Affinage

ASAP1

Arf-GAP with SH3 domain, ANK repeat and PH domain-containing protein 1 · UniProt Q9ULH1

Length
1129 aa
Mass
125.5 kDa
Annotated
2026-06-09
86 papers in source corpus 43 papers cited in narrative 43 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ASAP1 is a multi-domain scaffold and PIP2-dependent Arf GTPase-activating protein that integrates phospholipid signals, Arf GTPases, and the actomyosin cytoskeleton to control focal adhesion dynamics, invadopodium/podosome formation, dorsal ruffle generation, endocytic recycling, and ciliary receptor trafficking (PMID:9819391, PMID:10725410, PMID:18685082, PMID:22983554). It was originally purified as a PIP2-dependent GAP acting on Arf1 and Arf5 but not Arf6, with catalysis requiring the PH domain in concert with the Arf GAP domain (PMID:9819391, PMID:11773070, PMID:15212764). PIP2 binding to the PH domain is not merely a recruitment cue but an allosteric activator: cooperative binding at canonical and atypical sites drives a conformational switch that orients the PH domain to engage Arf·GTP at the membrane and accelerate hydrolysis, restricting the conformational motions of membrane-bound Arf1 to expose its catalytic regions (PMID:10734117, PMID:26365802, PMID:32998886, PMID:37989735). The N-terminal BAR domain serves dual roles—it autoinhibits GAP activity through intramolecular contacts with the PH/GAP domains, and it independently dimerizes to bend membranes, bind and bundle actin filaments via a lysine-rich cluster (K75/K76/K79), and bind nonmuscle myosin 2A, thereby coupling membrane remodeling to actin organization (PMID:16431365, PMID:19017632, PMID:26893376, PMID:31785555, PMID:32444496, PMID:35143843). GAP activity and BAR-domain actin/NM2A binding act coordinately to maintain focal adhesions and stress fibers, with Arf5 loss phenocopying ASAP1 depletion (PMID:40194952). The C-terminal SH3 domain, through a noncanonical acidic binding pocket, mediates interactions with proline-rich partners including FAK, Pyk2, and MICAL1, and Pyk2 phosphorylates ASAP1 to inhibit its GAP activity (PMID:12058076, PMID:12771146, PMID:36674928, PMID:39265663). ASAP1 is recruited to focal adhesions by CrkL and CD2AP and nucleates a ciliary trafficking complex with Arf4, Rab11, FIP3, and Rabin8 that targets rhodopsin to the cilium (PMID:12522101, PMID:15632162, PMID:18685082, PMID:22983554, PMID:25673879). In disease contexts, ASAP1 functions as an Arf6 effector promoting NFAT1-driven invasion in uveal melanoma and participates in TGFβ/SMAD and IQGAP1/CDC42 signaling in cancers (PMID:37500798, PMID:36792578, PMID:40742091).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1998 High

    Established ASAP1's defining biochemical activity—answering whether it was an enzyme by showing it is a PIP2-dependent Arf GAP physically coupled to Src-family signaling.

    Evidence Protein purification, in vitro GAP assay, GST pulldown, and in-cell phosphorylation

    PMID:9819391

    Open questions at the time
    • Did not resolve how PIP2 stimulates catalysis
    • Substrate specificity among Arf isoforms not yet defined
  2. 2000 High

    Linked the enzymatic activity to cellular function by localizing ASAP1 to focal adhesions and showing GAP activity is required for cell spreading and dorsal ruffle control.

    Evidence Fluorescence microscopy and cell spreading/PDGF assays with wild-type vs catalytically inactive mutant

    PMID:10725410

    Open questions at the time
    • GAP-independent functions hinted but not mechanistically separated
  3. 2000 High

    Resolved the role of PIP2 by showing the PH domain is an allosteric activator distinct from a membrane recruitment signal.

    Evidence In vitro GAP assays, limited proteolysis, and domain deletion analysis

    PMID:10734117

    Open questions at the time
    • Atomic structure of the conformational change unresolved
  4. 2001 High

    Defined in vivo substrate specificity (Arf1 not Arf6) and dissected two independent downstream pathways—GAP-dependent motility versus GAP-independent spreading inhibition.

    Evidence Cell-based ARF GAP assay, stable overexpression, motility assay, GAP-domain deletion mutant

    PMID:11773070

    Open questions at the time
    • Effectors of the GAP-independent spreading pathway not identified
  5. 2002 High

    Identified FAK as a direct SH3-domain partner linking ASAP1 to focal adhesion assembly.

    Evidence Yeast two-hybrid, reciprocal Co-IP/pulldown, cell spreading assay with binding/GAP mutants

    PMID:12058076

    Open questions at the time
    • Whether FAK binding regulates GAP activity not tested
  6. 2003 Medium

    Established phospho-regulation and adapter recruitment—Pyk2 phosphorylates ASAP1 to inhibit GAP activity, and CrkL directs it to peripheral adhesions.

    Evidence Yeast two-hybrid, Co-IP, in vitro kinase assay with mapped sites, fluorimetric GTPase assay; CrkL recruitment with SH2-mutant

    PMID:12522101 PMID:12771146

    Open questions at the time
    • Single-lab findings
    • Functional consequence of localization on Arf signaling not quantified
  7. 2005 High

    Defined the catalytic mechanism as a two-step conformational model with a composite PH–GAP substrate-binding site, and validated cellular function via CD2AP-dependent recruitment.

    Evidence Saturation kinetics, FRET, limited proteolysis, AUC; CD2AP mislocalization and siRNA with Arf1 GTP-loading readout

    PMID:15632162 PMID:16038802

    Open questions at the time
    • Atomic interface between PH and GAP domains not yet defined
  8. 2006 High

    Discovered the BAR domain as a membrane-bending module regulated by Arf1·GTP, expanding ASAP1's role into endocytic recycling of EGFR.

    Evidence In vitro membrane tubulation with EM, dimerization analysis, EGFR trafficking assay with BAR deletion

    PMID:16431365

    Open questions at the time
    • In vivo significance of tubulation for recycling not fully established
  9. 2007 High

    Provided rigorous catalytic kinetics and transition-state trapping, and defined ASAP1 as a coincidence detector for invadopodium/podosome formation requiring BAR, SH3, and Src phosphorylation but not GAP activity.

    Evidence Steady-state/single-turnover kinetics with AlF4- trapping; siRNA rescue with systematic domain mutants

    PMID:17112341 PMID:17893324

    Open questions at the time
    • How the distinct domain inputs are integrated spatially is unresolved
  10. 2008 High

    Resolved BAR autoinhibition and dynamic PH–GAP interactions, and connected ASAP1 to Rab11/FIP3-dependent recycling endosome trafficking.

    Evidence AUC, kinetics with BAR loop mutagenesis, NMR; yeast two-hybrid/Co-IP and transferrin trafficking with FIP3

    PMID:18675341 PMID:18685082 PMID:19017632

    Open questions at the time
    • How BAR autoinhibition is relieved in cells not defined
  11. 2011 Medium

    Identified GEFH1 as a BAR-binding negative regulator coupling Rho exchange activity to podosome assembly through ASAP1.

    Evidence Yeast two-hybrid, Co-IP, GAP assay, siRNA/overexpression

    PMID:21352810

    Open questions at the time
    • Single lab
    • Mechanism of GAP inhibition by GEFH1 not defined
  12. 2012 High

    Established ASAP1 as a scaffold for ciliary receptor targeting, assembling Arf4, Rab11, Rabin8, and rhodopsin and recognizing the rhodopsin ciliary targeting signal.

    Evidence siRNA knockdown, Co-IP, photoreceptor transport assay

    PMID:22983554

    Open questions at the time
    • Order of complex assembly not yet defined
  13. 2015 High

    Solved the PH domain structure revealing cooperative dual-site PIP2 binding, and showed FIP3 orchestrates the Rab11-Rabin8-Rab8 cascade by competing with rhodopsin for ASAP1.

    Evidence X-ray crystallography with mutagenesis; Co-IP competition and trafficking assays

    PMID:25673879 PMID:26365802

    Open questions at the time
    • Single-lab ciliary mechanism
    • Generality beyond rhodopsin cargo not tested
  14. 2015 Medium

    Extended ASAP1 function to immune cell migration and matrix degradation, linking it to dendritic cell motility relevant to tuberculosis susceptibility.

    Evidence siRNA knockdown in primary human dendritic cells, matrix degradation and migration assays

    PMID:25774636

    Open questions at the time
    • Single study in DCs
    • Molecular pathway to migration not dissected
  15. 2016 High

    Identified nonmuscle myosin 2A as a direct BAR-PH partner, positioning ASAP1 as a positive regulator of NM2A in adhesion, migration, and dorsal ruffle formation.

    Evidence In vitro binding, reciprocal Co-IP, siRNA knockdown with NM2A rescue

    PMID:26893376

    Open questions at the time
    • How ASAP1 modulates NM2A contractility mechanically not defined
  16. 2019 High

    Defined the BAR domain as a direct actin filament binding and bundling module dependent on a lysine cluster, and established the Arf1 N-terminal extension as the PIP2-dependent regulatory contact controlling GAP activity.

    Evidence Actin cosedimentation, domain-swap and point mutants, cell-based actin remodeling; GAP kinetics, peptide inhibition, NMR binding

    PMID:31591270 PMID:31785555

    Open questions at the time
    • Coupling of actin bundling to GAP catalysis in cells not resolved
  17. 2019 Medium

    Demonstrated ASAP1's requirement for mesenchymal progenitor differentiation in vivo, linking loss to growth retardation, delayed ossification, and impaired FAK/Src and PI3K/AKT signaling.

    Evidence Gene-trap mouse, in vitro differentiation assays, Western blotting for signaling components

    PMID:31246957

    Open questions at the time
    • Single lab
    • Direct molecular link from ASAP1 to the signaling defects not established
  18. 2020 High

    Resolved the atomic-level allosteric switch by which cooperative PIP2 binding orients the PH domain for Arf1 contact, and characterized BAR-driven unipolar actin bundling and filament stabilization.

    Evidence NMR, neutron reflectometry, MD simulation; actin cosedimentation, TIRF/EM, cell-based projection assays

    PMID:32444496 PMID:32998886

    Open questions at the time
    • Integration of bundling activity with membrane-bound GAP function in vivo unresolved
  19. 2021 Medium

    Showed ASAP1 regulates Mycobacterium tuberculosis uptake in macrophages through actin cytoskeleton remodeling.

    Evidence siRNA knockdown, confocal microscopy, CFU assay, F-actin staining

    PMID:34058694

    Open questions at the time
    • Single lab
    • Direct effector linking ASAP1 to uptake not identified
  20. 2022 High

    Pinpointed the lysine-rich cluster (K75/K76/K79) as the structural determinant for actin binding and bundling required for cellular stress fiber maintenance.

    Evidence Structural modeling, charge mutagenesis, cosedimentation/bundling assays, siRNA rescue in U2OS cells

    PMID:35143843

    Open questions at the time
    • Whether the same residues affect GAP activity not tested
  21. 2023 High

    Defined SH3-domain ligand recognition modes (MICAL1 PRM and ankyrin-B), establishing a noncanonical acidic binding pocket and expanding the ASAP1 partner network, and showed the PH domain restricts membrane-bound Arf1 conformational dynamics.

    Evidence X-ray crystallography with ITC and mutagenesis; NMR/neutron reflectometry/MD for Arf1 dynamics

    PMID:36674928 PMID:37989735 PMID:39265663

    Open questions at the time
    • Functional consequence of most newly predicted SH3 partners not validated
  22. 2023 Medium

    Placed ASAP1 in oncogenic signaling as an Arf6 effector driving NFAT1-mediated invasion and as a regulator of IQGAP1/CDC42-EGFR-MAPK signaling promoting chemoresistance.

    Evidence Co-IP, NFAT nuclear localization, ubiquitination assays, siRNA/overexpression, xenograft and tumor models

    PMID:36792578 PMID:37500798

    Open questions at the time
    • Single-lab cancer mechanisms
    • Direct enzymatic role of ASAP1 in these pathways unclear
  23. 2024 Medium

    Established that ASAP1 protein levels are controlled by SCF-FBXW7/CUL1-mediated ubiquitination affecting osteogenesis, and connected ASAP1 to neuronal tau seed internalization via A1AR/MSUT2.

    Evidence Co-IP, ubiquitination assays, osteogenesis and osteoporosis models; tau seeding assays with A1AR modulation

    PMID:38472475 PMID:39287759

    Open questions at the time
    • Single-lab findings
    • Mechanism of ASAP1 activity modulation by A1AR not defined
  24. 2025 Medium

    Demonstrated coordinate requirement of GAP and BAR-domain activities for adhesion/stress fiber maintenance, identified additional cytoskeletal partners (MYO1F), and placed ASAP1 in differentiation and EMT pathways (TAZ inactivation, TGFβ/SMAD).

    Evidence Domain-rescue siRNA in multiple cell lines with Arf5 epistasis; proximity proteomics; MEKi epistasis with WWTR1; Co-IP with SMAD2/3

    PMID:39495123 PMID:40194952 PMID:40742091 PMID:41208482

    Open questions at the time
    • Single-lab pathway placements
    • Direct molecular links between ASAP1 enzymatic activity and transcriptional outputs unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ASAP1's distinct domain activities—GAP catalysis, BAR membrane bending and actin bundling, and SH3 scaffolding—are spatially and temporally coordinated within single structures (focal adhesions, podosomes, cilia) in living cells remains unresolved.
  • No integrated model of in-cell domain coordination
  • Physiological triggers relieving BAR autoinhibition unknown
  • In vivo roles of most cancer/neuronal pathways not validated genetically

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0008092 cytoskeletal protein binding 4 GO:0008289 lipid binding 4 GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 4 GO:0005198 structural molecule activity 2
Localization
GO:0005856 cytoskeleton 3 GO:0005886 plasma membrane 3 GO:0005768 endosome 2 GO:0005929 cilium 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-1474244 Extracellular matrix organization 4 R-HSA-162582 Signal Transduction 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9609507 Protein localization 2
Partners
ARF1CD2APCRKLFAKFIP3MICAL1NM2APYK2
Complex memberships
ASAP1-FIP3-Rab11 ternary complexciliary targeting complex (Arf4-Rab11-Rabin8-rhodopsin)

Evidence

Reading pass · 43 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 ASAP1 was purified and cloned as a PIP2-dependent Arf1 GTPase-activating protein (GAP). The PH, zinc finger, and ANK repeat regions together possess PIP2-dependent GAP activity on Arf1 and Arf5 in vitro. ASAP1 associates with the SH3 domains of Src family members and Crk adapter protein in vitro, coprecipitates with Src from cell lysates, and is phosphorylated on tyrosine residues in cells expressing activated Src through the same proline-rich class II Src SH3 binding site. Protein purification, in vitro GAP assay, GST pulldown, co-immunoprecipitation, in-cell phosphorylation Molecular and cellular biology High 9819391
2000 ASAP1 localizes to focal adhesions and cycles with focal adhesion proteins during cell migration. Overexpression of ASAP1 altered focal adhesion morphology and blocked cell spreading and PDGF-induced dorsal ruffle formation; a GAP-inactive mutant had reduced effect on spreading and increased dorsal ruffle formation, demonstrating that GAP activity is required for these cytoskeletal functions. Fluorescence microscopy, cell spreading assay, PDGF-stimulation assay, overexpression of wild-type vs. catalytically inactive mutant Proceedings of the National Academy of Sciences of the United States of America High 10725410
2000 PIP2 activates ASAP1 GAP activity by binding the PH domain, which acts as an allosteric site rather than merely a membrane recruitment signal. The PH domain is necessary for GAP activity even in the absence of phospholipids; PIP2 binding causes a conformational change in the Arf GAP domain. Activation and membrane recruitment can be uncoupled. In vitro GAP activity assays, limited proteolysis, domain deletion/mutation analysis The Journal of biological chemistry High 10734117
2001 ASAP1 (DEF-1) functions as an ARF GAP for ARF1 but not ARF6 in vivo (cell-based ARF GAP assay), unlike ACAP1, ACAP2, and ARFGAP1 which act on both. Enhancement of cell motility by ASAP1 is dependent on GAP activity, whereas inhibition of cell spreading by ASAP1 is GAP-activity independent, indicating two distinct downstream pathways. Cell-based ARF GAP assay, stable overexpression, cell motility assay, GAP-domain deletion mutant The Journal of biological chemistry High 11773070
2002 ASAP1 binds to focal adhesion kinase (FAK) via an interaction between the C-terminal SH3 domain of ASAP1 and the second proline-rich motif in the C-terminal region of FAK. This interaction contributes to focal adhesion assembly; ASAP1 variants that could not bind FAK or lacked GAP activity showed reduced inhibition of cell spreading and failed to prevent paxillin/FAK organization in focal adhesions. Affinity chromatography, yeast two-hybrid, GST pulldown, co-immunoprecipitation, cell spreading assay, overexpression of mutants Molecular biology of the cell High 12058076
2003 CrkL binds ASAP1 via its N-terminal SH3 domain and directs ASAP1 to peripheral focal adhesions. CrkL co-expression recruited endogenous and exogenous ASAP1 to CrkL-induced focal adhesions; an SH2-mutated CrkL that cannot localize to focal adhesions failed to recruit ASAP1. Pulldown/mass spectrometry, co-immunoprecipitation, fluorescence microscopy, overexpression of wild-type vs. SH2-mutant CrkL The Journal of biological chemistry Medium 12522101
2003 Pyk2 interacts with ASAP1 through the proline-rich regions of Pyk2 and the SH3 domain of ASAP1. Pyk2 directly phosphorylates ASAP1 on tyrosine residues (Y308 and Y782) in vitro and in cells; this phosphorylation inhibits ASAP1 GAP activity toward Arf1 as measured by fluorimetric GTPase assay. Yeast two-hybrid, pulldown, co-immunoprecipitation, in vitro kinase assay, fluorimetric Arf-GTPase assay The Journal of biological chemistry High 12771146
2004 ASAP1 interacts with the N-terminus (amino acids 2–17) of Arf1 at an interface distinct from other Arf GAPs (AGAP1, ArfGAP1). Specific mutations in Arf1 alpha-helix 3 and switch regions (notably I46D reducing ASAP1-catalyzed hydrolysis ~10,000-fold with isolated effect on kcat) distinguish ASAP1's catalytic interface from other Arf GAPs. In vitro GAP activity assay, Arf1 mutagenesis, antibody epitope sequestration, in vivo localization studies Cellular signalling High 15212764
2005 ASAP1 regulation by phospholipids requires a direct interaction between its PH and Arf GAP domains; the two domains form a composite substrate-binding site. Saturation kinetics, limited proteolysis, FRET, and fluorescence spectrometry support a two-step model: conformational change upon membrane recruitment followed by a second change upon PIP2 binding. Saturation kinetics, limited proteolysis, FRET, fluorescence spectrometry, analytical ultracentrifugation Cellular signalling High 16038802
2005 CD2AP (CD2-associated protein) binds ASAP1 through its N-terminal SH3 domains. Sequestration of endogenous ASAP1 to mitochondria via a CD2AP SH3-mito fusion protein inhibited cell spreading and migration in response to fibronectin and caused increased GTP loading on Arf1 and loss of paxillin from adhesions. siRNA knockdown of ASAP1 produced the same phenotypes. Affinity chromatography/mass spectrometry, co-immunoprecipitation, GST pulldown, mitochondria mislocalization strategy, siRNA knockdown, GTP-loading assay, fluorescence microscopy The Journal of biological chemistry High 15632162
2005 Arf1 mutant I46D selectively abolishes ASAP1-catalyzed GTP hydrolysis (~10,000-fold reduction in kcat) while having minimal effect on AGAP1 (~3-fold). In vivo, [I46D]Arf1 acts as a constitutively active mutant at the cell periphery, disrupting ASAP1 and paxillin localization. In vitro GAP assay with kinetic analysis, in vivo localization by fluorescence microscopy, mutagenesis Current biology High 16332543
2006 ASAP1 contains an N-terminal BAR domain that together with the PH domain dimerizes into an extended structure that binds acidic phospholipid-containing vesicles and bends membranes to form tubular structures. This bending activity is regulated by Arf1·GTP binding to the Arf GAP domain (acting as an Arf effector). ASAP1 colocalizes with EGFR in tubular recycling structures; the BAR domain is necessary for ASAP1 function in EGFR trafficking and cell spreading. In vitro membrane tubulation assay with electron microscopy, vesicle sedimentation, dimerization analysis, live-cell imaging, EGFR trafficking assay, BAR domain deletion mutant Current biology High 16431365
2007 ASAP1 uses Arf1-GTP as substrate with kcat ~57 s−1 and Km ~2.2 μM (steady-state). AlF4− stabilizes an Arf1-GDP·ASAP1 transition-state complex. Arg-497 mutation severely affects kcat with minimal effect on Km. Mutations of residues predicted to affect Arf1 affinity (W479, I490, R505, L511, D512) instead primarily affected kcat, supporting a conformational change in the Arf1-GTP·ASAP1 complex during catalysis. Steady-state and single-turnover kinetics, AlF4− trapping, mutagenesis, in vivo dorsal ruffle assay The Biochemical journal High 17112341
2007 ASAP1 is required for formation of invadopodia and podosomes. The BAR domain, SH3 domain, and Src phosphorylation site of ASAP1 are each required for podosome formation. The Src binding site and GAP activity are dispensable for podosome formation, suggesting ASAP1 functions as a coincidence detector integrating SH3-domain protein interactions, BAR domain scaffolding, and Src phosphorylation. siRNA knockdown, rescue with ASAP1 mutants (BAR-deleted, SH3-deleted, phosphorylation site mutant, GAP-inactive), fluorescence microscopy Molecular and cellular biology High 17893324
2008 ASAP1 directly binds FIP3 (a Rab11 and Arf6 effector) through its BAR domain as identified by yeast two-hybrid and confirmed by co-immunoprecipitation and in vitro pulldown. FIP3 binding to the BAR domain stimulates ASAP1 GAP activity against Arf1 but not Arf6. ASAP1 forms a ternary complex with Rab11 via FIP3. ASAP1 colocalizes with FIP3 in pericentrosomal recycling endosomes; ASAP1 or FIP3 depletion alters transferrin receptor localization and transferrin trafficking. Yeast two-hybrid, co-immunoprecipitation, in vitro pulldown, GAP activity assay, siRNA knockdown, fluorescence microscopy, transferrin trafficking assay Molecular biology of the cell High 18685082
2008 The BAR domain of ASAP1 autoinhibits GAP activity by intramolecular interaction with the PH and/or Arf GAP domains. The catalytic power of PZA (PH+GAP+Ank) is greater than BAR-PZA; the BAR domain increases Km and decreases kcat. The effect requires the N-terminal loop of the BAR domain and is not due to differential membrane association or membrane curvature changes. Sedimentation velocity analytical ultracentrifugation, in vitro GAP assay on large unilamellar vesicles, steady-state and single-turnover kinetics, BAR loop mutagenesis The Journal of biological chemistry High 19017632
2008 NMR spectroscopy reveals a dynamic interaction between the PH and Arf GAP domains of ASAP1: the domains interact transiently, with the interaction partially occluding the PIP2 binding site in solution. PIP2 binding alters PH domain conformation but has little effect on Arf GAP domain structure. PH domain loop mutations at the GAP-domain interface affect PIP2 binding and both Km and kcat for Arf1 GTP hydrolysis. NMR spectroscopy, in vitro GAP kinetics, mutagenesis, analytical ultracentrifugation, lipid binding assays Cellular signalling High 18675341
2011 GEFH1 (a RhoA guanine nucleotide exchange factor) binds the BAR domain of ASAP1, colocalizes with ASAP1 in podosomes, inhibits ASAP1 GAP activity, and negatively regulates podosome assembly. GEFH1 overexpression inhibited podosome assembly and a GEFH1 mutant lacking the BAR-binding domain was less effective; GEFH1 siRNA knockdown increased the rate of podosome assembly. Yeast two-hybrid, co-immunoprecipitation, fluorescence colocalization, GAP activity assay, overexpression, siRNA knockdown Biochemical and biophysical research communications Medium 21352810
2012 ASAP1 is a scaffold for ciliary receptor targeting that brings together Arf4, Rab11, Rab8-GEF Rabin8, and rhodopsin. Ablation of ASAP1 abolishes ciliary targeting of rhodopsin and causes actin-rich periciliary membrane projections with mislocalized rhodopsin. ASAP1 recognizes the FR ciliary targeting signal of rhodopsin; rhodopsin FR-AA mutant fails to interact with Rab8 and cannot cross the periciliary diffusion barrier. siRNA knockdown, fluorescence microscopy, co-immunoprecipitation, transport assay in photoreceptors The EMBO journal High 22983554
2015 Crystal structure of the ASAP1 PH domain was solved in unliganded and dibutyryl-PIP2-bound forms. PIP2 contacts both a canonical site (C site) and an atypical site (A site); PIP2 dependence of vesicle binding and GAP activity is sigmoidal (cooperative), distinct from the hyperbolic binding seen for PLC-δ1 PH domain. Mutations in either the C or A site reduced PIP2-dependent vesicle binding and GAP activity, supporting cooperative binding mechanism for rapid switching. X-ray crystallography, vesicle binding assay, in vitro GAP activity assay, site-directed mutagenesis Structure High 26365802
2015 ASAP1-depleted dendritic cells show impaired matrix degradation and migration. ASAP1 is involved in actin and membrane remodeling associated with podosomes in dendritic cells; genetic variants reducing ASAP1 expression in M. tuberculosis-infected dendritic cells may impair their migration. siRNA knockdown of ASAP1 in primary human dendritic cells, matrix degradation assay, migration assay Nature genetics Medium 25774636
2015 FIP3 competes with rhodopsin for binding to ASAP1 and displaces it from the ternary complex with Arf4-GTP and ASAP1. FIP3 promotes Rab11a activity and coordinates ASAP1 and Rab11a interactions with Rabin8, facilitating orderly Rab11-Rabin8-Rab8 cascade assembly for ciliary receptor trafficking. Ablation of FIP3 abolishes ciliary targeting similarly to ASAP1 ablation. Co-immunoprecipitation, competition binding assay, siRNA knockdown, fluorescence microscopy, trafficking assay Journal of cell science Medium 25673879
2016 The ASAP1 BAR domain together with the PH domain directly binds nonmuscle myosin 2A (NM2A) in vitro. ASAP1 and NM2A co-immunoprecipitate and colocalize in cells. ASAP1 knockdown reduced colocalization of NM2A and F-actin. Knockdown of either ASAP1 or NM2A produced similar defects in focal adhesions, cell migration, spreading, and circular dorsal ruffles. Exogenous NM2A rescued ASAP1-knockdown CDR defects, positioning ASAP1 as a positive regulator of NM2A. In vitro binding assay, co-immunoprecipitation, siRNA knockdown, rescue experiments, fluorescence microscopy The Journal of biological chemistry High 26893376
2019 PIP2 controls binding of the N-terminal extension (residues 2–17) of ARF1 to the PH domain of ASAP1 and thereby regulates GAP activity. Deletion of the ARF1 N-terminus ([Δ17]ARF1) makes GAP activity largely PIP2-independent. A peptide of residues 2–17 inhibits GAP activity and binds PIP2-dependently to the PH domain including a 17-amino acid interdomain linker N-terminal to the first β-strand. Mutations in the linker or C-terminal α-helix of the PH domain decrease both ARF1 N-terminal binding and GAP activity, and reduce cellular actin remodeling. In vitro GAP assay with truncation and point mutants, peptide inhibition assay, NMR binding assay, cell-based actin remodeling assay The Journal of biological chemistry High 31591270
2019 ASAP1 depletion causes defects in actin stress fiber organization. The BAR-PH fragment is sufficient to affect actin; the N-BAR domain of ASAP1 directly binds and bundles actin filaments in vitro, whereas the Arf GAP and C-terminal SH3 domain reduce BAR-PH binding and bundling. Overexpression of ASAP1 enhanced actin remodeling; replacing the ASAP1 BAR domain with the ACAP1 BAR domain abolished actin effects. siRNA knockdown, overexpression, actin co-sedimentation, domain swap mutants, fluorescence microscopy iScience High 31785555
2019 NMR methyl-geoHARD analysis of the ASAP1 ZA (PH-ArfGAP) domain reveals wide-range conformational dynamics (kex 10²–10⁵ s⁻¹) in the hydrophobic interior, including collective and local motions that may correlate with catalytic function and substrate recognition. Methyl-TROSY NMR, adiabatic relaxation dispersion, CPMG relaxation dispersion Journal of the American Chemical Society Low 31293161
2019 Loss of ASAP1 in mice (gene-trap) impairs adipogenic and osteogenic differentiation of mesenchymal progenitor cells, causing growth retardation and delayed ossification. Mechanistically, FAK/Src and PI3K/AKT signaling is compromised in ASAP1-null MEFs, leading to impaired adipogenic and osteogenic differentiation. Gene-trap mouse model, in vitro differentiation assays, Western blotting for FAK/Src and PI3K/AKT pathway components PLoS genetics Medium 31246957
2020 Binding of multiple PI(4,5)P2 molecules to the ASAP1 PH domain triggers a functionally relevant allosteric conformational switch and maintains the PH domain in a defined orientation that allows critical contacts with Arf1 at the membrane, as determined by combining NMR, neutron reflectometry, and molecular dynamics simulation. NMR, neutron reflectometry, molecular dynamics simulation Science advances High 32998886
2020 The ASAP1 N-BAR domain directly binds F-actin, homodimerization of ASAP1 aligns F-actin in predominantly unipolar bundles, and ASAP1 stabilizes actin filaments against depolymerization. The N-BAR domain moderately reduces spontaneous G-actin polymerization. Overexpression of ASAP1 BAR-PH tandem induced actin-filled cellular projections; an ASAP1 construct lacking the N-BAR domain failed to induce projections. Actin cosedimentation, polymerization and depolymerization assays, TIRF microscopy, confocal microscopy, electron microscopy, overexpression in fibroblasts The Journal of biological chemistry High 32444496
2021 Knockdown of ASAP1 in THP1-derived macrophages increased efficiency of Mycobacterium tuberculosis H37Ra entry and enhanced F-actin aggregation and vinculin/paxillin-rich puncta formation, identifying ASAP1 as a regulator of Mtb uptake through actin cytoskeleton remodeling. siRNA knockdown, fluorescence confocal microscopy, colony forming unit assay, F-actin staining Tuberculosis Medium 34058694
2022 A lysine-rich cluster (K75, K76, K79) in the N-BAR domain of ASAP1 is required for binding and bundling actin filaments. Charge-neutralizing or charge-reversing mutations at these positions reduced BAR-PH binding to F-actin and abrogated actin bundle formation in vitro and cellular actin remodeling in U2OS cells; [K75E, K76E, K79E] full-length ASAP1 did not rescue endogenous ASAP1 knockdown-induced reduction of stress fibers. Structural modeling, mutagenesis, actin co-sedimentation, in vitro bundling assay, cell-based actin remodeling assay, siRNA rescue The Journal of biological chemistry High 35143843
2023 Membrane-bound active Arf1 (Myr-Arf1) explores large conformational dynamics with its G domain oscillating between membrane-associated and membrane-distal conformations. Interaction with the ASAP1 PH domain restricts Arf1 G domain motions and locks it in a conformation exposing functionally relevant regions for catalysis. NMR, neutron reflectometry, molecular dynamics simulations Nature communications High 37989735
2023 Crystal structure of the ASAP1 SH3 domain in complex with the MICAL1 proline-rich motif (PRM) revealed a unique binding mode: ASAP1 SH3 contains two negatively charged patches that recognize the 'xPx+Px+' sequence in MICAL1 PRM, yielding sub-μM affinity. This binding pocket (termed SH3AGS) is also found in GRAF and SKAP1 SH3 domains. X-ray crystallography, ITC/binding affinity measurement, mutagenesis International journal of molecular sciences High 36674928
2023 ASAP1 acts as an effector for ARF6 and mediates HGF/IGF-1 signaling to promote nuclear localization and transcriptional activity of NFAT1 in uveal melanoma. HGF and IGF-1 hyperactivate ARF6, which then interacts with ASAP1 to induce NFAT1 nuclear translocation; inhibition of ASAP1 or NFAT impairs cellular invasiveness and reduces metastasis in a xenograft model. Co-immunoprecipitation (ARF6-ASAP1), NFAT nuclear localization assay, siRNA knockdown, xenograft mouse model Oncogene Medium 37500798
2023 ASAP1 activates the IQGAP1/CDC42 pathway by inhibiting ubiquitin-mediated degradation of IQGAP1, thereby enhancing CDC42 activity. Activated CDC42 upregulates the EGFR-MAPK pathway to promote chemotherapy resistance in gastric cancer. siRNA/overexpression, Co-IP, ubiquitination assay, Western blotting for CDC42/EGFR/MAPK pathway, in vitro and in vivo tumor assays Cell death & disease Medium 36792578
2024 CUL1 promotes ubiquitination and degradation of ASAP1 via the SCF-FBXW7 complex, suppressing osteoblast proliferation and osteogenesis. CUL1 silencing moderated Dex-induced inhibition of proliferation and osteogenesis by restoring ASAP1 levels. Co-immunoprecipitation, ubiquitination assay, CUL1 siRNA knockdown, osteogenesis assay, mouse osteoporosis model Hormones Medium 39287759
2024 The SH3 domain of ASAP1 binds a 12-residue positively charged peptide from the neuronal scaffold protein 440 kDa ankyrin-B via a noncanonical SH3-ligand binding mode. The crystal structure of ASAP1-SH3 in complex with this gAnkB peptide defined a consensus ASAP1-SH3 binding motif, enabling identification of novel binding partners including Clasp1/2, ALS2, β-Pix, DAPK3, PHIP, and Limk1. Crystal structure determination, ITC/binding affinity measurement, mutagenesis, in silico database search The Journal of biological chemistry High 39265663
2024 MSUT2 regulates tau seed internalization into neurons via adenosine receptor 1 (A1AR)-mediated modulation of ASAP1 activity. Down-regulation or inhibition of A1AR modulates ASAP1 activity, reducing internalization of pathogenic tau seeds and tau pathology in neuron cultures and mouse models. siRNA knockdown, tau seeding assay, A1AR inhibitor treatment, neuron culture and mouse model of tau pathology Acta neuropathologica Medium 38472475
2025 ASAP1 and ARF1 are necessary for myogenic differentiation in FN-RMS. Loss of ASAP1 or ARF1/ARF5 (GAP substrates) blocks differentiation and prevents MEK-inhibition-induced inactivation of TAZ (WWTR1), a pro-proliferative transcriptional co-activator. Dual knockdown of ASAP1 and WWTR1 rescued MEKi-induced differentiation, placing ASAP1 upstream of TAZ inactivation. siRNA knockdown, MEK inhibitor treatment, Western blotting for TAZ phosphorylation/activation, myogenic transcription factor expression assay, epistasis rescue experiment Molecular cancer research Medium 39495123
2025 MYO1F interacts with ASAP1 through an SH3-domain-dependent interaction (proximity labeling proteomics, structural modeling, mutagenesis), and ASAP1 colocalizes with MYO1F at actin-rich podosomes and phagocytic cups in macrophages and microglia. Proximity labeling/proteomics, structural modeling, mutagenesis, immunofluorescence colocalization Journal of cell science Medium 41208482
2025 ASAP1 interacts with the SMAD2/3 complex and forms a positive feedback loop with TGFβ signaling, promoting EMT and cell invasiveness in papillary thyroid cancer cells. ASAP1 knockdown reduced p-SMAD2 levels; co-immunoprecipitation confirmed ASAP1-SMAD2/3 interaction. Co-immunoprecipitation, immunofluorescence, Western blotting for p-SMAD2, luciferase reporter assay, lentiviral knockdown/overexpression Cancer medicine Medium 40742091
2025 Both the Arf GAP domain activity and the BAR domain actin/NM2A-binding activity of ASAP1 are required coordinately to maintain focal adhesions and actin stress fibers; neither domain alone is sufficient. Arf5 (a GAP substrate) loss-of-function phenocopies ASAP1 knockdown on SFs and FAs. siRNA knockdown, rescue with domain mutants (GAP-inactive, BAR-deleted), dominant negative and GTPase-deficient Arf5 mutants, fluorescence microscopy in four cell lines Biology of the cell Medium 40194952
2024 The PH domain of ASAP1 enhances GAP activity by >7 orders of magnitude by acting as an active catalytic component, not merely a membrane recruitment signal. NMR and MD simulations show the PH domain directly contacts Arf·GTP at the membrane and allosterically drives conformational rearrangements of the GTP binding site to facilitate charge stabilization and accelerate GTP hydrolysis; mathematical modeling indicates this allosteric contribution equals membrane recruitment in importance. NMR, molecular dynamics simulation, kinetic assays, mutagenesis, mathematical modeling bioRxivpreprint Medium 39763923

Source papers

Stage 0 corpus · 86 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 ASAP1, a phospholipid-dependent arf GTPase-activating protein that associates with and is phosphorylated by Src. Molecular and cellular biology 212 9819391
2000 The Arf GTPase-activating protein ASAP1 regulates the actin cytoskeleton. Proceedings of the National Academy of Sciences of the United States of America 182 10725410
2021 EIF4A3-induced circular RNA ASAP1 promotes tumorigenesis and temozolomide resistance of glioblastoma via NRAS/MEK1/ERK1-2 signaling. Neuro-oncology 170 32926734
2002 The association of ASAP1, an ADP ribosylation factor-GTPase activating protein, with focal adhesion kinase contributes to the process of focal adhesion assembly. Molecular biology of the cell 142 12058076
2015 Susceptibility to tuberculosis is associated with variants in the ASAP1 gene encoding a regulator of dendritic cell migration. Nature genetics 138 25774636
2000 Phosphoinositide-dependent activation of the ADP-ribosylation factor GTPase-activating protein ASAP1. Evidence for the pleckstrin homology domain functioning as an allosteric site. The Journal of biological chemistry 109 10734117
2005 DDEF1 is located in an amplified region of chromosome 8q and is overexpressed in uveal melanoma. Clinical cancer research : an official journal of the American Association for Cancer Research 108 15897555
2012 The Arf GAP ASAP1 provides a platform to regulate Arf4- and Rab11-Rab8-mediated ciliary receptor targeting. The EMBO journal 107 22983554
2007 Src-dependent phosphorylation of ASAP1 regulates podosomes. Molecular and cellular biology 88 17893324
2001 DEF-1/ASAP1 is a GTPase-activating protein (GAP) for ARF1 that enhances cell motility through a GAP-dependent mechanism. The Journal of biological chemistry 81 11773070
2008 ASAP1, a gene at 8q24, is associated with prostate cancer metastasis. Cancer research 78 18519696
2006 A BAR domain in the N terminus of the Arf GAP ASAP1 affects membrane structure and trafficking of epidermal growth factor receptor. Current biology : CB 78 16431365
2008 Arf GTPase-activating protein ASAP1 interacts with Rab11 effector FIP3 and regulates pericentrosomal localization of transferrin receptor-positive recycling endosome. Molecular biology of the cell 65 18685082
2008 Autoinhibition of Arf GTPase-activating protein activity by the BAR domain in ASAP1. The Journal of biological chemistry 64 19017632
2005 Mislocalization or reduced expression of Arf GTPase-activating protein ASAP1 inhibits cell spreading and migration by influencing Arf1 GTPase cycling. The Journal of biological chemistry 62 15632162
2015 Molecular Basis for Cooperative Binding of Anionic Phospholipids to the PH Domain of the Arf GAP ASAP1. Structure (London, England : 1993) 56 26365802
2016 Long non-coding RNAs, ASAP1-IT1, FAM215A, and LINC00472, in epithelial ovarian cancer. Gynecologic oncology 52 27667152
2015 The Arf and Rab11 effector FIP3 acts synergistically with ASAP1 to direct Rabin8 in ciliary receptor targeting. Journal of cell science 49 25673879
2003 CrkL directs ASAP1 to peripheral focal adhesions. The Journal of biological chemistry 49 12522101
2003 The tyrosine kinase Pyk2 regulates Arf1 activity by phosphorylation and inhibition of the Arf-GTPase-activating protein ASAP1. The Journal of biological chemistry 45 12771146
2007 Kinetic analysis of GTP hydrolysis catalysed by the Arf1-GTP-ASAP1 complex. The Biochemical journal 38 17112341
2020 Novel ASAP1-USP6, FAT1-USP6, SAR1A-USP6, and TNC-USP6 fusions in primary aneurysmal bone cyst. Genes, chromosomes & cancer 34 32011035
2019 Loss of ASAP1 in mice impairs adipogenic and osteogenic differentiation of mesenchymal progenitor cells through dysregulation of FAK/Src and AKT signaling. PLoS genetics 34 31246957
2005 Regulation of ASAP1 by phospholipids is dependent on the interface between the PH and Arf GAP domains. Cellular signalling 34 16038802
2016 The Arf GTPase-activating Protein, ASAP1, Binds Nonmuscle Myosin 2A to Control Remodeling of the Actomyosin Network. The Journal of biological chemistry 31 26893376
2012 A SNP in ASAP1 gene is associated with meat quality and production traits in Nelore breed. Meat science 31 22682072
2018 LncRNA ASAP1-IT1 positively modulates the development of cholangiocarcinoma via hedgehog signaling pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 30 29653361
2004 Differences between AGAP1, ASAP1 and Arf GAP1 in substrate recognition: interaction with the N-terminus of Arf1. Cellular signalling 30 15212764
2020 Membrane surface recognition by the ASAP1 PH domain and consequences for interactions with the small GTPase Arf1. Science advances 29 32998886
2015 A pooled shRNA screen for regulators of primary mammary stem and progenitor cells identifies roles for Asap1 and Prox1. BMC cancer 29 25879659
2020 Integrative analysis of genomic amplification-dependent expression and loss-of-function screen identifies ASAP1 as a driver gene in triple-negative breast cancer progression. Oncogene 28 32235890
2019 The ArfGAP ASAP1 Controls Actin Stress Fiber Organization via Its N-BAR Domain. iScience 27 31785555
2016 eIF5B increases ASAP1 expression to promote HCC proliferation and invasion. Oncotarget 25 27694689
2020 The BAR domain of the Arf GTPase-activating protein ASAP1 directly binds actin filaments. The Journal of biological chemistry 24 32444496
2023 ASAP1 activates the IQGAP1/CDC42 pathway to promote tumor progression and chemotherapy resistance in gastric cancer. Cell death & disease 23 36792578
2005 Mutational analysis of the Arf1*GTP/Arf GAP interface reveals an Arf1 mutant that selectively affects the Arf GAP ASAP1. Current biology : CB 23 16332543
2020 Expression of ASAP1 and FAK in gastric cancer and its clinicopathological significance. Oncology letters 22 32566028
2018 Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells. Oncology letters 21 29541211
2008 Dynamic interaction between Arf GAP and PH domains of ASAP1 in the regulation of GAP activity. Cellular signalling 21 18675341
2018 Long non-coding RNA ASAP1-IT1 promotes cell proliferation, invasion and metastasis through the PTEN/AKT signaling axis in non-small cell lung cancer. European review for medical and pharmacological sciences 20 29364481
2008 The AsaP1 peptidase of Aeromonas salmonicida subsp. achromogenes is a highly conserved deuterolysin metalloprotease (family M35) and a major virulence factor. Journal of bacteriology 20 18952802
2023 Myr-Arf1 conformational flexibility at the membrane surface sheds light on the interactions with ArfGAP ASAP1. Nature communications 19 37989735
2016 Loss of EGFR-ASAP1 signaling in metastatic and unresectable hepatoblastoma. Scientific reports 16 27910913
2011 GEFH1 binds ASAP1 and regulates podosome formation. Biochemical and biophysical research communications 16 21352810
2021 Long non‑coding RNA ASAP1‑IT1 suppresses ovarian cancer progression by regulating Hippo/YAP signaling. International journal of molecular medicine 15 33576454
2019 Probing the Broad Time Scale and Heterogeneous Conformational Dynamics in the Catalytic Core of the Arf-GAP ASAP1 via Methyl Adiabatic Relaxation Dispersion. Journal of the American Chemical Society 13 31293161
2019 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 13 31591270
2016 No Significant Effect of ASAP1 Gene Variants on the Susceptibility to Tuberculosis in Chinese Population. Medicine 13 27227929
2023 Activation of NFAT by HGF and IGF-1 via ARF6 and its effector ASAP1 promotes uveal melanoma metastasis. Oncogene 11 37500798
2019 A Common Variant of ASAP1 Is Associated with Tuberculosis Susceptibility in the Han Chinese Population. Disease markers 11 31089398
2022 A lysine-rich cluster in the N-BAR domain of ARF GTPase-activating protein ASAP1 is necessary for binding and bundling actin filaments. The Journal of biological chemistry 9 35143843
2013 Innate and adaptive immune responses of Arctic charr (Salvelinus alpinus, L.) during infection with Aeromonas salmonicida subsp. achromogenes and the effect of the AsaP1 toxin. Fish & shellfish immunology 9 23811350
2018 ASAP1 gene polymorphisms are associated with susceptibility to tuberculosis in a Chinese Xinjiang Muslim population. Experimental and therapeutic medicine 8 29545860
2023 Crystal Structure of the SH3 Domain of ASAP1 in Complex with the Proline Rich Motif (PRM) of MICAL1 Reveals a Unique SH3/PRM Interaction Mode. International journal of molecular sciences 7 36674928
2022 Loss of ASAP1 in the MMTV-PyMT model of luminal breast cancer activates AKT, accelerates tumorigenesis, and promotes metastasis. Cancer letters 7 35181478
2022 Clinicopathological Implications of ASAP1 Expression in Hepatocellular Carcinoma. Pathology oncology research : POR 7 36110251
2021 LncRNA ASAP1-IT1 enhances cancer cell stemness via regulating miR-509-3p/YAP1 axis in NSCLC. Cancer cell international 7 34715859
2020 Asap1 Affects the Susceptibility of Zebrafish to Mycobacterium by Regulating Macrophage Migration. Frontiers in cellular and infection microbiology 7 33194781
2023 miR-212/132 attenuates OVA-induced airway inflammation by inhibiting mast cells activation through MRGPRX2 and ASAP1. Experimental cell research 6 37875175
2020 Knockout of ASAP1 induces autophagy in papillary thyroid carcinoma by inhibiting the mTOR signaling pathway. Pathology, research and practice 6 32307199
2024 MSUT2 regulates tau spreading via adenosinergic signaling mediated ASAP1 pathway in neurons. Acta neuropathologica 5 38472475
2023 Expression profiling of circular RNA reveals a potential miR-145-5p sponge function of circ-AFF2 and circ-ASAP1 in renal cell carcinoma. American journal of translational research 5 36777845
2025 ASAP1 protein macromolecule promotes the growth and development of gastric cancer cells and the remodeling of F-actin cytoskeleton: Expression of VEGF and HIF-1 α proteins. International journal of biological macromolecules 4 40424906
2021 ASAP1 regulates the uptake of Mycobacterium tuberculosis H37Ra in THP1-derived macrophages by remodeling actin cytoskeleton. Tuberculosis (Edinburgh, Scotland) 4 34058694
1999 Monoclonal antibodies against AsaP1, a major exotoxin of the fish pathogen Aeromonas salmonicida subsp. achromogenes, and their application in ELISA. Journal of applied microbiology 4 10583691
2024 CUL1 exacerbates glucocorticoid-induced osteoporosis by enhancing ASAP1 ubiquitination. Hormones (Athens, Greece) 3 39287759
2022 Novel Role of Long Non-Coding RNA ASAP1-IT1 in Progression of Hepatocellular Carcinoma. Frontiers in oncology 3 35712508
2022 Polymorphisms in the ASAP1 and SP110 Genes and Its Association with the Susceptibility to Pulmonary Tuberculosis in a Mongolian Population. Journal of immunology research 3 36249417
2012 Toxoid construction of AsaP1, a lethal toxic aspzincin metalloendopeptidase of Aeromonas salmonicida subsp. achromogenes, and studies of its activity and processing. Veterinary microbiology 3 23031341
2025 ASAP1 and ARF1 Regulate Myogenic Differentiation in Rhabdomyosarcoma by Modulating TAZ Activity. Molecular cancer research : MCR 2 39495123
2025 Actin Binding to the BAR Domain and Arf GAP Activity of ASAP1 Coordinately Control Actin Stress Fibers and Focal Adhesions. Biology of the cell 2 40194952
2025 The MYO1F interactome reveals ASAP1, CD2AP and SH3KBP1 as novel adaptor proteins in podosomes and phagosomes. Journal of cell science 2 41208482
2024 Inhibition of ASAP1 Modulates the Tumor Immune Microenvironment and Suppresses Lung Cancer Metastasis via the p-STAT3 Signaling Pathway. Cell biochemistry and biophysics 2 38874840
2024 The PH domain in the ArfGAP ASAP1 drives catalytic activation through an unprecedented allosteric mechanism. bioRxiv : the preprint server for biology 2 39763923
2015 Regulator of dendritic cell migration, ASAP1 is associated with increased susceptibility to tuberculosis. Clinical genetics 2 25970765
2009 Crystallization and preliminary X-ray diffraction studies of AsaP1_E294A and AsaP1_E294Q, two inactive mutants of the toxic zinc metallopeptidase AsaP1 from Aeromonas salmonicida subsp. achromogenes. Acta crystallographica. Section F, Structural biology and crystallization communications 2 19574642
2023 An Uncharacterised lncRNA Coded by the ASAP1 Locus Is Downregulated in Serum of Type 2 Diabetes Mellitus Patients. International journal of molecular sciences 1 37686290
2019 [ASAP1 knockdown reduces migration of RAW264.7 cells infected with Mycobacterium tuberculosis]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 1 31894003
2005 Assay and functional properties of the tyrosine kinase Pyk2 in regulation of Arf1 through ASAP1 phosphorylation. Methods in enzymology 1 16413287
2026 Case Report: Novel ASAP1::BRAF fusion in a young adult with low-grade temporal lobe glioma. Frontiers in oncology 0 41659712
2026 ASAP1 gene InDel variants are associated with enhanced goat resistance against Brucella infection. Animal bioscience 0 41856082
2025 The PH domain in the ArfGAP ASAP1 drives catalytic activation through an unprecedented allosteric mechanism. Research square 0 40166026
2025 Redefining PH Domain Function: An Active Allosteric Mechanism in ASAP1-Mediated Arf1 GTP Hydrolysis. Research square 0 40470248
2025 ASAP1 Promotes Epithelial to Mesenchymal Transition by Activating the TGFβ Pathway in Papillary Thyroid Cancer. Cancer medicine 0 40742091
2024 New targets and designed inhibitors of ASAP Arf-GAPs derived from structural characterization of the ASAP1/440-kD ankyrin-B interaction. The Journal of biological chemistry 0 39265663
2024 ASAP1 promotes extrahepatic cholangiocarcinoma progression by regulating the Wnt/β-catenin pathway in vitro and in vivo. American journal of cancer research 0 39659924

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