndrome, with increased levels of output of free fatty acids and heparin-binding EGF-like growth factor from the adipose tissue of the mice. Thus, L-SACC1 mice provide a model for the mechanistic link between increased cell proliferation in states of impaired metabolism and visceral obesity.

Indexed as

AnimalsAntigens, CDAntigens, DifferentiationCarcinoembryonic AntigenCell Adhesion MoleculesCell DivisionCell Line, TumorCOS CellsErbB ReceptorsHumansInsulinLiverMaleMAP Kinase Signaling SystemMiceMice, TransgenicAntigens, CDAntigens, DifferentiationCarcinoembryonic AntigenCD66 antigensCeacam1 protein, mouseCell Adhesion MoleculesErbB ReceptorsInsulinRecombinant Fusion Proteins

Identifiers

PMID15467833
PMCPMC518664
OpenAlexW1982365731

What OpenQuestion holds

Textmetadata
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.