Evidence map›Paper›PMID 11980921›Full record

ArticleThe Journal of cell biology2002

Defective Rac-mediated proliferation and survival after targeted mutation of the beta1 integrin cytodomain.

Emilio Hirsch, Laura Barberis, Mara Brancaccio, Ornella Azzolino, Dazhong Xu, John M Kyriakis, Lorenzo Silengo, Filippo G Giancotti, Guido Tarone, Reinhard Fässler and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 80 citations in OpenAlex.

  1. Breast cancer (Dove Medical Press) · 2023
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Integrins in development and cancer.Biophysical reviews · 2014
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Analysis of conserved residues in the betapat-3 cytoplasmic tail reveals important functions of integrin in multiple tissues.Developmental dynamics : an official publication of the American Association of Anatomists · 2010
    Article
  16. Article
  17. Integrins in lens development and disease.Experimental eye research · 2009
    Review
  18. Integrins and cell-fate determination.Journal of cell science · 2009
    Review
  19. Article
  20. Synergistic control of cell adhesion by integrins and syndecans.Nature reviews. Molecular cell biology · 2007
    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

11 authors at 5 institutions in 4 countries.

Emilio HirschDipartimento di Genetica, Biologia, e Biochimica, Università di Torino, 10126 Torino, Italy. emilio.hirsch@unito.it
Laura Barberis
Mara Brancaccio
Ornella Azzolino
Dazhong Xu
John M Kyriakis
Lorenzo Silengo
Filippo G Giancotti
Guido Tarone
Reinhard Fässler
Fiorella Altruda
Azienda Ospedaliero Universitaria San Giovanni Battista · ITUniversity of Turin · ITMassachusetts General Hospital · USLund University · SEMemorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell matrix adhesion is required for cell proliferation and survival. Here we report that mutation by gene targeting of the cytoplasmic tail of beta1 integrin leads to defective proliferation and survival both in vivo and in vitro. Primary murine embryonic fibroblasts (MEFs) derived from mutant homozygotes display defective cell cycle coupled to impaired activation of the FAK-PI3K-Akt and Rac-JNK signaling pathways. Expression in homozygous MEFs of a constitutively active form of Rac is able to rescue proliferation, survival, and JNK activation. Moreover, although showing normal Erk phosphorylation, mutant cells fail to display Erk nuclear translocation upon fibronectin adhesion. However, expression of the constitutively activated form of Rac restores Erk nuclear localization, suggesting that adhesion-dependent Rac activation is necessary to integrate signals directed to promote MAPK activity. Altogether, our data provide the evidence for an epistatic interaction between the beta1 integrin cytoplasmic domain and Rac, and indicate that this anchorage-dependent signaling pathway is crucial for cell growth control.

Indexed as

AllelesAnimalsCell AdhesionCell CycleCell DivisionCell SurvivalFetal DeathFibroblastsGene TargetingHomozygoteIntegrin beta1MiceMitogen-Activated Protein KinasesMutationPhosphatidylinositol 3-KinasesProtein IsoformsIntegrin beta1Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Isoformsrac GTP-Binding Proteins

Identifiers

PMID11980921
PMCPMC2173276
OpenAlexW2114474216

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.