Evidence map›Paper›PMID 26391662›Full record

ArticleThe Journal of cell biology2015

Integrins activate trimeric G proteins via the nonreceptor protein GIV/Girdin.

Anthony Leyme, Arthur Marivin, Lorena Perez-Gutierrez, Lien T Nguyen, Mikel Garcia-Marcos

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.8field-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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Small-molecule targeting of GPCR-independent noncanonical G-protein signaling in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Article
  7. Regulating cellular cyclic adenosine monophosphate: "Sources," "sinks," and now, "tunable valves".Wiley interdisciplinary reviews. Systems biology and medicine · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. DAPLE protein inhibits nucleotide exchange on GαThe Journal of biological chemistry · 2020
    Article
  14. Article
  15. PI3Kβ links integrin activation and PI(3,4)PMolecular biology of the cell · 2019
    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

5 authors at 1 institution in 1 country.

Anthony LeymeDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118.
Arthur MarivinDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118.
Lorena Perez-GutierrezDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118.
Lien T NguyenDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118.
Mikel Garcia-MarcosDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118 mgm1@bu.edu.
Boston University · US

Funding

Alternative mechanisms of signaling via trimeric G proteinsR01GM108733 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GARCIA-MARCOS, MIKEL · 2014 to 2018
$1.6M
Identification of chemical probes that specifically disrupt the GIV-Gi interfaceR01GM112631 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GARCIA-MARCOS, MIKEL · 2015 to 2017
$933k
NIGMS NIH HHS GM108733NIGMS NIH HHS GM112631NIGMS NIH HHS R01 GM108733NIGMS NIH HHS R01 GM112631
6 · The paper itself

Abstract

Signal transduction via integrins and G protein-coupled receptors is critical to control cell behavior. These two receptor classes have been traditionally believed to trigger distinct and independent signaling cascades in response to extracellular cues. Here, we report a novel mechanism of integrin signaling that requires activation of the trimeric G protein Gαi by the nonreceptor guanine nucleotide exchange factor (GEF) GIV (also known as Girdin), a metastasis-associated protein. We demonstrate that GIV enhances integrin-dependent cell responses upon extracellular matrix stimulation and makes tumor cells more invasive. These responses include remodeling of the actin cytoskeleton and PI3K-dependent signaling, resulting in enhanced haptotaxis and invasion. We show that both GIV and its substrate Gαi3 are recruited to active integrin complexes and that tumor cells engineered to express GEF-deficient GIV fail to transduce integrin signals into proinvasive responses via a Gβγ-PI3K axis. Our discoveries delineate a novel mechanism by which integrin signaling is rewired during metastasis to result in increased tumor invasiveness.

Indexed as

AnimalsGTP-Binding Protein alpha Subunits, Gi-GoHeLa CellsHumansIntegrinsMCF-7 CellsMiceMicrofilament ProteinsNIH 3T3 CellsPhosphatidylinositol 3-KinasesSignal TransductionVesicular Transport ProteinsCCDC88A protein, humanCcdc88a protein, mouseGNAI3 protein, humanGnai3 protein, mouseGTP-Binding Protein alpha Subunits, Gi-GoIntegrinsMicrofilament ProteinsPhosphatidylinositol 3-KinasesVesicular Transport Proteins

Identifiers

PMID26391662
PMCPMC4586755
OpenAlexW2181198026

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.