Evidence map›Paper›PMID 38580321›Full record

ArticleThe journal of physical chemistry. B2024

G Protein Activation Occurs via a Largely Universal Mechanism.

Neha Vithani, Tyson D Todd, Sukrit Singh, Tony Trent, Kendall J Blumer, Gregory R Bowman

Abstract read
In one paragraph

Article in The journal of physical chemistry. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Tyrosine kinases sample unique activation ensembles.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. The G protein inhibitor YM-254890 is an allosteric glue.bioRxiv : the preprint server for biology · 2024
    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.

Neha VithaniDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, Missouri 63110, United States.ORCID 0000-0003-4375-8762
Tyson D ToddDepartment of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, United States.ORCID 0000-0002-9044-8313
Sukrit SinghDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, Missouri 63110, United States.
Tony TrentDepartments of Biochemistry & Biophysics and Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States.
Kendall J BlumerDepartment of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, United States.
Gregory R BowmanDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, Missouri 63110, United States.ORCID 0000-0002-2083-4892

Funding

PHARMACOLOGICAL TARGETING OF GALPHA SUBUNITS IN DISEASER01GM124093 · NIGMS · WASHINGTON UNIVERSITY · PI BLUMER, KENDALL J, MOELLER, KEVIN DAVID · 2017 to 2024
$3.6M
MSMs, adaptive sampling, and data sharing on the cloudR01GM124007 · NIGMS · WASHINGTON UNIVERSITY · PI BOWMAN, GREGORY · 2017 to 2021
$2.0M
NIGMS NIH HHS R01 GM124007NIGMS NIH HHS R01 GM124093
6 · The paper itself

Abstract

Understanding how signaling proteins like G proteins are allosterically activated is a long-standing challenge with significant biological and medical implications. Because it is difficult to directly observe such dynamic processes, much of our understanding is based on inferences from a limited number of static snapshots of relevant protein structures, mutagenesis data, and patterns of sequence conservation. Here, we use computer simulations to directly interrogate allosteric coupling in six G protein α-subunit isoforms covering all four G protein families. To analyze this data, we introduce automated methods for inferring allosteric networks from simulation data and assessing how allostery is conserved or diverged among related protein isoforms. We find that the allosteric networks in these six G protein α subunits are largely conserved and consist of two pathways, which we call pathway-I and pathway-II. This analysis predicts that pathway-I is generally dominant over pathway-II, which we experimentally corroborate by showing that mutations to pathway-I perturb nucleotide exchange more than mutations to pathway-II. In the future, insights into unique elements of each G protein family could inform the design of isoform-specific drugs. More broadly, our tools should also be useful for studying allostery in other proteins and assessing the extent to which this allostery is conserved in related proteins.

Indexed as

GTP-Binding Protein alpha SubunitsProteinsAllosteric RegulationComputer SimulationGTP-Binding Protein alpha SubunitsProteins

Identifiers

PMID38580321
PMCPMC11034501

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Registered trials

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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.