ArticleCellular signalling2008
Dynamic interaction between Arf GAP and PH domains of ASAP1 in the regulation of GAP activity.
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.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- The PH domain in the ArfGAP ASAP1 drives catalytic activation through an unprecedented allosteric mechanism.bioRxiv : the preprint server for biology · 2024Article
- ASAP1 activates the IQGAP1/CDC42 pathway to promote tumor progression and chemotherapy resistance in gastric cancer.Cell death & disease · 2023Article
- Interaction of the N terminus of ADP-ribosylation factor with the PH domain of the GTPase-activating protein ASAP1 requires phosphatidylinositol 4,5-bisphosphate.The Journal of biological chemistry · 2019Article
- ACAP1 assembles into an unusual protein lattice for membrane deformation through multiple stages.PLoS computational biology · 2019Article
- Invited review: Small GTPases and their GAPs.Biopolymers · 2016Review
- Molecular Basis for Cooperative Binding of Anionic Phospholipids to the PH Domain of the Arf GAP ASAP1.Structure (London, England : 1993) · 2015Article
- Efficient and generalized processing of multidimensional NUS NMR data: the NESTA algorithm and comparison of regularization terms.Journal of biomolecular NMR · 2015Article
- The Arf GAP AGAP2 interacts with β-arrestin2 and regulates β2-adrenergic receptor recycling and ERK activation.The Biochemical journal · 2013Article
- Quantitative Analysis of Guanine Nucleotide Exchange Factors (GEFs) as Enzymes.Cellular logistics · 2013Article
- On the supertertiary structure of proteins.Nature chemical biology · 2012Article
- GTP-binding protein-like domain of AGAP1 is protein binding site that allosterically regulates ArfGAP protein catalytic activity.The Journal of biological chemistry · 2012Article
- A PH domain in the Arf GTPase-activating protein (GAP) ARAP1 binds phosphatidylinositol 3,4,5-trisphosphate and regulates Arf GAP activity independently of recruitment to the plasma membranes.The Journal of biological chemistry · 2009Article
- Autoinhibition of Arf GTPase-activating protein activity by the BAR domain in ASAP1.The Journal of biological chemistry · 2009Article
- Allosteric properties of PH domains in Arf regulatory proteins.Cellular logisticsReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
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.