Affinage

Showing WIPF1 — WIP is a alias.

WIPF1

WAS/WASL-interacting protein family member 1 · UniProt O43516

Length
503 aa
Mass
51.3 kDa
Annotated
2026-06-11
100 papers in source corpus 48 papers cited in narrative 48 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

WIPF1 (WIP) is an intrinsically disordered scaffold protein that couples actin nucleation machinery to upstream signals and controls the stability and localization of WASP/N-WASP at sites of actin polymerization (PMID:9405671, PMID:11331876). It was first identified through its direct interaction with WASP, binding at a site distinct from the Cdc42-binding region while carrying its own N-terminal actin- and profilin-binding motifs required to drive actin polymerization (PMID:9405671); the structural basis of the C-terminal interaction was resolved as a peptide that wraps around the N-WASP EVH1/WH1 domain, explaining how WAS disease mutations disrupt WIP binding (PMID:12437929, PMID:29215267). A central function of WIP is to act as a chaperone that protects WASP from calpain- and proteasome-mediated degradation: WASP protein but not mRNA is lost in WIP-deficient cells and restored by re-expression, a mechanism conserved from C. elegans through mouse to a human WIPF1 stop-codon patient in whom WASP was undetectable (PMID:17213309, PMID:22231303, PMID:16378591). WIP positions and activates the N-WASP–Arp2/3 system at diverse actin structures, integrating signals from Nck, cortactin, the F-BAR proteins Toca-1/FBP17 in a membrane-curvature-dependent manner, and DOCK8 (PMID:9694849, PMID:12620186, PMID:15260990, PMID:18923421, PMID:23707428, PMID:27599296). Through these activities WIP drives filopodia, membrane ruffling, pathogen actin tails, podosomes and invadopodia with associated matrix degradation, and clathrin-mediated endocytosis (PMID:10878810, PMID:11331876, PMID:12724353, PMID:17141616, PMID:20952093, PMID:27009365, PMID:28813247). In the immune system WIP is essential for T-cell activation, immune-synapse formation, and IL-2 signaling, for FcεRI-driven mast cell signaling via stabilization of Syk, and for NK-cell cytotoxicity through WASP-independent polarization of lytic granules (PMID:11869681, PMID:14757742, PMID:18258743, PMID:19359486). WIP also exerts WASP-independent functions through direct actin binding, supporting cytoskeletal integrity and T-cell migration, focal adhesion assembly via an actin–MRTF–SRF axis, and regulation of neuronal maturation and synaptic activity (PMID:25246631, PMID:24797074, PMID:21810783). Loss-of-function WIPF1 mutation in humans causes a WAS-like primary immunodeficiency with absent WASP (PMID:22231303).

Mechanistic history

Synthesis pass · year-by-year structured walk · 25 steps
  1. 1997 High

    Established WIP as a physical and functional partner of WASP, defining its core domain architecture (actin/profilin-binding N-terminus, distinct WASP-binding site) and its capacity to drive actin polymerization.

    Evidence Yeast two-hybrid, co-IP from lymphocytes, and truncation-mutant expression in B cells

    PMID:9405671

    Open questions at the time
    • Did not establish whether WIP regulates WASP stability or only localization
    • Mechanism of actin polymerization induction not resolved biochemically
  2. 1998 Medium

    Showed WIP links the adaptor Nck and profilin to the cytoskeleton through domain-specific interactions, placing WIP within receptor-proximal signaling adaptor networks.

    Evidence GST-Nck pulldown and WIP fragment domain mapping in B-cell lysates

    PMID:9694849

    Open questions at the time
    • Single lab, no functional readout for the Nck–WIP interaction
    • Did not test reciprocity in vivo
  3. 1999 High

    Demonstrated functional conservation of the WIP–WASP partnership in endocytosis and cell polarity, mapping the requirement to the WH2 actin- and profilin-binding domains.

    Evidence Yeast genetic suppression/complementation with verprolin orthologs and WIP domain mutants

    PMID:10358064 PMID:9742397

    Open questions at the time
    • Yeast system may not capture mammalian-specific regulatory inputs
    • Did not address WASP stabilization role
  4. 2000 High

    Defined WIP as the recruiter of N-WASP to actin-polymerization sites via the N-WASP WH1 domain, integrating Cdc42 and SH2/SH3-adaptor pathways during pathogen actin-based motility.

    Evidence Cell-based vaccinia and Shigella actin-tail assays with domain mutants and dominant negatives

    PMID:10878810

    Open questions at the time
    • Did not resolve how upstream signals choose between recruitment and activation
    • Quantitative contribution of WIP vs other recruiters unclear
  5. 2001 High

    Established the biochemical activity of WIP: direct N-WASP and actin binding, F-actin stabilization, and a required role with N-WASP in filopodium formation.

    Evidence In vitro pyrene-actin assays, microinjection with function-blocking antibodies, and co-IP/imaging

    PMID:11331876 PMID:11687573

    Open questions at the time
    • Apparent inhibition of Arp2/3 nucleation in vitro vs activation in cells not reconciled
    • Regulation of the WIP–N-WASP unit by phosphorylation not yet addressed
  6. 2002 High

    Genetic loss-of-function established WIP as essential for T-cell activation and immune synapse formation, with cell-type-specific (T vs B) consequences, and showed WIP supports N-WASP recruitment at vesicle surfaces.

    Evidence WIP-knockout mouse T/B cell assays and N-WASP-deficient cell reconstitution with domain mutants

    PMID:11869681 PMID:12147689

    Open questions at the time
    • Did not distinguish actin-scaffolding from WASP-stabilizing contributions to the T-cell phenotype
    • Molecular basis of the divergent B-cell phenotype unresolved
  7. 2002 High

    Resolved the structural recognition mechanism between WIP and the N-WASP EVH1/WH1 domain, providing a molecular explanation for WAS-associated missense mutations that disrupt WIP binding.

    Evidence NMR structure of the N-WASP WH1 domain bound to a WIP peptide

    PMID:12437929

    Open questions at the time
    • Structure of full-length disordered WIP not determined
    • Did not address the actin-dependent second interface
  8. 2003 High

    Extended WIP's effector network to cortactin and to Rac1/PDGF-driven membrane dynamics, with the actin-binding domain required for ruffle formation.

    Evidence Cortactin SH3 pulldowns and in vitro Arp2/3 assays; anti-WIP microinjection and domain mutants in fibroblasts

    PMID:12620186 PMID:12724353

    Open questions at the time
    • How cortactin and N-WASP inputs are coordinated on WIP not resolved
    • In vivo relevance of cortactin synergy to specific actin structures untested
  9. 2004 High

    Identified F-BAR protein Toca-1 as an activator of the predominant cellular N-WASP–WIP complex, establishing cooperative Cdc42 effector logic, and broadened WIP's signaling roles to mast cell FcεRI signaling through Syk stabilization.

    Evidence Biochemical purification and in vitro actin assembly; WIP-/- mast cells with Syk co-IP and stability assays

    PMID:14757742 PMID:15260990

    Open questions at the time
    • Whether Syk stabilization is mechanistically analogous to WASP chaperoning untested
    • Toca-1 vs FBP17 specificity not yet defined
  10. 2006 High

    Established WIP as essential for podosome formation and revealed its role in regulating calpain-mediated WASP cleavage, and identified a WASP-containing actin/myosin megacomplex in NK cells modulated by PKCθ phosphorylation.

    Evidence WIP-/- dendritic cells with calpain inhibitors; co-IP/gel filtration and RNAi in NK cell lines

    PMID:16606694 PMID:17141616

    Open questions at the time
    • How phosphorylation controls complex composition not mechanistically resolved
    • Link between podosome defect and WASP degradation only correlative
  11. 2007 High

    Defined WIP's chaperone function in molecular terms—the WASP-binding domain protects WASP from calpain and proteasomal degradation—while showing this minimal protection is insufficient for full WASP-dependent signaling, and extended conserved WIP–WASP partnership to Drosophila myoblast fusion.

    Evidence WIP-/- T cells with in vitro calpain assays and proteasome/calpain inhibitors; K562 co-expression and domain mapping; Drosophila genetics

    PMID:17205972 PMID:17213309 PMID:17419994 PMID:17711847

    Open questions at the time
    • Identity of the proteasomal E3 ligase for free WASP not defined
    • How the WIP N-terminus inhibits NFAT activation mechanistically unclear
  12. 2008 High

    Established a WASP-independent role for WIP in NK-cell cytotoxicity through lytic granule polarization, demonstrating WIP functions beyond the WIP–WASP axis.

    Evidence RNAi/overexpression in NK cell lines with cytotoxicity assays, subcellular fractionation, and co-localization with lytic granules

    PMID:18258743 PMID:18923421

    Open questions at the time
    • Molecular tether linking WIP to lytic granules unidentified
    • Membrane-curvature activation studied in vitro only
  13. 2009 High

    Used a WIP/WASP double knockout to show WIP is required for IL-2/STAT5 signaling and subcortical actin integrity beyond WASP loss alone, separating WIP-specific from WASP-shared functions.

    Evidence WIP/WASP double-KO mouse T cells with STAT5 phosphorylation, CD25, and F-actin readouts versus single-KO controls

    PMID:19359486

    Open questions at the time
    • Direct molecular link between WIP and the IL-2 receptor signaling apparatus not defined
    • Whether actin defect causes the signaling defect untested
  14. 2010 High

    Mapped the cortactin-binding region of WIP as essential for matrix-degrading function of podosomes, dissociating podosome assembly from degradative activity.

    Evidence WIP-/- dendritic cells rescued with a domain-deletion mutant and gelatin degradation assays

    PMID:20952093

    Open questions at the time
    • How the cortactin-binding region directs MMP delivery not resolved
    • Direct cortactin requirement not genetically isolated
  15. 2011 High

    Revealed dynamic competitive regulation of the WASP–WIP complex (by Blow in Drosophila) driving rapid component exchange required for fusion-pore formation, and identified WIP as a negative regulator of neuronal maturation and synaptic activity.

    Evidence Drosophila genetics with competition and FRAP assays; WIP-/- mouse hippocampal neuron morphometry and electrophysiology

    PMID:21571220 PMID:21810783

    Open questions at the time
    • Whether mammalian factors analogous to Blow regulate WASP–WIP exchange unknown
    • Molecular pathway underlying the neuronal phenotype not yet defined here
  16. 2012 High

    Confirmed in humans that WIPF1 loss-of-function abolishes WASP protein and causes a WAS-like immunodeficiency, validating the chaperone model as clinically relevant.

    Evidence Patient cells with a homozygous WIPF1 stop-codon mutation, WASP immunoblotting, and lentiviral WIP rescue

    PMID:22231303

    Open questions at the time
    • Genotype-phenotype range of WIPF1 deficiency not delineated
    • Did not address WASP-independent contributions to patient phenotype
  17. 2013 High

    Established WIP (or WIRE) as the obligatory link between Nck and N-WASP for Arp2/3-dependent actin assembly, separating the recruitment step from the actin-stimulation step within Nck.

    Evidence Nck-, WIP-, and N-WASP-deficient MEFs in vaccinia actin-tail assays with Nck/WIP domain mutants

    PMID:23707428

    Open questions at the time
    • How the first/third Nck SH3 domains stimulate assembly mechanistically unresolved
    • Generality beyond pathogen tails to physiological structures not tested
  18. 2014 High

    Defined two distinct WIP–WASP interfaces (a phosphorylation-dependent WH1 interface and an actin-dependent VCA interface) and showed WASP activation couples interface remodeling to exposure of its ubiquitylation site, mechanistically linking activation to degradation; also isolated WIP's WASP-independent actin-binding functions in T-cell migration and focal-adhesion/MRTF–SRF signaling, and resolved the disordered actin-binding motif by NMR.

    Evidence Triple-color FRET in live T cells with PKCθ inhibitors/phosphomimetics; Btk kinase identification with phosphomutants; WIPΔABD knock-in mice; WIP-/- fibroblasts with MRTF/SRF rescue; NMR of the ABM

    PMID:24797074 PMID:24962707 PMID:25246631 PMID:25413351 PMID:25495558

    Open questions at the time
    • How phospho- and actin-dependent interfaces are temporally coordinated in vivo not fully resolved
    • Identity of the WASP ubiquitin ligase still unaddressed
  19. 2015 Medium

    Extended the WIP scaffold to intersectin adaptors, forming an ITSN1–WIP–N-WASP trimer that localizes to invadopodia.

    Evidence Co-IP, GST-SH3 pulldown, and co-localization in breast cancer cells

    PMID:25797047

    Open questions at the time
    • Functional requirement of ITSN1 for invadopodia not tested here
    • Single lab, no reciprocal in vivo validation
  20. 2016 High

    Bridged DOCK8 to WASP-dependent actin regulation via WIP in T cells, distinguished non-redundant WIP versus WIRE roles in invadopodium assembly versus maturation, and uncovered a WASP-independent oncogenic role for WIP in stabilizing YAP/TAZ via endosomal sequestration of the β-catenin destruction complex.

    Evidence Co-IP and functional T-cell assays in DOCK8/WAS patient cells; RNAi with invadopodium assays; WIP knockdown/overexpression with fractionation, inhibitors, and xenografts

    PMID:27009365 PMID:27599296 PMID:27851961

    Open questions at the time
    • Mechanism of endosomal sequestration of the destruction complex not resolved at molecular detail
    • How DOCK8 GEF activity is coupled to the WIP scaffold unclear
  21. 2017 High

    Provided high-resolution structure of the WIP C-terminus–WASp complex linking specific residues to WASp affinity and ubiquitylation, and placed WIP downstream of AKT2 in mutant-p53-driven tumorigenesis controlling YAP/TAZ and cancer stem-cell markers.

    Evidence NMR/FRET of the WIP–WASp complex with peptide mutants and ubiquitylation assays; co-IP, phosphorylation, and in vivo tumor assays

    PMID:28166194 PMID:29215267

    Open questions at the time
    • Structural data did not capture the full intact complex in cells
    • AKT2-WIP phosphosite functional consequences from single lab
  22. 2018 Low

    Implicated WIP in RAB4-positive recycling endosome trafficking with ITSN1 and in RhoA-dependent cancer cell invasion, broadening its membrane-trafficking and tumor-promoting roles.

    Evidence Co-IP, transferrin recycling and co-localization assays in MCF-7; co-IP and invasion assays in lung adenocarcinoma

    PMID:27939884 PMID:29958948

    Open questions at the time
    • Co-IP/co-localization only without domain dissection of vesicle function
    • RhoA interaction shown by single co-IP without reciprocal validation
  23. 2019 Medium

    Demonstrated a WASP-independent endocytic function of WIP-1 in scission of clathrin-coated pits via direct G-actin binding and cortactin-domain-mediated recruitment of DBN-1/Abp1 and dynamin.

    Evidence RNAi and live imaging in C. elegans intestine with domain mapping of the WIP-1–DBN-1 interaction

    PMID:31118234

    Open questions at the time
    • Conservation of this WASP-independent scission role in mammals untested
    • How G-actin binding triggers scission mechanistically unresolved
  24. 2020 Medium

    Connected WIP to the NRF2 oxidative-stress response, showing WIP restrains KEAP1 E3 activity through actin-cytoskeleton-dependent KEAP1–F-actin binding rather than autophagic protection.

    Evidence WIP/KEAP1 knockdown, NRF2 mutant overexpression, ROS measurement, and KEAP1–F-actin co-IP in glioblastoma cells

    PMID:32825452

    Open questions at the time
    • Single lab, no in vivo confirmation
    • Direct mechanism by which actin organization controls KEAP1 activity unresolved
  25. 2023 Medium

    Extended WIPF1 actin functions to extravillous trophoblast podosomes via ACTN4 interaction and to MYOCD-driven PI3K/AKT signaling in gastric cancer, implicating WIPF1 in trophoblast differentiation/disease and tumor progression.

    Evidence Co-IP with ARG54 site mutagenesis and migration/podosome assays in trophoblasts; knockdown/overexpression with pathway readouts and MYOCD rescue in gastric cancer

    PMID:38026208 PMID:40821124

    Open questions at the time
    • ACTN4 interaction from single lab without reciprocal in vivo validation
    • Gastric cancer mechanism not dissected at molecular level

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple WIP interfaces, phosphorylation inputs (PKCθ, Btk, AKT2), and partner choices are integrated in space and time to switch between WASP stabilization, WASP activation/degradation, and WASP-independent functions remains unresolved.
  • No unified model coupling signal input to interface remodeling in vivo
  • E3 ligase mediating WASP/WIP-regulated ubiquitylation unidentified
  • Structural basis of full-length WIP scaffolding not determined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 5 GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 4 GO:0140313 molecular sequestering activity 3
Localization
GO:0005856 cytoskeleton 4 GO:0005886 plasma membrane 3 GO:0031410 cytoplasmic vesicle 3 GO:0005829 cytosol 2
Pathway
R-HSA-168256 Immune System 5 R-HSA-162582 Signal Transduction 4 R-HSA-5653656 Vesicle-mediated transport 4 R-HSA-1643685 Disease 3
Partners
CORTACTINDOCK8ITSN1N-WASPNCKPROFILINTOCA-1WASP
Complex memberships
ITSN1–WIP–N-WASP trimeric complexN-WASP–WIP–Arp2/3 nucleation complexWIP–WASP/N-WASP complexWIP–WASp–actin–myosin IIA megacomplex (NK cells)

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 WIP (WIPF1) was identified as a WASP-interacting protein via yeast two-hybrid; it coimmunoprecipitates with WASP from lymphocytes, binds WASP at a site distinct from the Cdc42 binding site, and has actin and profilin binding motifs. Expression of WIP in B cells induced actin polymerization and cerebriform projections; a WIP truncation mutant lacking the actin-binding motif failed to do so, establishing the actin-binding domain as required for this function. Yeast two-hybrid, co-immunoprecipitation, expression in human B cells with truncation mutant Proceedings of the National Academy of Sciences of the United States of America High 9405671
1998 WIP binds to the adaptor protein Nck via the second SH3 domain of Nck; the Nck-binding site on WIP (amino acids 321–415) is distinct from the WASP-binding site (amino acids 416–488). Profilin is found in Nck precipitates, suggesting Nck links to the cytoskeleton via WIP and profilin. GST pulldown with recombinant Nck from BJAB cell lysates, domain mapping with WIP fragments The Journal of biological chemistry Medium 9694849
1998 The yeast WIP homologue End5p/verprolin interacts with the WASp homologue Las17p (yeast ortholog of WASP); high-copy LAS17 partially suppresses end5-1 growth and endocytosis defects, establishing that the WIP–WASP functional partnership is conserved in yeast and essential for endocytosis. Yeast two-hybrid, high-copy suppressor screen, endocytosis assay in yeast Current biology : CB High 9742397
1999 Human WIP functionally complements yeast vrp1 (verprolin) mutations, restoring cytoskeletal organization and endocytosis; this complementation requires the WH2 actin-binding domain and the profilin-binding domain of WIP, establishing these as the functional core of WIP's role in cell polarity and actin organization. Yeast complementation assay, WIP domain mutants, immunofluorescence localization in yeast The Journal of biological chemistry High 10358064
2000 WIP mediates recruitment of N-WASP to vaccinia virus actin tails via the WH1 domain of N-WASP (not the polyproline region). For Shigella, N-WASP recruits WIP. The N-WASP–WIP complex integrates signaling cascades (SH2/SH3-adaptor pathway and Cdc42 pathway) leading to Arp2/3-dependent actin polymerization and pathogen actin-based motility. Cell-based actin tail assays with domain mutants, co-localization, dominant-negative experiments Nature cell biology High 10878810
2001 WIP directly interacts with N-WASP and with actin; WIP retards N-WASP/Cdc42-activated actin polymerization by the Arp2/3 complex and stabilizes actin filaments. Microinjection of WIP induces filopodia in an N-WASP-dependent manner; anti-WIP antibody blocks filopodium induction by bradykinin, Cdc42(V12), and N-WASP, establishing WIP and N-WASP as a functional unit in filopodium formation. In vitro actin polymerization assay (pyrene-actin), microinjection with function-blocking antibodies, immunofluorescence Nature cell biology High 11331876
2001 Rat WIP co-immunoprecipitates with N-WASP in vivo and co-localizes with actin stress fibers. Co-expression of WIP and N-WASP redistributes N-WASP from the nucleus to perinuclear/actin-associated locations and dissolves stress fibers while promoting filopodia formation, indicating WIP controls N-WASP subcellular localization. Co-immunoprecipitation, immunofluorescence, co-expression in fibroblasts and tumor cells The Journal of biological chemistry Medium 11687573
2002 NMR structure of the N-WASP EVH1 (WH1) domain in complex with a 25-residue WIP motif revealed a novel recognition mechanism: the WIP peptide wraps around the EVH1 domain contacting an extended surface, mechanistically explaining how WAS missense mutations in this domain disrupt WIP binding. NMR structure determination with WIP peptide Cell High 12437929
2002 WIP-deficient mice have T cells that fail to proliferate, secrete IL-2, increase F-actin content, polarize, or form immune synapses after TCR ligation, establishing WIP as essential for T cell activation and immunological synapse formation. WIP-deficient B cells show enhanced proliferation, indicating differential roles in T vs B cells. WIP knockout mouse model, T cell proliferation/activation assays, F-actin staining, conjugate formation assay Immunity High 11869681
2002 Phosphatidylinositol 4,5-bisphosphate (PIP2)-induced vesicle motility requires N-WASP and involves WIP recruitment alongside Nck and Grb2; reconstitution in N-WASP-defective cells with mutants showed that both the WH1 domain (which recruits WIP) and the polyproline domain contribute significantly to N-WASP recruitment/activation at vesicle surfaces. Reconstitution of vesicle motility in N-WASP-deficient cells with domain mutants, fluorescence microscopy The Journal of biological chemistry High 12147689
2003 Cortactin SH3 domain interacts with WIP in an SH3-dependent manner (GST pulldown). WIP increases the efficiency of cortactin-mediated Arp2/3 complex activation in a concentration-dependent manner, and co-expression of cortactin and WIP stimulates membrane protrusions. Yeast two-hybrid, GST-cortactin pulldown, in vitro Arp2/3 actin polymerization assay, overexpression/localization Current biology : CB High 12620186
2003 WIP participates in PDGF-induced ruffle formation: overexpression enhances ruffling, microinjection of anti-WIP antibody or WIP deficiency decreases ruffling, and a WIP mutant lacking the actin-binding site blocks PDGF-induced membrane ruffling in murine fibroblasts, establishing WIP's actin-binding domain as required for ruffle formation downstream of PDGF/Rac1. Microinjection of anti-WIP antibody, WIP overexpression, domain mutant (lacking actin-binding site), immunofluorescence, video microscopy in 3T3 and WIP-/- fibroblasts Journal of cell science High 12724353
2004 Toca-1 (a PCH/F-BAR protein) binds both N-WASP and Cdc42 and activates the N-WASP–WIP complex (the predominant form of N-WASP in cells) to promote actin nucleation; two distinct Cdc42 effectors (N-WASP–WIP and Toca-1) cooperate and are both required for Cdc42-induced actin assembly. Biochemical purification of Toca-1, in vitro actin assembly assays, co-IP, depletion experiments Cell High 15260990
2004 WIP-deficient mast cells show impaired degranulation, IL-6 secretion, calcium mobilization, and reduced phosphorylation of Syk, PLCγ2, and JNK after FcεRI ligation. WIP co-immunoprecipitates with Syk after FcεRI ligation and inhibits Syk degradation, establishing WIP as a regulator of FcεRI signaling via maintenance of Syk levels. WIP-/- bone marrow-derived mast cells, degranulation assay, co-immunoprecipitation with Syk, immunoblotting for Syk levels The Journal of experimental medicine High 14757742
2006 WIP is essential for podosome formation in dendritic cells (DCs): WIP-/- DCs cannot form actin cores containing WASP and cortactin. WIP regulates podosome structure by controlling calpain-mediated cleavage of WASP and by facilitating WASP localization to actin polymerization sites at podosomes. WIP-/- DCs, immunofluorescence, live imaging, calpain inhibitor experiments Current biology : CB High 17141616
2006 WIP, WASp, actin, and myosin IIA form a multiprotein complex (~1.3 MDa) in activated NK cells. Inhibitory KIR signaling decreases actin and myosin IIA recruitment to the constitutive WIP–WASp complex. PKCθ-mediated phosphorylation of WIP correlates with increased complex formation. WIP knockdown inhibits NK cell cytotoxicity. Co-immunoprecipitation/gel filtration, RNAi, kinase inhibitor studies in YTS NK cell line The Journal of cell biology High 16606694
2007 WIP acts as a chaperone for WASP: WASP protein (but not mRNA) levels are severely reduced in T cells from WIP-/- mice and restored by WIP re-introduction. The WIP WASP-binding domain protects WASP from calpain-mediated degradation in vitro. Proteasome inhibitors increase WASP levels in WIP-deficient cells, indicating WASP is degraded by both calpain and the proteasome when unbound from WIP. WIP-/- mouse T cells, immunoblotting for WASP, in vitro calpain degradation assay, proteasome inhibitor treatment (MG132, bortezomib), calpain inhibitor (calpeptin) Proceedings of the National Academy of Sciences of the United States of America High 17213309
2007 Drosophila D-WIP (WIP ortholog) is expressed specifically in myoblasts and bridges the WASp-Arp2/3 actin nucleation system to the myoblast adhesion molecules Dumbfounded and Sticks and Stones, recruiting the actin polymerization machinery to fusion sites. Loss of D-WIP or Wsp blocks myoblast fusion at the stage of fusion pore enlargement. Drosophila genetic analysis, immunoprecipitation, immunofluorescence in embryos Developmental cell High 17419994
2007 WASP expression requires WIP: WASP gene transfer yields high WASP expression only when WIP is co-expressed in K562 cells; WIP knockdown in T cells reduces WASP levels. The minimal WIP region that rescues WASP expression is the WASP-binding domain, but this minimal domain is insufficient to rescue WASP-dependent NFAT-mediated IL-2 transcription. Co-expression in K562 cells, siRNA knockdown in T cells, domain-mapping WIP mutants, reporter assay International immunology High 17205972
2007 WIP–WASP complex mediates TCR-induced NFAT activation without dissociation: PKCθ-mediated phosphorylation of WIP Ser488 does not cause WIP–WASP dissociation; WIP–WASP complexes persist after TCR stimulation; a WIP–WASP fusion protein efficiently mediates NFAT activation. The WIP N-terminus (polyproline and WH2 domain) is inhibitory for TCR-mediated NFAT activation. Co-IP after TCR stimulation, WIP-WASP fusion protein, domain truncation, NFAT reporter assay in Jurkat cells The Journal of biological chemistry Medium 17711847
2008 WIP is indispensable for NK cell cytotoxicity: WIP knockdown completely inhibits cytolysis; WIP overexpression enhances cytolytic ability. WIP co-localizes with lytic granules and segregates to the lysosomal fraction. WIP knockdown inhibits polarization of lytic granules to the immune synapse (but not conjugate formation), and granule-WIP interaction is independent of WASp. RNAi knockdown and overexpression in YTS NK cells, cytotoxicity assays, subcellular fractionation, immunofluorescence co-localization Proceedings of the National Academy of Sciences of the United States of America High 18258743
2008 EFC/F-BAR proteins (FBP17 and Toca-1) activate N-WASP–WIP complex-mediated actin polymerization in a membrane curvature-dependent manner, requiring phosphatidylserine-containing membranes and Toca-1/FBP17 but not Cdc42 or PIP2. Toca-1/FBP17 recruit N-WASP–WIP to the membrane via conserved acidic residues near their SH3 domains. In vitro actin polymerization assays with liposomes of defined curvature, domain mutants The EMBO journal High 18923421
2009 WIP is essential for IL-2 signaling in T cells: WIP/WASP double-KO (DKO) T cells (unlike WASP-KO alone) fail to respond to IL-2, as evidenced by failure to up-regulate CD25, phosphorylate STAT5, or induce STAT5-dependent genes after antigen stimulation. DKO T cells have a disrupted subcortical actin cytoskeleton and impaired TCR-triggered actin polymerization. WIP/WASP double-KO mouse model, IL-2 signaling assays (STAT5 phosphorylation, CD25 up-regulation), F-actin content measurements Proceedings of the National Academy of Sciences of the United States of America High 19359486
2010 The cortactin-binding domain of WIP (residues 110–170) is essential for podosome formation and MMP-mediated extracellular matrix degradation by dendritic cells; WIP-/- DCs can synthesize MMPs but fail to degrade matrix. Lentiviral rescue with WIPΔ110–170 restores disorganized podosomes but not matrix degradation. WIP-/- DCs, lentiviral rescue with domain deletion mutant, gelatin degradation assay, immunofluorescence for MMP localization European journal of cell biology High 20952093
2011 Blown fuse (Blow), an FCM-specific Drosophila protein, modulates the stability of the WASP–WIP complex by competing with WASP for WIP binding; this competition drives rapid exchange of WASP, WIP, and G-actin within the podosome-like structure, which is required for fusion pore formation in myoblast fusion. Drosophila genetics, biochemical competition assays, co-IP, FRAP Developmental cell High 21571220
2012 WIP deficiency caused by a homozygous WIPF1 stop codon mutation (c.1301C>G) results in undetectable WASP protein (despite normal WAS mRNA), establishing that WIP stabilizes WASP in human T cells. Introduction of WIP into patient T cells restored WASP expression. Patient cells with WIPF1 mutation, immunoblotting for WASP, lentiviral WIP re-introduction The Journal of experimental medicine High 22231303
2013 WIP (or its homolog WIRE) is an essential link between Nck and N-WASP for Arp2/3-dependent actin assembly: N-WASP recruitment to vaccinia virus depends on WIP (not on direct Nck–N-WASP interaction). WIP contains two Nck-binding sites and is recruited to virus by the second SH3 domain of Nck while bound to N-WASP. The first and third SH3 domains of Nck are required to stimulate actin assembly but not to recruit the WIP:N-WASP complex. MEFs lacking Nck, WIP, or N-WASP; vaccinia actin-tail assay; domain mutants of Nck and WIP; co-IP Current biology : CB High 23707428
2014 WIP and WASp form two distinct molecular interfaces in cells: (i) WH1 domain of WASp with C-terminal WIP, dependent on PKCθ-mediated WIP phosphorylation (in response to TCR activation); (ii) VCA domain of WASp with N-terminal WIP, dependent on actin (inhibited by latrunculin A). WASp activation involves dissociation of interface (i) while interface (ii) remains, exposing the WASp ubiquitylation site and promoting degradation. Triple-color FRET (3FRET) in live T cells, PKCθ inhibitors, latrunculin A, phosphomimetic WIP mutants Science signaling High 24962707
2014 Tyrosine phosphorylation of WIP (mediated by Bruton's tyrosine kinase, Btk) releases bound WASP from the WIP–WASP complex; in the absence of WIP–WASP binding, WASP is rapidly degraded. WIP phosphomimics abolish WIP–WASP interaction and disrupt podosomes; WIP lacking tyrosine phosphorylation extends podosome lifetimes. Btk was identified as a kinase regulating WIP tyrosine phosphorylation. WIP knockdown, phosphomimic/phosphonull WIP mutants, kinase screen with inhibitors, podosome assay, matrix degradation assay in macrophages Journal of cell science High 25413351
2014 WIP binding to actin (via its actin-binding domain, ABD), independently of its binding to WASp, is critical for the integrity of the actin cytoskeleton in T cells and for their migration; WIPΔABD mice have T cells with normal WASp levels but decreased F-actin, disorganized actin cytoskeleton, impaired chemotaxis, and defective homing to lymph nodes. Knock-in mice expressing WIP lacking the ABD (WIPΔABD), F-actin staining, chemotaxis assays, lymph node homing assays Molecular and cellular biology High 25246631
2014 WIP binding to F-actin (via ABD) is required for focal adhesion assembly and stress fiber formation in fibroblasts. WIP-/- fibroblasts have defective focal adhesions, increased G-actin levels, and reduced nuclear MRTF-A/SRF activity; constitutively nuclear MRTF-A or active SRF restores these defects, establishing a WIP–actin–MRTF–SRF axis in cell adhesion. WIP-/- fibroblasts, knock-in WIP mutant (fails to bind actin), MRTF-A nuclear translocation, SRF reporter, focal adhesion immunostaining Molecular and cellular biology High 24797074
2014 NMR structural characterization showed WIP N-terminal ABM is intrinsically disordered but has residual helical (residues 30–42) and β-strand (residues 44–62) propensities that echo the actin-bound conformation; residues 17–25 preceding the canonical ABM also show β-strand propensity, suggesting the WIP–actin interaction epitope extends to the N-terminal polyproline region. NMR (protonless 13C'-detected spectroscopy), secondary chemical shifts, RDC measurements The FEBS journal Medium 25495558
2015 Intersectin adaptor proteins ITSN1 and ITSN2 interact with WIP via SH3 domain–proline-rich motif interactions (middle part of WIP proline-rich region). ITSN1, WIP, and N-WASP form a trimeric complex in cells. Endogenous ITSN1 co-localizes with WIP at invadopodia in breast cancer cells. Co-immunoprecipitation, GST-SH3 pulldown, immunofluorescence co-localization in MDA-MB-231 cells Cellular signalling Medium 25797047
2016 DOCK8 is connected to WASp and actin in T cells through WIP acting as a bridge: WIP co-immunoprecipitates with DOCK8 and WASp. DOCK8 guanine nucleotide exchange factor activity is essential for WASp activation, F-actin assembly, immune synapse/actin foci formation, mechanotransduction, T cell transendothelial migration, and lymph node homing—all of which also depend on WASp, placing DOCK8 and WASp in the same actin-regulatory pathway via WIP. Co-immunoprecipitation, T cell functional assays (immune synapse, foci, migration), T cells from DOCK8-deficient and WAS patients The Journal of clinical investigation High 27599296
2016 WIP and WICH/WIRE play non-redundant roles in invadopodium formation in breast cancer cells: WIP interacts with N-WASP and cortactin and is essential for invadopodium assembly, while WICH/WIRE regulates N-WASP activation to control invadopodium maturation and degradative activity. Nck interaction with WIP modulates invadopodium maturation. RNAi knockdown of WIP and WICH/WIRE, co-immunoprecipitation, invadopodium formation/matrix degradation assays, TIRF microscopy Scientific reports High 27009365
2016 WIP controls tumor growth by stabilizing the YAP/TAZ complex via the endocytic/endosomal system: when WIP levels are high, the β-catenin destruction complex (APC–axin–GSK3) is sequestered to multi-vesicular body compartments, inhibiting YAP/TAZ degradation. YAP/TAZ stability is dependent on Rac, PAK, and mDia, and is Hippo-independent. WIP knockdown/overexpression in cancer cells, subcellular fractionation, co-IP for destruction complex, Rac/PAK/mDia inhibitors, in vivo xenograft Cell reports Medium 27851961
2017 Mutant p53 oncogenic activity is driven by WIP: WIP is phosphorylated by AKT2 downstream of mtp53/p63-enhanced PI3K/AKT2-mediated integrin/receptor recycling pathways. WIP regulates YAP/TAZ stability; WIP knockdown reduces CSC markers (CD133, CD44, YAP/TAZ) and tumor growth in vivo. WIP knockdown/overexpression, mtp53 overexpression, co-IP for AKT2-WIP interaction, in vivo tumor growth assays Oncogene Medium 28166194
2017 NMR and FRET analysis of the WIP C-terminal (residues 442–492)–WASp (residues 20–158) complex revealed a pleckstrin homology-like domain with mixed α/β fold; WIP residues 454–456 are the major contributor to WASp affinity, and residues 449–451 have the largest effect on WASp ubiquitylation and degradation. WIP binding to WASp is inversely linked to WASp ubiquitylation. NMR structure of complex, FRET in vivo, biochemical ubiquitylation assays, WIP peptide mutants ACS chemical biology High 29215267
2017 At yeast endocytic sites, WASP and WIP accumulate to a threshold level through multivalent SH3 domain–PRM interactions involving linker proteins; Arp2/3-mediated actin assembly initiation is tightly coupled to reaching threshold levels of WASP and WIP (not to recruitment kinetics or autoinhibition release), giving actin assembly onset switch-like behavior. Quantitative live-cell fluorescence imaging of endocytic sites, yeast genetics (SH3/PRM mutants) eLife High 28813247
2018 WIP interacts with RhoA: in lung adenocarcinoma cells, WIP knockdown reduces RhoA levels and WIP co-immunoprecipitates with RhoA; WIP regulates invasion, EMT, and anchorage-independent growth via RhoA. Co-immunoprecipitation, siRNA knockdown, invasion assays, RhoA immunoblotting Biochemical and biophysical research communications Low 27939884
2018 WIP/ITSN1 complex co-localizes with RAB4-positive fast-recycling endosomes and is involved in transferrin receptor recycling. ITSN1 recruits WIP to RAB4-positive vesicles. WIP enhances N-WASP–ITSN1 interaction and ITSN1/β-actin association, and the WIP/ITSN1-L complex promotes filopodia-like protrusion formation. Co-immunoprecipitation, transferrin recycling assay, co-localization with Rab4, overexpression in MCF-7 cells Gene Low 29958948
2019 In C. elegans intestine, WIP-1 promotes scission of clathrin-coated pits by directly binding G-actin (independent of WSP-1/WASP); the cortactin-binding domain of WIP-1 serves as the binding interface for DBN-1 (Abp1), and DBN-1–F-actin interaction is essential for Dynamin-1 (DYN-1) recruitment at endocytic sites. RNAi knockdown, live imaging of CCP scission in C. elegans intestine, domain mapping for WIP-1–DBN-1 interaction Journal of cell science Medium 31118234
2020 WIP depletion increases reactive oxygen species and reduces NRF2 levels in glioblastoma cells. WIP stabilizes NRF2 by restraining KEAP1 E3 ligase activity; increased KEAP1 activity in WIP-depleted cells depends on actin cytoskeleton organization (via KEAP1–F-actin binding), not protection of KEAP1 from autophagic degradation. WIP knockdown, KEAP1 knockdown, NRF2ΔETGE overexpression, ROS measurements, co-IP of KEAP1–F-actin Antioxidants (Basel, Switzerland) Medium 32825452
2023 WIPF1 interacts with ACTN4 to regulate podosome formation, matrix degradation, and actin polymerization in extravillous trophoblasts (EVTs); the ARG54 site of WIPF1 is implicated in this interaction. WIPF1 knockdown impairs EVT cell migration and trophoblast differentiation; WIPF1 is downregulated in RSA patient EVTs. Co-immunoprecipitation, WIPF1 knockdown in hTSC-derived EVTs, podosome/matrix degradation assays, site-directed mutagenesis (ARG54) Genes & diseases Medium 40821124
2023 WIPF1 promotes gastric cancer cell proliferation, invasion, and migration in a myocardin (MYOCD)-dependent manner by activating the PI3K/AKT signaling pathway; MYOCD transactivates WIPF1 transcription and silencing WIPF1 significantly represses PI3K/AKT activation. siRNA knockdown, overexpression, in vitro and xenograft assays, PI3K/AKT pathway immunoblotting, MYOCD rescue experiments iScience Low 38026208
2005 C. elegans WIP-1 physically interacts with WSP-1 (WASP/N-WASP homolog) by yeast two-hybrid. RNAi knockdown of wip-1 decreases WSP-1 protein levels (not mRNA), and wsp-1 RNAi decreases WIP-1 protein levels (not mRNA), establishing mutual protein stabilization. WIP-1 RNAi causes embryonic lethality with hypodermal cell migration defects (ventral enclosure) similar to wsp-1 RNAi. Yeast two-hybrid, RNAi, Western blot, immunostaining in C. elegans embryos Biochemical and biophysical research communications High 16378591
2011 WIP-deficient hippocampal neurons show enlarged somas, overgrowth of neuritic and dendritic branches at early developmental stages, increased dendritic arborization, and increased amplitude and frequency of miniature excitatory postsynaptic currents, identifying WIP as a negative regulator of neuronal maturation and synaptic activity. WIP-/- mouse hippocampal neurons, morphometric analysis, electrophysiology (mEPSC recording) Cerebral cortex (New York, N.Y. : 1991) High 21810783
2014 WIP absence in dendritic spines increases spine size and F-actin levels through a RhoA/ROCK/profilinIIa-dependent (N-WASP/Arp2/3-independent) mechanism. WIP deficiency causes transcriptional upregulation of neutral sphingomyelinase (NSM) via active RhoA, reducing membrane sphingomyelin, which in turn enhances RhoA membrane association and raft partitioning. NSM inhibition or sphingomyelin addition reverses RhoA, F-actin, and functional anomalies in WIP-/- synapses. WIP-/- mouse neurons, pharmacological inhibition of NSM, sphingomyelin supplementation, RhoA localization assay, F-actin staining, Arp2/3 co-IP Human molecular genetics Medium 24698977

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Toca-1 mediates Cdc42-dependent actin nucleation by activating the N-WASP-WIP complex. Cell 368 15260990
1997 WIP, a protein associated with wiskott-aldrich syndrome protein, induces actin polymerization and redistribution in lymphoid cells. Proceedings of the National Academy of Sciences of the United States of America 311 9405671
2000 A complex of N-WASP and WIP integrates signalling cascades that lead to actin polymerization. Nature cell biology 282 10878810
2001 WIP regulates N-WASP-mediated actin polymerization and filopodium formation. Nature cell biology 238 11331876
2008 EFC/F-BAR proteins and the N-WASP-WIP complex induce membrane curvature-dependent actin polymerization. The EMBO journal 152 18923421
2003 Cortactin interacts with WIP in regulating Arp2/3 activation and membrane protrusion. Current biology : CB 151 12620186
2002 A. thaliana TRANSPARENT TESTA 1 is involved in seed coat development and defines the WIP subfamily of plant zinc finger proteins. Genes & development 144 11782451
2012 A novel primary human immunodeficiency due to deficiency in the WASP-interacting protein WIP. The Journal of experimental medicine 132 22231303
1998 The WASp homologue Las17p functions with the WIP homologue End5p/verprolin and is essential for endocytosis in yeast. Current biology : CB 131 9742397
2007 WIP is a chaperone for Wiskott-Aldrich syndrome protein (WASP). Proceedings of the National Academy of Sciences of the United States of America 130 17213309
2002 Structure of the N-WASP EVH1 domain-WIP complex: insight into the molecular basis of Wiskott-Aldrich Syndrome. Cell 130 12437929
2002 WIP deficiency reveals a differential role for WIP and the actin cytoskeleton in T and B cell activation. Immunity 128 11869681
2007 WIP/WASp-based actin-polymerization machinery is essential for myoblast fusion in Drosophila. Developmental cell 127 17419994
2002 Phosphatidylinositol 4,5-biphosphate (PIP2)-induced vesicle movement depends on N-WASP and involves Nck, WIP, and Grb2. The Journal of biological chemistry 123 12147689
1998 The Wiskott-Aldrich syndrome protein-interacting protein (WIP) binds to the adaptor protein Nck. The Journal of biological chemistry 113 9694849
2006 WIP regulates the stability and localization of WASP to podosomes in migrating dendritic cells. Current biology : CB 104 17141616
2016 A DOCK8-WIP-WASp complex links T cell receptors to the actin cytoskeleton. The Journal of clinical investigation 98 27599296
2006 Formation of a WIP-, WASp-, actin-, and myosin IIA-containing multiprotein complex in activated NK cells and its alteration by KIR inhibitory signaling. The Journal of cell biology 82 16606694
2017 Mutant p53 oncogenic functions in cancer stem cells are regulated by WIP through YAP/TAZ. Oncogene 75 28166194
2005 WIP and WASP play complementary roles in T cell homing and chemotaxis to SDF-1alpha. International immunology 74 16141245
2007 WASP-interacting protein (WIP): working in polymerisation and much more. Trends in cell biology 67 17949983
2002 Identification of novel SH3 domain ligands for the Src family kinase Hck. Wiskott-Aldrich syndrome protein (WASP), WASP-interacting protein (WIP), and ELMO1. The Journal of biological chemistry 66 12029088
2013 WIP provides an essential link between Nck and N-WASP during Arp2/3-dependent actin polymerization. Current biology : CB 64 23707428
1999 The human WASP-interacting protein, WIP, activates the cell polarity pathway in yeast. The Journal of biological chemistry 56 10358064
2003 WIP participates in actin reorganization and ruffle formation induced by PDGF. Journal of cell science 55 12724353
2011 Competition between Blown fuse and WASP for WIP binding regulates the dynamics of WASP-dependent actin polymerization in vivo. Developmental cell 54 21571220
2009 Recent advances in the biology of WASP and WIP. Immunologic research 53 19018480
2015 Plant nuclear shape is independently determined by the SUN-WIP-WIT2-myosin XI-i complex and CRWN1. Nucleus (Austin, Tex.) 52 25759303
2008 WIP is essential for lytic granule polarization and NK cell cytotoxicity. Proceedings of the National Academy of Sciences of the United States of America 46 18258743
2017 Switch-like Arp2/3 activation upon WASP and WIP recruitment to an apparent threshold level by multivalent linker proteins in vivo. eLife 45 28813247
2016 WIP Drives Tumor Progression through YAP/TAZ-Dependent Autonomous Cell Growth. Cell reports 45 27851961
2008 WASP and WIP regulate podosomes in migrating leukocytes. Journal of microscopy 45 18755005
2005 WIP: a multifunctional protein involved in actin cytoskeleton regulation. European journal of cell biology 44 16546573
2002 The novel adaptor protein, Mti1p, and Vrp1p, a homolog of Wiskott-Aldrich syndrome protein-interacting protein (WIP), may antagonistically regulate type I myosins in Saccharomyces cerevisiae. Genetics 44 11901111
2004 WIP regulates signaling via the high affinity receptor for immunoglobulin E in mast cells. The Journal of experimental medicine 41 14757742
2018 GhWIP2, a WIP zinc finger protein, suppresses cell expansion in Gerbera hybrida by mediating crosstalk between gibberellin, abscisic acid, and auxin. The New phytologist 40 29681133
2008 The Wip1 phosphatase and Mdm2: cracking the "Wip" on p53 stability. Cell cycle (Georgetown, Tex.) 39 18333294
2012 WIP: WASP-interacting proteins at invadopodia and podosomes. European journal of cell biology 37 22823953
2010 The cortactin-binding domain of WIP is essential for podosome formation and extracellular matrix degradation by murine dendritic cells. European journal of cell biology 37 20952093
2001 The rat homologue of Wiskott-Aldrich syndrome protein (WASP)-interacting protein (WIP) associates with actin filaments, recruits N-WASP from the nucleus, and mediates mobilization of actin from stress fibers in favor of filopodia formation. The Journal of biological chemistry 36 11687573
2003 X-linked thrombocytopenia caused by a mutation in the Wiskott-Aldrich syndrome (WAS) gene that disrupts interaction with the WAS protein (WASP)-interacting protein (WIP). Experimental hematology 34 12591280
2015 SUN anchors pollen WIP-WIT complexes at the vegetative nuclear envelope and is necessary for pollen tube targeting and fertility. Journal of experimental botany 33 26409047
2007 The expression of Wiskott-Aldrich syndrome protein (WASP) is dependent on WASP-interacting protein (WIP). International immunology 32 17205972
2010 Weird fingers: functional analysis of WIP domain proteins. FEBS letters 31 20541552
2000 Cutting edge: WIP, a binding partner for Wiskott-Aldrich syndrome protein, cooperates with Vav in the regulation of T cell activation. Journal of immunology (Baltimore, Md. : 1950) 31 10706671
2020 Long noncoding RNA HCG18 up-regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR-141-3p in gastric cancer. Cancer medicine 30 32725768
2007 WIP null mice display a progressive immunological disorder that resembles Wiskott-Aldrich syndrome. The Journal of pathology 30 17086554
2023 CLDN6 inhibits breast cancer metastasis through WIP-dependent actin cytoskeleton-mediated autophagy. Journal of experimental & clinical cancer research : CR 28 36935496
2014 WIP: more than a WASp-interacting protein. Journal of leukocyte biology 28 25210148
2014 Triple-color FRET analysis reveals conformational changes in the WIP-WASp actin-regulating complex. Science signaling 27 24962707
2012 The enteropathogenic E. coli effector EspH promotes actin pedestal formation and elongation via WASP-interacting protein (WIP). Cellular microbiology 27 22372637
2009 Downregulation of Wip-1 phosphatase expression in MCF-7 breast cancer cells enhances doxorubicin-induced apoptosis through p53-mediated transcriptional activation of Bax. Cancer biology & therapy 26 19242108
2011 A peptide derived from the Wiskott-Aldrich syndrome (WAS) protein-interacting protein (WIP) restores WAS protein level and actin cytoskeleton reorganization in lymphocytes from patients with WAS mutations that disrupt WIP binding. The Journal of allergy and clinical immunology 25 21376381
2012 WIP-ing out atherosclerosis with autophagy. Autophagy 23 22895013
2005 Caenorhabditis elegans WASP-interacting protein homologue WIP-1 is involved in morphogenesis through maintenance of WSP-1 protein levels. Biochemical and biophysical research communications 23 16378591
2016 WIP and WICH/WIRE co-ordinately control invadopodium formation and maturation in human breast cancer cell invasion. Scientific reports 22 27009365
2014 WIP is necessary for matrix invasion by breast cancer cells. European journal of cell biology 22 25169059
2013 WIP regulates persistence of cell migration and ruffle formation in both mesenchymal and amoeboid modes of motility. PloS one 22 23950925
2020 Integrative genome-wide analysis reveals the role of WIP proteins in inhibition of growth and development. Communications biology 21 32415243
2016 WIP promotes in-vitro invasion ability, anchorage independent growth and EMT progression of A549 lung adenocarcinoma cells by regulating RhoA levels. Biochemical and biophysical research communications 21 27939884
2009 WIP is critical for T cell responsiveness to IL-2. Proceedings of the National Academy of Sciences of the United States of America 20 19359486
2018 The Phenotype and Treatment of WIP Deficiency: Literature Synopsis and Review of a Patient With Pre-transplant Serial Donor Lymphocyte Infusions to Eliminate CMV. Frontiers in immunology 19 30450104
2015 Intersectin adaptor proteins are associated with actin-regulating protein WIP in invadopodia. Cellular signalling 19 25797047
2006 WASP suppresses the growth defect of Saccharomyces cerevisiae las17Delta strain in the presence of WIP. Biochemical and biophysical research communications 19 16488394
2006 A novel anti-WIP monoclonal antibody detects an isoform of WIP that lacks the WASP binding domain. Biochemical and biophysical research communications 19 17207458
2018 WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma. Cancers 18 29890731
2014 Binding of WIP to actin is essential for T cell actin cytoskeleton integrity and tissue homing. Molecular and cellular biology 18 25246631
2014 Tyrosine phosphorylation of WIP releases bound WASP and impairs podosome assembly in macrophages. Journal of cell science 18 25413351
2007 Structure-function analysis of the WIP role in T cell receptor-stimulated NFAT activation: evidence that WIP-WASP dissociation is not required and that the WIP NH2 terminus is inhibitory. The Journal of biological chemistry 18 17711847
2021 LncRNA PAXIP1-AS1 fosters the pathogenesis of pulmonary arterial hypertension via ETS1/WIPF1/RhoA axis. Journal of cellular and molecular medicine 16 34245091
2018 The Lack of WIP Binding to Actin Results in Impaired B Cell Migration and Altered Humoral Immune Responses. Cell reports 16 30021160
2014 Binding of the WASP/N-WASP-interacting protein WIP to actin regulates focal adhesion assembly and adhesion. Molecular and cellular biology 16 24797074
2018 WIP/ITSN1 complex is involved in cellular vesicle trafficking and formation of filopodia-like protrusions. Gene 15 29958948
2017 Epigenetically upregulated WIPF1 plays a major role in BRAF V600E-promoted papillary thyroid cancer aggressiveness. Oncotarget 15 27863429
2016 Similar efficacy and tolerability of raltegravir-based antiretroviral therapy in HIV-infected patients, irrespective of age group, burden of comorbidities and concomitant medication: Real-life analysis of the German 'WIP' cohort. International journal of STD & AIDS 15 28385065
2012 WIP remodeling actin behind the scenes: how WIP reshapes immune and other functions. International journal of molecular sciences 15 22837718
2009 Platelet-associated IgAs and impaired GPVI responses in platelets lacking WIP. Blood 15 19692704
2016 Invadopodia proteins, cortactin, N-WASP and WIP differentially promote local invasiveness in ameloblastoma. Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology 13 26752341
2016 Wip 1 inhibits intestinal inflammation in inflammatory bowel disease. Cellular immunology 13 27687530
2011 WIP is a negative regulator of neuronal maturation and synaptic activity. Cerebral cortex (New York, N.Y. : 1991) 13 21810783
2006 A role for WASP Interacting Protein, WIP, in fibroblast adhesion, spreading and migration. The international journal of biochemistry & cell biology 13 17008118
2015 WASP-WIP complex in the molecular pathogenesis of Wiskott-Aldrich syndrome. Pediatrics international : official journal of the Japan Pediatric Society 12 26331277
2014 WIP modulates dendritic spine actin cytoskeleton by transcriptional control of lipid metabolic enzymes. Human molecular genetics 12 24698977
2023 The transcription factor GhTCP7 suppresses petal expansion by interacting with the WIP-type zinc finger protein GhWIP2 in Gerbera hybrida. Journal of experimental botany 11 37102769
2023 WIPF1 promotes gastric cancer progression by regulating PI3K/Akt signaling in a myocardin-dependent manner. iScience 11 38026208
2021 WIP, YAP/TAZ and Actin Connections Orchestrate Development and Transformation in the Central Nervous System. Frontiers in cell and developmental biology 11 34195190
2018 Crosstalk between WIP and Rho family GTPases. Small GTPases 11 29172947
2013 PP1α, PP1β and Wip-1 regulate H4S47 phosphorylation and deposition of histone H3 variant H3.3. Nucleic acids research 10 23828041
2019 WIP-1 and DBN-1 promote scission of endocytic vesicles by bridging actin and Dynamin-1 in the C. elegans intestine. Journal of cell science 8 31118234
2020 The Disordered Cellular Multi-Tasker WIP and Its Protein-Protein Interactions: A Structural View. Biomolecules 7 32708183
2020 WIP Modulates Oxidative Stress through NRF2/KEAP1 in Glioblastoma Cells. Antioxidants (Basel, Switzerland) 7 32825452
2017 New Structural Insights into Formation of the Key Actin Regulating WIP-WASp Complex Determined by NMR and Molecular Imaging. ACS chemical biology 5 29215267
2016 A J-modulated protonless NMR experiment characterizes the conformational ensemble of the intrinsically disordered protein WIP. Journal of biomolecular NMR 5 27844185
2015 New insights into the role of the disordered WIP N-terminal domain revealed by NMR structural characterization. The FEBS journal 5 25495558
2015 Neuritic complexity of hippocampal neurons depends on WIP-mediated mTORC1 and Abl family kinases activities. Brain and behavior 5 26664784
2024 Multifaceted role of the actin-binding protein WIP: Promotor and inhibitor of tumor progression and dissemination. Cytoskeleton (Hoboken, N.J.) 4 39329352
2025 Camellia sinensis WIP domain protein 3 (CsWIP3), a C2H2 zinc finger protein, mediates lignin content and regulates plant growth in tea plants. International journal of biological macromolecules 2 40107543
2025 Unraveling the role of the WIPF1/ACTN4 complex in podosome formation of human placental EVTs: Insights into recurrent spontaneous abortion. Genes & diseases 2 40821124
2020 Controlling Smad4 signaling with a Wip. EMBO reports 1 32189449
2025 WIPF1 regulates stemness in small cell lung cancer. Science progress 0 40415347

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