Evidence map›Paper›PMID 27864364›Full record

ArticleThe Journal of biological chemistry2016

Membrane Recruitment of the Non-receptor Protein GIV/Girdin (Gα-interacting, Vesicle-associated Protein/Girdin) Is Sufficient for Activating Heterotrimeric G Protein Signaling.

Kshitij Parag-Sharma, Anthony Leyme, Vincent DiGiacomo, Arthur Marivin, Stefan Broselid, Mikel Garcia-Marcos

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Receptor tyrosine kinases activate heterotrimeric G proteins via phosphorylation within the interdomain cleft of Gαi.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Regulating cellular cyclic adenosine monophosphate: "Sources," "sinks," and now, "tunable valves".Wiley interdisciplinary reviews. Systems biology and medicine · 2020
    Review
  11. Article
  12. DAPLE protein inhibits nucleotide exchange on GαThe Journal of biological chemistry · 2020
    Article
  13. Structural basis for GPCR-independent activation of heterotrimeric Gi proteins.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Article
  15. Article
  16. Specific inhibition of GPCR-independent G protein signaling by a rationally engineered protein.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. 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

6 authors at 1 institution in 1 country.

Kshitij Parag-SharmaFrom the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118.
Anthony LeymeFrom the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118.
Vincent DiGiacomoFrom the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118.
Arthur MarivinFrom the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118.
Stefan BroselidFrom the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118.
Mikel Garcia-MarcosFrom the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 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 R01 GM108733NIGMS NIH HHS R01 GM112631
6 · The paper itself

Abstract

GIV (aka Girdin) is a guanine nucleotide exchange factor that activates heterotrimeric G protein signaling downstream of RTKs and integrins, thereby serving as a platform for signaling cascade cross-talk. GIV is recruited to the cytoplasmic tail of receptors upon stimulation, but the mechanism of activation of its G protein regulatory function is not well understood. Here we used assays in humanized yeast models and G protein activity biosensors in mammalian cells to investigate the role of GIV subcellular compartmentalization in regulating its ability to promote G protein signaling. We found that in unstimulated cells GIV does not co-fractionate with its substrate G protein Gα

Indexed as

Cell MembraneHeLa CellsHeterotrimeric GTP-Binding ProteinsHumansImmunoblottingMembrane MicrodomainsMicrofilament ProteinsSaccharomyces cerevisiaeVesicular Transport ProteinsCCDC88A protein, humanHeterotrimeric GTP-Binding ProteinsMicrofilament ProteinsVesicular Transport Proteinsbioluminescence resonance energy transfer (BRET)G protein-coupled receptor (GPCR)guanine nucleotide exchange factor (GEF)heterotrimeric G proteinreceptor tyrosine kinase

Identifiers

PMID27864364
PMCPMC5207140
OpenAlexW2551025503

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.