Evidence map›Paper›PMID 15489914›Full record

ArticleOncogene2004

Not so strange bedfellows: G-protein-coupled receptors and Src family kinases.

Deirdre K Luttrell, Louis M Luttrell

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

105 citing papers in PubMed, 218 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. CSK-mediated signalling by integrins in cancer.Frontiers in cell and developmental biology · 2023
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. CRFFrontiers in endocrinology · 2019
    Article
  19. Article
  20. Article

45 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Deirdre K LuttrellDepartment of Medicine, Medical University of South Carolina, Charleston, SC, 29425, USA.
Louis M Luttrell
Medical University of South Carolina · USRalph H. Johnson VA Medical Center · US

Funding

TYROSINE KINASES IN G PROTEIN MEDIATED SIGNALINGR01DK055524 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 1998 to 2017
$4.6M
Parathyroid Hormone and Osteoblast MitogenesisR01DK064353 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 2002 to 2005
$937k
Receptor 'transactivation'in insulin signaling.R01DK058283 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 2001 to 2004
$854k
Tyrosine Kinases in G Protein Mediated SignalingR56DK055524 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 2008 to 2008
$284k
NIDDK NIH HHS DK55524NIDDK NIH HHS DK58283NIDDK NIH HHS DK64353
6 · The paper itself

Abstract

Src family nonreceptor tyrosine kinases are an integral component of the signal transduction apparatus employed by growth factor receptor tyrosine kinases. As such, their role in cellular growth control and malignant transformation has been the subject of intensive investigation. In contrast, classical G-protein-coupled receptor (GPCR) signaling involves activation of second messenger-regulated serine/threonine kinases or ion channels, and is primarily involved in neurotransmission and the short-term regulation of intermediary metabolism. Over the past decade, this strictly dichotomous model of transmembrane signaling has been challenged by the discovery that GPCRs also exert control over cellular growth, proliferation, and differentiation, and do so by stimulating tyrosine phosphorylation cascades. Several mechanisms, from the direct association of Src family kinases with GPCRs or receptor-associated proteins, to the transactivation of receptor tyrosine kinases and focal adhesion complexes by G-protein-mediated signals, permit GPCRs to activate Src family kinases. Conversely, Src activity plays a central role in controlling GPCR trafficking and effects on cell proliferation and cytoskeletal rearrangement. It is now clear that GPCRs and Src family kinases do not belong to separate, exclusive clubs. Rather, these strange bedfellows are intimately involved in multilayered forms of crosstalk that influence a host of cellular processes.

Indexed as

AnimalsArrestinsbeta-ArrestinsGTP-Binding ProteinsHumansProtein BindingReceptors, G-Protein-CoupledSignal Transductionsrc-Family KinasesArrestinsbeta-ArrestinsGTP-Binding ProteinsReceptors, G-Protein-Coupledsrc-Family Kinases

Identifiers

PMID15489914
OpenAlexW2011792786

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.