Evidence map›Paper›PMID 9679153›Full record

ArticleThe Journal of cell biology1998

Integrin-mediated signals regulated by members of the rho family of GTPases.

E A Clark, W G King, J S Brugge, M Symons, R O Hynes

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed
19.8field-weighted citation impact, top 1% 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

187 citing papers in PubMed, 606 citations in OpenAlex.

  1. Review
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  8. Toxicological research · 2023
    Article
  9. Article
  10. Article
  11. CSK-mediated signalling by integrins in cancer.Frontiers in cell and developmental biology · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

127 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

5 authors at 2 institutions in 1 country.

E A ClarkHoward Hughes Medical Institute, Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
W G King
J S Brugge
M Symons
R O Hynes
Center for Cancer Research · USHoward Hughes Medical Institute · US

Funding

CELL-SURFACE STRUCTURE AND TRANSFORMATIONSR01CA017007 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HYNES, RICHARD O · 1985 to 2005
$2.9M
STUDIES ON THE C-SRC PROTO-ONCOGENE PRODUCT IN NEURONSR01CA047572 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BRUGGE, JOAN SIEFERT · 1988 to 1997
–
NCI NIH HHS CA17007NCI NIH HHS CA47572NCI NIH HHS R01 CA017007
6 · The paper itself

Abstract

The organization of the actin cytoskeleton can be regulated by soluble factors that trigger signal transduction events involving the Rho family of GTPases. Since adhesive interactions are also capable of organizing the actin-based cytoskeleton, we examined the role of Cdc42-, Rac-, and Rho-dependent signaling pathways in regulating the cytoskeleton during integrin-mediated adhesion and cell spreading using dominant-inhibitory mutants of these GTPases. When Rat1 cells initially adhere to the extracellular matrix protein fibronectin, punctate focal complexes form at the cell periphery. Concomitant with focal complex formation, we observed some phosphorylation of the focal adhesion kinase (FAK) and Src, which occurred independently of Rho family GTPases. However, subsequent phosphorylation of FAK and paxillin occurs in a Rho-dependent manner. Moreover, we found Rho dependence of the assembly of large focal adhesions from which actin stress fibers radiate. Initial adhesion to fibronectin also stimulates membrane ruffling; we show that this ruffling is independent of Rho but is dependent on both Cdc42 and Rac. Furthermore, we observed that Cdc42 controls the integrin-dependent activation of extracellular signal-regulated kinase 2 and of Akt, a kinase whose activity has been demonstrated to be dependent on phosphatidylinositol (PI) 3-kinase. Since Rac-dependent membrane ruffling can be stimulated by PI 3-kinase, it appears that Cdc42, PI 3-kinase, and Rac lie on a distinct pathway that regulates adhesion-induced membrane ruffling. In contrast to the differential regulation of integrin-mediated signaling by Cdc42, Rac, and Rho, we observed that all three GTPases regulate cell spreading, an event that may indirectly control cellular architecture. Therefore, several separable signaling pathways regulated by different members of the Rho family of GTPases converge to control adhesion-dependent changes in the organization of the cytoskeleton, changes that regulate cell morphology and behavior.

Indexed as

GTPase-Activating ProteinsActinsAnimalscdc42 GTP-Binding ProteinCell AdhesionCell Cycle ProteinsCell LineCytoskeletonFibronectinsGTP-Binding ProteinsGTP PhosphohydrolasesIntegrinsMutationRatsrhoA GTP-Binding ProteinSignal TransductionActinscdc42 GTP-Binding ProteinCell Cycle ProteinsFibronectinsGTPase-Activating ProteinsGTP-Binding ProteinsGTP PhosphohydrolasesIntegrinsrhoA GTP-Binding Proteinrho GTPase-activating protein

Identifiers

PMID9679153
PMCPMC2133065
OpenAlexW2149352954

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.