Evidence map›Paper›PMID 12972543›Full record

ArticleMolecular biology of the cell2003

The association between integrin-associated protein and SHPS-1 regulates insulin-like growth factor-I receptor signaling in vascular smooth muscle cells.

Laura A Maile, Jane Badley-Clarke, David R Clemmons

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  2. IGF-1R targeting in cancer - does sub-cellular localization matter?Journal of experimental & clinical cancer research : CR · 2023
    Review
  3. Review
  4. CD47 (Cluster of Differentiation 47).Atlas of genetics and cytogenetics in oncology and haematology · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Insulin-like growth factor-binding protein-2 is required for osteoclast differentiation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012
    Article
  13. Article
  14. An essential role for the association of CD47 to SHPS-1 in skeletal remodeling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2011
    Article
  15. Spatial association of the Cav1.2 calcium channel with α5β1-integrin.American journal of physiology. Cell physiology · 2011
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors.

Laura A MaileDivision of Endocrinology, University of North Carolina, Chapel Hill, North Carolina 27599-7170, USA.
Jane Badley-Clarke
David R Clemmons

Funding

MECHANISMS BY WHICH IGF-I STIMULATES SMOOTH MUSCLE CELLSR01HL056850 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CLEMMONS, DAVID ROBERT · 1996 to 2007
$2.5M
NHLBI NIH HHS HL56850NHLBI NIH HHS R01 HL056850
6 · The paper itself

Abstract

Growth factor signaling is usually analyzed in isolation without considering the effect of ligand occupancy of transmembrane proteins other than the growth factor receptors themselves. In smooth muscle cells, the transmembrane protein Src homology 2 domain containing protein tyrosine phosphatase substrate-1 (SHPS-1) has been shown to be an important regulator of insulin-like growth factor-I (IGF-I) signaling. SHPS-1 is phosphorylated in response to IGF-I, leading to recruitment of Src homology 2 domain tyrosine phosphatase (SHP-2). Subsequently, SHP-2 is transferred to IGF-I receptor and regulates the duration of IGF-I receptor phosphorylation. Whether ligand occupancy of SHPS-1 influences SHPS-1 phosphorylation or SHP-2 recruitment, thereby altering growth factor signaling, is unknown. Previous studies have shown that integrin associated protein (IAP) associates with SHPS-1. We undertook these studies to determine whether this interaction controlled SHPS-1 phosphorylation and/or SHP-2 recruitment and thereby regulated IGF-I signaling. Disruption of IAP-SHPS-1 binding, by using an IAP monoclonal antibody or cells expressing mutant forms of IAP that did not bind to SHPS-1, inhibited IGF-I-stimulated SHPS-1 phosphorylation and SHP-2 recruitment. This was associated with a lack of SHP-2 transfer to IGF-I receptor and sustained receptor phosphorylation. This resulted in an inability of IGF-I to stimulate sustained mitogen-activated protein kinase activation, cell proliferation, and cell migration. The effect was specific for IGF-I because disruption of the IAP-SHPS-1 interaction had no effect on platelet-derived growth factor-stimulated SHPS-1 phosphorylation or cell migration. In summary, our results show that 1) ligand occupancy of SHPS-1 is a key determinant of its ability to be phosphorylated after IGF-I stimulation, and 2) the interaction between IAP and SHPS-1 is an important regulator of IGF-I signaling because disruption of the results in impaired SHP-2 recruitment and subsequent inhibition of IGF-I-stimulated cell proliferation and migration.

Indexed as

Antigens, DifferentiationAnimalsAntigens, CDCarrier ProteinsCD47 AntigenCell MovementCells, CulturedCloning, MolecularIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMitogen-Activated Protein KinasesMuscle, Smooth, VascularNeural Cell Adhesion Molecule L1PhosphorylationProtein BindingProtein Structure, TertiaryAntigens, CDAntigens, DifferentiationCarrier ProteinsCD47 AntigenIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMitogen-Activated Protein KinasesNeural Cell Adhesion Molecule L1Protein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine PhosphatasesReceptor, IGF Type 1Receptors, Immunologic

Identifiers

PMID12972543
PMCPMC196546

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.