| 2004 |
Abi1 directly binds the WHD domain of WAVE2, increases WAVE2 actin polymerization activity in vitro, and mediates assembly of a WAVE2-Abi1-Nap1-PIR121 complex identified by tandem mass spectrometry. This complex is as active as WAVE2-Abi1 sub-complex in stimulating Arp2/3, and re-localizes to the leading edge of ruffles following Rac activation. RNAi inhibition of Abi1 abrogates Rac-dependent lamellipodia protrusion. |
Tandem mass spectrometry, Co-IP, in vitro actin polymerization assay, RNAi knockdown, live-cell imaging |
Nature cell biology |
High |
15048123
|
| 2003 |
WAVE2 is specifically required for peripheral ruffle formation and directed cell migration (without ECM) downstream of PDGF stimulation in fibroblasts, whereas WAVE1 is required for dorsal ruffle formation. Loss of WAVE2 impairs leading-edge extension for directed migration. |
Gene-specific siRNA knockdown, live-cell migration assays, immunofluorescence |
Developmental cell |
High |
14536061
|
| 2004 |
WAVE2 binds PtdIns(3,4,5)P3 through its basic domain. PtdIns(3,4,5)P3 produced by PI(3)K at the cell membrane is sufficient to recruit WAVE2 to the polarized membrane even in the presence of dominant-negative Rac; a lipid-binding-deficient full-length WAVE2 mutant inhibits proper lamellipodia formation. |
Lipid-binding assays, myristoylated PI3K expression, dominant-negative Rac, mutant WAVE2 expression, fluorescence microscopy |
Nature cell biology |
High |
15107862
|
| 2003 |
Genetic disruption of WAVE2 in mice causes embryonic lethality (~E10) with haemorrhages and impaired angiogenic sprouting/branching of endothelial cells; WAVE2-null endothelial cells fail to form lamellipodia at leading edges in response to VEGF, establishing WAVE2 as essential for Rac-regulated actin reorganization during angiogenesis in vivo. |
Gene-targeted knockout mouse, embryological analysis, endothelial cell migration and lamellipodia assays |
Nature |
High |
12879075
|
| 2003 |
WAVE2-deficient mouse embryonic fibroblasts exhibit severe defects in cell motility, lamellipodium formation, and Rac-mediated actin polymerization in response to PDGF, while proliferation is normal, establishing a non-redundant role for WAVE2 downstream of Rac in actin-based cell movement. |
Gene-targeted knockout mouse/MEFs, PDGF stimulation, actin polymerization and cell migration assays |
The EMBO journal |
High |
12853475
|
| 2005 |
Abi-1 couples WAVE2 to Abl kinase after cell stimulation, promoting Abl-mediated tyrosine phosphorylation of WAVE2 at Y150, which is required for WAVE2 activation, actin polymerization induction, and membrane translocation with activated Rac. Mutation of Y150 or disruption of WAVE2-Abi-1 binding impairs membrane actin rearrangement; Abl/Arg-null fibroblasts fail to phosphorylate WAVE2 or form membrane actin rearrangements. |
Co-IP, in vitro and in vivo phosphorylation assays, site-directed mutagenesis (Y150F), RNAi, fibroblast knockout cells |
Proceedings of the National Academy of Sciences of the United States of America |
High |
15657136
|
| 2006 |
c-Abl interacts with the WAVE2 complex via Abi-1 and phosphorylates WAVE2 on tyrosine 150 to activate membrane ruffling; WAVE2-Y150F rescue cells fail to ruffle or form microspikes, and RNAi of WAVE2 in Abl/Arg-null cells has no additive effect on membrane ruffling, placing Abl upstream of WAVE2 in this pathway. |
Co-IP, in vitro kinase assay, site-directed mutagenesis (Y150F), RNAi, genetic epistasis in Abl/Arg-null cells |
The Journal of biological chemistry |
High |
16899465
|
| 2006 |
WAVE2 complex (with Sra1/PIR121, Nap1, Abi1, HSPC300) isolated from the membrane fraction is fully active in stimulating Arp2/3 in an IRSp53-dependent manner in vitro, while cytosolic WAVE2 complex is not. Purified WAVE2 and WAVE2 complex are activated by IRSp53 in a Rac-dependent manner with PIP3-containing liposomes; IRSp53 knockdown reduces lamellipodia formation without decreasing WAVE2 complex levels. |
In vitro Arp2/3 activity assay, membrane fractionation, IRSp53 RNAi, purified protein reconstitution with PIP3 liposomes |
The Journal of cell biology |
High |
16702231
|
| 2011 |
ERK directly phosphorylates both WAVE2 and Abi1 within the WRC at lamellipodial leading edges. These phosphorylations are required for functional WRC interaction with Arp2/3 and actin during cell protrusion, as shown by phospho-deficient mutants failing to support protrusion. |
In vitro kinase assay, phospho-mutant analysis, co-localization by microscopy, cell protrusion assay |
Molecular cell |
High |
21419341
|
| 2006 |
WAVE2 is recruited to the T cell immunological synapse following TCR crosslinking, undergoes biochemical modification, and is required for actin cytoskeletal reorganization, beta-integrin-mediated adhesion, and calcium entry at a step distal to PLCgamma1 activation and IP3-mediated store release (CRAC channel activation). |
Co-IP, RNAi knockdown, live-cell imaging, calcium flux assays, integrin adhesion assays |
Current biology : CB |
High |
16401421
|
| 2007 |
WAVE2 VCA domain mediates formation of an Arp2/3-vinculin-talin signaling complex at the T cell immunological synapse; TCR stimulation induces WAVE2-ARP2/3-dependent F-actin nucleation leading to talin recruitment and high-affinity integrin binding to VCAM-1. Vinculin is required for talin recruitment but not for F-actin or integrin accumulation. |
RNAi knockdown, Co-IP, immunofluorescence, integrin binding assay (VCAM-1) |
Molecular and cellular biology |
High |
17591693
|
| 2008 |
The WAVE2 complex associates with Abl tyrosine kinase in T cells; TCR ligation induces WAVE2-dependent membrane recruitment of Abl. WAVE2 regulates TCR-mediated Rap1 activation via recruitment of CrkL-C3G exchange complex; Abl phosphorylates C3G to enable its GEF activity toward Rap1, controlling integrin clustering and affinity maturation. |
Co-IP, RNAi, dominant-negative constructs, Rap1 activation assay, integrin clustering assay |
The Journal of cell biology |
High |
18809728
|
| 2008 |
Cdk5 phosphorylates WAVE2 at Ser-137 in vitro, downstream of Fyn kinase activation by PDGF, to control oligodendrocyte precursor cell migration. WAVE2-S137A mutant impairs PDGF-dependent OPC migration. |
In vitro kinase assay, site-directed mutagenesis (S137A), retroviral shRNA knockdown, cell migration assay |
The Journal of neuroscience : the official journal of the Society for Neuroscience |
High |
18701695
|
| 2018 |
LRRK2 binds WAVE2 and phosphorylates it at Thr470, stabilizing WAVE2 and preventing its proteasomal degradation. LRRK2-G2019S (gain-of-function PD mutation) causes increased WAVE2-mediated phagocytic responses in macrophages/microglia; Lrrk2 loss causes the opposite. WAVE2 mediates LRRK2-G2019S-induced dopaminergic neuronal death. |
Co-IP, in vitro kinase assay, proteasome inhibitor treatment, siRNA knockdown, macrophage/microglia phagocytosis assay, in vivo mouse model |
Proceedings of the National Academy of Sciences of the United States of America |
High |
29760073
|
| 2021 |
Conditional T cell-specific ablation of WAVE2 causes severe autoimmunity with increased mTOR activation. WAVE2 directly bound mTOR and inhibited its activation by impeding mTOR interactions with RAPTOR and RICTOR. Both T cell defects and autoimmunity were ameliorated by pharmacological mTOR inhibitors. |
Conditional KO mouse, Co-IP (WAVE2-mTOR direct binding), mTOR inhibitor rescue, phosphoproteomic/metabolic analysis |
Science (New York, N.Y.) |
High |
33766857
|
| 2010 |
Dysbindin-1 forms a ternary complex with WAVE2 and Abi-1 in neurons (but not N-WASP); dysbindin-1 promotes binding of WAVE2 to Abi-1. RNAi knockdown of dysbindin-1 generates abnormally elongated immature dendritic protrusions, implicating the complex in dendritic spine morphogenesis. |
Co-IP, immunofluorescence, RNAi knockdown in hippocampal neurons |
Molecular psychiatry |
Medium |
20531346
|
| 2007 |
ERK2 directly phosphorylates WAVE2 in vitro at sites in the proline-rich region and VCA domain. Phosphorylation of the VCA region increases its affinity for Arp2/3 but paradoxically reduces Arp2/3-mediated actin polymerization activity in vitro. |
In vitro kinase assay with ERK2, actin polymerization assay, binding assay |
Journal of biochemistry |
Medium |
17202194
|
| 2007 |
MAP kinase phosphorylation sites within WAVE2 regulate persistent cell migration and Golgi polarization; fibroblasts expressing phospho-defective WAVE2 show increased migration speed, decreased persistence, and disrupted Golgi polarization—effects mimicked by acute WAVE2 RNAi knockdown. |
Site-directed mutagenesis of MAP kinase phosphosites, transgene expression, scratch-wound migration assay, RNAi |
Journal of cell science |
Medium |
18032787
|
| 2009 |
Casein kinase 2 (CK2) phosphorylates five serine residues (482, 484, 488, 489, 497) in the WAVE2 VCA domain; phosphorylation is required for high-affinity Arp2/3 interaction, while phosphorylation of Ser482/484 specifically inhibits Arp2/3 activation. Non-phosphorylatable alanine mutations inhibit WAVE2-dependent cell ruffling and leading-edge integrity in vivo. |
In vitro CK2 phosphorylation, mutagenesis, Arp2/3 binding/activation assay, cell ruffling assay |
Cell motility and the cytoskeleton |
Medium |
19012317
|
| 2011 |
Abi1 knockout cells display reduced WAVE1 and WAVE2 protein levels along with Nap1 and Sra-1/PIR121, demonstrating that Abi1 is required for the stability and integrity of the entire WAVE complex. Abi1 KO causes decreased migration rate and distance but increased directional persistence, without affecting peripheral ruffling but impairing dorsal ruffling. |
Conditional Abi1 KO mouse/MEFs, Western blot of complex components, migration assays |
Proceedings of the National Academy of Sciences of the United States of America |
High |
21482783
|
| 2001 |
The basic region of WAVE2 (between WH1 and CRIB domains) binds ADP actin filaments, enhancing Arp2/3 branching efficiency on pre-existing ADP filaments by ~2-fold compared to VCA domain alone. This basic region is required for actin-based bead motility in cytosol; VCA domain alone or constructs lacking the basic region fail to support bead movement. |
In vitro actin polymerization/branching assay, bead motility assay in brain cytosol, deletion constructs |
Journal of cell science |
High |
11792818
|
| 2001 |
The basic region of WAVE2 is required for actin-based motility in cell extracts; beads coated with full-length WAVE2 but not WAVE2 lacking the basic clusters (Delta basic) or VCA alone support movement in brain cytosol, and VCA/Delta-basic constructs are much less able to induce actin polymerization in cytosol. |
Polystyrene bead motility assay in brain cytosol, in vitro actin polymerization assay, deletion constructs |
Biochemical and biophysical research communications |
High |
11401525
|
| 2005 |
WAVE2 is required for Rac1-induced membrane ruffling, invasion into ECM, and pulmonary metastasis of B16F10 melanoma cells. WAVE2 acts as the primary downstream effector of Rac to achieve invasion; co-expression of RacCA and WAVE2 in parental B16 cells additively increases invasiveness beyond RacCA alone. |
RNAi knockdown, constitutively active Rac co-expression, Matrigel invasion assay, in vivo metastasis assay |
Oncogene |
High |
15608687
|
| 2010 |
WAVE2 directly binds Abl kinase and activates HIV-1 Arp2/3-dependent actin polymerization; Tiam-1 (Rac GEF) associates with IRSp53 to link Rac to the WAVE2 complex. Rac and Abl activate the WAVE2 complex for pore expansion at the hemifusion stage of HIV-1 entry; siRNA knockdown of WAVE2, Abl, IRSp53, or Arp3 attenuates HIV-1 fusion and infection. |
siRNA knockdown, fusion assay, virus-cell infection assay, Abl kinase inhibitors (imatinib, nilotinib, dasatinib), fluorescence microscopy with membrane curving agents |
PLoS pathogens |
Medium |
20585556
|
| 2014 |
HIV-1 gp120 binding to CXCR4 or CCR5 triggers WAVE2 phosphorylation at serine 351 via both Gαi-dependent and -independent pathways; WAVE2-mediated Arp2/3 activity is required for HIV-1 nuclear migration. Stable shRNA knockdown of Arp3 or Arp2/3 inhibitor CK548 prevented HIV-1 nuclear migration and infection of CD4 T cells. |
Phosphorylation mapping, shRNA knockdown, Arp2/3 inhibitor, HIV-1 infection/nuclear migration assay in primary cells |
The Journal of biological chemistry |
Medium |
24415754
|
| 2011 |
IL-2 activates WAVE2 in NK cells to enable WASp-independent F-actin accumulation at the immunological synapse and NK cell cytotoxicity. WAVE2 was required for IL-2-induced WASp-independent NK function but not for baseline innate NK activity, defining WAVE2 and WASp as parallel pathways to F-actin reorganization. |
WASp inhibitor, WAS patient cells, siRNA knockdown of WAVE2, NK cytotoxicity assay, F-actin quantification at IS |
The Journal of clinical investigation |
Medium |
21383498
|
| 2011 |
WAVE2 regulates meiotic spindle stability, peripheral positioning, and polar body emission in mouse oocytes via an actin-mediated pathway. siRNA-mediated and antibody-mediated disruption of WAVE2 causes failure of chromosome congression, spindle formation, spindle positioning, polar body extrusion, actin cap and cortical granule-free domain formation. WAVE2 regulation of chromosome migration is independent of microtubules. |
siRNA knockdown, antibody microinjection, immunofluorescence, nocodazole treatment (microtubule depletion) |
Cell cycle (Georgetown, Tex.) |
Medium |
21543895
|
| 2009 |
Pak1 constitutively binds WAVE2 and is transported with WAVE2 to the leading edge upon HGF stimulation. Pak1 mediates kinesin-dependent WAVE2 transport along microtubules by phosphorylating stathmin/Op18 at Ser38 and recruiting phospho-stathmin to the kinesin-WAVE2 complex. Pak1 inhibition or depletion abrogates HGF-induced WAVE2 transport and lamellipodia formation. |
Co-IP, siRNA knockdown of Pak1, Pak1 inhibitor (IPA-3), phospho-specific antibodies, lamellipodia assay |
Cellular signalling |
Medium |
19162178
|
| 2008 |
Kinesin heavy chain KIF5B forms a complex with WAVE2 and IQGAP1; HGF-induced WAVE2 transport to the cell periphery and lamellipodia formation require KIF5B-mediated transport along microtubules in a Rac1-dependent manner. Downregulation of KIF5B or microtubule depolymerization abrogates WAVE2 transport. |
Co-IP (WAVE2-KIF5B), siRNA knockdown of KIF5B, nocodazole treatment, lamellipodia quantification |
Experimental cell research |
Medium |
18514191
|
| 2010 |
PKA forms a complex with WAVE2 in breast cancer cells and brain extracts; two separate regions of WAVE2 mediate PKA binding. WAVE2 serves as an A-kinase-anchoring protein (AKAP) that recruits PKA to membrane protrusions; WAVE2 depletion impairs PKA localization at protrusions and PKA activation-induced enlargement of membrane protrusions. |
Co-IP, siRNA knockdown, PKA activator treatment, immunofluorescence of protrusion size |
The Journal of biological chemistry |
Medium |
21119216
|
| 2007 |
WAVE2 complex is required for Rac-Abi-1-dependent actin recruitment and entry of Chlamydia trachomatis into epithelial cells; siRNA depletion of WAVE2 and Abi-1 abrogates chlamydia-induced actin recruitment and significantly reduces pathogen uptake. C. trachomatis infection promotes Rac interaction with WAVE2 and Abi-1 but not with IRSp53. |
Co-IP, siRNA knockdown, bacterial invasion/infection assay, immunofluorescence |
Cellular microbiology |
Medium |
17501982
|
| 2005 |
WAVE2-Abi1 complex is required for CSF-1-induced F-actin protrusions and macrophage migration. WAVE2 and Abi1 are co-recruited to protrusions; reducing WAVE2 by dominant-negative, antibody, or RNAi impairs CSF-1-elicited actin protrusions, and targeting Abi1 reduces WAVE2 levels and impairs migration. |
Dominant-negative expression, antibody microinjection, RNAi, Co-IP, cell migration assay |
Journal of cell science |
Medium |
16280551
|
| 2008 |
Membrane targeting of WAVE2 alone is insufficient for WAVE2-dependent actin polymerization; IRSp53 links Rac1 to WAVE2-Abi1 in a Rac1-activation-dependent immunoprecipitable complex in macrophages. Reduction of IRSp53 or expression of IRSp53 lacking the WAVE2-binding SH3 domain significantly reduces Rac1 association with WAVE2 and Abi1, and diminishes CSF-1-induced protrusions and migration. |
RNAi, Co-IP, dominant-negative IRSp53, membrane-targeted WAVE2 expression, migration/protrusion assays |
Journal of cell science |
Medium |
18198193
|
| 2014 |
Cortactin directly binds both WAVE2 and Arp2/3 at the epithelial zonula adherens; both interactions are necessary for actin assembly at the ZA. Cortactin binding to the cadherin cytoplasmic tail was demonstrated by cell-free protein expression and fluorescent single-molecule coincidence assays. |
Cell-free protein expression, fluorescent single-molecule coincidence assay, siRNA knockdown, in vitro binding assays |
The Journal of biological chemistry |
Medium |
24469447
|
| 2011 |
WAVE2 and mDia1 interact directly with IRSp53 within filopodia, as shown by acceptor photobleaching FRET. mDia1 and WAVE2 synergize with IRSp53 to form filopodia; depletion of either mDia1 or WAVE2 decreases IRSp53-induced filopodia formation. |
Acceptor photobleaching FRET, siRNA knockdown, time-lapse imaging of filopodium formation |
The Journal of biological chemistry |
Medium |
22179776
|
| 2012 |
WAVE2-Abi2 complex activity is regulated by Abl kinase (via Y150 phosphorylation) and Cdk5 (via S137 phosphorylation) to control growth cone activity and the multipolar-to-bipolar neuronal transition, as well as initiation of glia-guided migration in the developing neocortex. |
In utero electroporation, mutagenesis (Y150, S137), time-lapse imaging of migrating neurons |
Cerebral cortex (New York, N.Y. : 1991) |
Medium |
22617848
|
| 2005 |
WAVE2 is required for efficient invasion of polarized epithelial cells by Salmonella typhimurium. Disruption of the PIR121/Nap1/Abi1/WAVE2/HSPC300 pentameric complex potently inhibits bacterial uptake, while the IRSp53/WAVE2 complex is not required for invasion despite being formed during infection. |
siRNA knockdown, dominant-negative complex disruption, bacterial invasion/internalization assay |
The Journal of biological chemistry |
Medium |
15929989
|
| 2004 |
N-WASP and WAVE2 act downstream of phosphatidylinositol 3-kinase to mediate HGF-induced lamellipodia formation and myogenic cell migration; dominant-negative WAVE2 or WAVE2 RNAi prevents HGF-induced lamellipodial formation and both non-directional and directional migration of C2C12 myoblasts. |
Dominant-negative expression, RNAi knockdown, PI3K inhibitor (LY294002), cell migration and chemotaxis assays |
The Journal of biological chemistry |
Medium |
15496413
|
| 2010 |
Nonmuscle myosin IIA (MYH9) constitutively associates with WAVE2 in a myosin II activity-dependent manner; the MYH9-WAVE2 complex co-localizes to PIP3 at the leading edge after IGF-I stimulation. Depletion of MYH9 or inhibition of myosin II by blebbistatin abrogates F-actin arc and lamellipodia formation, indicating MYH9 is required for lamellipodia through binding to WAVE2. |
Co-IP (identified by mass spectrometry), siRNA knockdown, blebbistatin treatment, immunofluorescence |
Biochemical and biophysical research communications |
Medium |
21184743
|
| 2015 |
Cortactin phosphorylation on S405/S418 by PLCβ3-PKCδ downstream of MCP1/CCR2/Gαq11 signaling is required for cortactin interaction with WAVE2; this interaction mediates G-actin polymerization, F-actin stress fiber formation, and smooth muscle cell migration. |
Co-IP, siRNA knockdown of PLCβ3/PKCδ/CCR2/Gαq11, phosphomimetic/phosphodeficient mutants, actin polymerization and migration assays |
Molecular biology of the cell |
Medium |
26490115
|
| 2012 |
SKAP2 physically associates with both WAVE2 and cortactin and inhibits their interaction; cortactin is required for membrane localization of WAVE2, and SKAP2 suppresses WAVE2/cortactin-mediated actin polymerization in vitro. SKAP2 knockdown enhances WAVE2 translocation to cell membrane and accelerates cell migration in a SKAP2-WAVE2 binding-dependent manner. |
Co-IP, in vitro actin polymerization assay, siRNA knockdown, cell migration assay, binding-deficient mutant |
The Journal of biological chemistry |
Medium |
23161539
|
| 2017 |
Following T cell activation, WAVE2 undergoes ubiquitylation at lysine 45 (mapped by mutagenesis), leading to proteasomal degradation. The autoinhibitory conformation of the WRC stabilizes WAVE2 in resting cells (shown by FRET); release of autoinhibition upon activation exposes K45 to ubiquitylation and degradation. |
FRET (to detect WRC conformational state), ubiquitylation assays, mutagenesis (K45), proteasome inhibitor treatment, T cell activation |
Scientific reports |
Medium |
28332566
|
| 2014 |
WAVE2 recruitment to the TCR signaling site requires ZAP-70, LAT, SLP-76, and Nck (similar to WASp). However, unlike WASp, WAVE2 leaves this complex and migrates peripherally with vinculin to the membrane leading edge. These dynamics were demonstrated using FRET and triple-color FRET technology in live T cells. |
FRET, triple-color FRET (3FRET), siRNA knockdown, live T cell imaging |
The Journal of biological chemistry |
Medium |
25342748
|
| 2018 |
Hem-1 (Nap1) scaffold loss leads to degradation of the entire WAVE2 complex and loss of c-Abl survival signaling from the complex, causing failure of fetal liver HSC engraftment in bone marrow. This engraftment defect is not due to defects in actin-dependent chemotaxis, homing, or adhesion, but to loss of Abl signaling. |
Hem-1 KO mouse, HSC transplantation, homing/migration/adhesion assays, Western blot of complex components, Abl signaling analysis |
Nature communications |
Medium |
29915352
|
| 2006 |
Vinexin beta interacts with the proline-rich region of WAVE2 through its first and second SH3 domains and increases WAVE2 protein levels by reducing proteasomal degradation in a PKA-dependent manner. PKA activation alone increases WAVE2 expression; PKA inhibition suppresses vinexin-induced WAVE2 increase. |
Co-IP, domain mapping by mutagenesis, proteasome inhibitor treatment, PKA activation/inhibition, Western blot |
Genes to cells : devoted to molecular & cellular mechanisms |
Medium |
16483316
|
| 2015 |
NESH/Abi-3 forms a WAVE2 complex that is functionally distinct from the Abi-1-based WAVE2 complex: NESH/Abi-3 neither binds c-Abl nor promotes c-Abl-mediated WAVE2 phosphorylation, and expression of NESH/Abi-3 reduces WAVE2 translocation to the plasma membrane and disrupts lamellipodial protrusion. A linker region between proline-rich regions and the SH3 domain of Abi-1 is required for its c-Abl interaction and c-Abl-mediated WAVE2 phosphorylation. |
Co-IP, domain mapping, imatinib inhibition, siRNA, fluorescence microscopy of WAVE2 localization |
Cell communication and signaling : CCS |
Medium |
26428302
|
| 2016 |
TrkC activation by neurotrophin-3 leads to ERK-dependent phosphorylation of WAVE2 at Thr346 and Ser351, causing a WAVE2 mobility shift; mutagenesis of these sites or ERK inhibition abolishes TrkC-induced WAVE2 shift and podocyte migration. WAVE2 shRNA knockdown abolishes TrkC-induced podocyte migration. |
Mutagenesis of ERK phosphosites (T346/S351), ERK inhibition, shRNA knockdown, podocyte migration assay |
FASEB journal : official publication of the Federation of American Societies for Experimental Biology |
Medium |
29162704
|
| 2013 |
WAVE2 knockdown in 3D epithelial acini causes cadherin isoform switching (decreased E-cadherin, increased N-cadherin) and upregulation of Twist1 mRNA; knockdown of Twist1 in WAVE2-KD cells reverses cadherin switching and rescues the aberrant morphological phenotype. Abl kinase activity is increased in WAVE2-KD cells, and Abl inhibition rescues the multi-lobular phenotype, placing WAVE2 upstream as a repressor of Abl/Twist1 activity. |
shRNA knockdown, 3D acini culture, Abl inhibitor (STI571), Twist1 knockdown rescue, qRT-PCR, immunostaining |
PloS one |
Medium |
23691243
|
| 2020 |
WAVE1 and WAVE2 are redundant for lamellipodia formation and motility in B16-F1 melanoma cells; however, WAVE2 KO decreases the rate of leading-edge actin extension while WAVE1 KO increases it. WAVE1 restricts the rate of actin extension and couples actin networks to the membrane to drive protrusion. |
CRISPR knockout of WAVE1 and WAVE2 individually and together, leading-edge actin extension measurement, retrograde flow measurement |
Molecular biology of the cell |
High |
32697617
|
| 2009 |
HSPC300 interacts with WAVE2 protein and its silencing results in WAVE2 degradation in vitro, indicating HSPC300 is required for WAVE2 stability within the complex. |
siRNA knockdown, Western blot of WAVE2 levels, Co-immunoprecipitation |
Lung cancer (Amsterdam, Netherlands) |
Low |
19576655
|