Evidence map›Paper›PMID 18675341›Full record

ArticleCellular signalling2008

Dynamic interaction between Arf GAP and PH domains of ASAP1 in the regulation of GAP activity.

Ruibai Luo, Lisa M Miller Jenkins, Paul A Randazzo, James Gruschus

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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  10. On the supertertiary structure of proteins.Nature chemical biology · 2012
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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

4 authors at 2 institutions in 1 country.

Ruibai LuoLaboratory of Cellular and Molecular Biology, National Institutes of Health, Bethesda, MD 20892, United Sates.
Lisa M Miller Jenkins
Paul A Randazzo
James Gruschus
National Institutes of Health · USNational Cancer Institute · US

Funding

Regulation of ADP-ribosylation factorZIABC007365 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RANDAZZO, PAUL A · 2009 to 2025
$27.9M
REGULATION OF ADP-RIBOSYLATION FACTORZ01BC007365 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RANDAZZO, PAUL A · 1996 to 2008
$3.3M
Intramural NIH HHS Z01 BC007365Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

ASAP family Arf GAPs induce the hydrolysis of GTP bound to the Ras superfamily protein Arf1, regulate cell adhesion and migration and have been implicated in carcinogenesis. The ASAP proteins have a core catalytic domain of PH, Arf GAP and Ank repeat domains. The PH domain is necessary for both biological and catalytic functions of ASAP1 and has been proposed to be integrally folded with the Arf GAP domain. Protection studies and analytical ultracentrifugation studies previously reported indicated that the domains are, at least partly, folded together. Here, using NMR spectroscopy and biochemical analysis, we have further tested this hypothesis and characterized the interdomain interaction. A comparison of NMR spectra of three recombinant proteins comprised of either the isolated PH domain of ASAP1, the Arf GAP and ankyrin repeat domain or all three domains indicated that the PH domain did interact with the Arf GAP and Ank repeat domains; however, we found a significant amount of dynamic independence between the PH and Arf GAP domains, consistent with the interactions being transient. In contrast, the Arf GAP and Ank repeat domains form a relatively rigid structure. The PH-Arf GAP domain interaction partially occluded the phosphoinositide binding site in the soluble protein, but binding studies indicated the PIP2 binding site was accessible in ASAP1 bound to a lipid bilayer surface. Phosphoinositide binding altered the conformation of the PH domain, but had little effect on the structure of the Arf GAP domain. Mutations in a loop of the PH domain that contacts the Arf GAP domain affected PIP2 binding and the K(m) and k(cat) for converting Arf1 GTP to Arf1 GDP. Based on these results, we generated a homology model of a composite PH/Arf GAP/Ank repeat domain structure. We propose that the PH domain contributes to Arf GAP activity by either binding to or positioning Arf1 GTP that is simultaneously bound to the Arf GAP domain.

Indexed as

Adaptor Proteins, Signal TransducingADP-Ribosylation FactorsBinding SitesCatalysisGTPase-Activating ProteinsInositol PhosphatesLipid BilayersMagnetic Resonance SpectroscopyModels, MolecularMutationPhosphatidylinositol 4,5-DiphosphatePhospholipidsProtein BindingProtein Structure, SecondaryProtein Structure, TertiaryAdaptor Proteins, Signal TransducingADP-Ribosylation FactorsGTPase-Activating ProteinsInositol PhosphatesLipid BilayersPhosphatidylinositol 4,5-DiphosphatePhospholipids

Identifiers

PMID18675341
PMCPMC2574850
OpenAlexW2021597866

What OpenQuestion holds

Textmetadata
LicenceTDM
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.