Evidence map›Paper›PMID 15610010›Full record

ArticleBiochemistry2004

GRP1 pleckstrin homology domain: activation parameters and novel search mechanism for rare target lipid.

John A Corbin, Ronald A Dirkx, Joseph J Falke

Open access · greenAbstract read
In one paragraph

Article in Biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

64 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Two-step mechanism of Bruton's tyrosine kinase membrane recruitment and activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Switch-like activation of Bruton's tyrosine kinase by membrane-mediated dimerization.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  20. Article

4 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

3 authors at 1 institution in 1 country.

John A CorbinMolecular Biophysics Program and The Department of Chemistry and Biochemistry, University of Colorado, Boulder, Colorado 80309-0215, USA.
Ronald A Dirkx
Joseph J Falke
University of Colorado Boulder · US

Funding

Mechanisms of Signaling on Membrane SurfacesR01GM063235 · NIGMS · UNIVERSITY OF COLORADO AT BOULDER · PI FALKE, JOSEPH J · 2001 to 2021
$6.4M
NIGMS NIH HHS GM R01-63235NIGMS NIH HHS R01 GM063235
6 · The paper itself

Abstract

Pleckstrin homology (PH) domains play a central role in a wide array of signaling pathways by binding second messenger lipids of the phosphatidylinositol phosphate (PIP) lipid family. A given type of PIP lipid is formed in a specific cellular membrane where it is generally a minor component of the bulk lipid mixture. For example, the signaling lipid PI(3,4,5)P(3) (or PIP(3)) is generated primarily in the inner leaflet of the plasma membrane where it is believed to never exceed 0.02% of the bulk lipid. The present study focuses on the PH domain of the general receptor for phosphoinositides, isoform 1 (GRP1), which regulates the actin cytoskeleton in response to PIP(3) signals at the plasma membrane surface. The study systematically analyzes both the equilibrium and kinetic features of GRP1-PH domain binding to its PIP lipid target on a bilayer surface. Equilibrium binding measurements utilizing protein-to-membrane fluorescence resonance energy transfer (FRET) to detect GRP1-PH domain docking to membrane-bound PIP lipids confirm specific binding to PIP(3). A novel FRET competitive binding measurement developed to quantitate docking affinity yields a K(D) of 50 +/- 10 nM for GRP1-PH domain binding to membrane-bound PIP(3) in a physiological lipid mixture approximating the composition of the plasma membrane inner leaflet. This observed K(D) lies in a suitable range for regulation by physiological PIP(3) signals. Interestingly, the affinity of the interaction decreases at least 12-fold when the background anionic lipids phosphatidylserine (PS) and phosphatidylinositol (PI) are removed from the lipid mixture. Stopped-flow kinetic studies using protein-to-membrane FRET to monitor association and dissociation time courses reveal that this affinity decrease arises from a corresponding decrease in the on-rate for GRP1-PH domain docking with little or no change in the off-rate for domain dissociation from membrane-bound PIP(3). Overall, these findings indicate that the PH domain interacts not only with its target lipid, but also with other features of the membrane surface. The results are consistent with a previously undescribed type of two-step search mechanism for lipid binding domains in which weak, nonspecific electrostatic interactions between the PH domain and background anionic lipids facilitate searching of the membrane surface for PIP(3) headgroups, thereby speeding the high-affinity, specific docking of the domain to its rare target lipid.

Indexed as

Lipid MetabolismBlood ProteinsData Interpretation, StatisticalFluorescence Resonance Energy TransferHumansKineticsPhosphoproteinsProtein BindingProtein Structure, TertiaryReceptors, Cytoplasmic and NuclearSequence HomologyTime FactorsBlood Proteinsphosphatidylinositol receptorsPhosphoproteinsplatelet protein P47Receptors, Cytoplasmic and Nuclear

Identifiers

PMID15610010
PMCPMC3625374
OpenAlexW2039921700

What OpenQuestion holds

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Read underepoch 390

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.