Affinage

WBP2

WW domain-binding protein 2 · UniProt Q969T9

Length
261 aa
Mass
28.1 kDa
Annotated
2026-06-11
33 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

WBP2 is a PPXY-motif adaptor protein that functions principally as a transcriptional co-activator within the Hippo pathway, where its C-terminal PPXY-containing region is recognized by the WW domains of YAP/TAZ to potentiate YAP/TAZ–TEAD-driven oncogenic transcription (PMID:20972459, PMID:21981024); this role is evolutionarily conserved, as Drosophila Wbp2 binds Yorkie and genetically acts downstream of the Salvador-Warts-Hippo pathway to control tissue growth (PMID:21311569), and in mammalian epidermal stem cells WBP2 serves as a YAP co-factor governing proliferation under adhesion control (PMID:28332498). WBP2 additionally suppresses Hippo kinase activity directly, binding and inhibiting LATS2 (PMID:33475198) and competitively displacing LATS1 from WWC3 via its PPXY motifs (PMID:33837178), driving YAP nuclear translocation and tumor progression. WBP2 protein levels are tightly governed by PPXY–WW-mediated ubiquitination: the E3 ligases ITCH and WWP1 bind WBP2 and target it for proteasomal degradation (PMID:27578003, PMID:41891541, PMID:32459862, PMID:39709035), a fate counteracted by Wnt/EGFR-driven tyrosine phosphorylation and competitive WW-domain occupancy by TAZ/YAP, with stabilized nuclear WBP2 engaging β-catenin to activate TCF transcription (PMID:27578003). Beyond Hippo/Wnt, WBP2 acts as a co-activator for the steroid hormone receptors ERα and PGR, controlling MDR1 (ABCB1) transcription and chemoresistance (PMID:29937544, PMID:26881968), stabilizes BTRC mRNA to drive NF-κB signaling and TNBC invasion (PMID:34197030), physically blocks microprocessor (DGCR8/DDX5/DDX17) assembly to suppress microRNA biogenesis (PMID:34117091), and protects GPX4 from chaperone-mediated autophagy by competing with HSC70, thereby restraining ferroptosis (PMID:37516014). WBP2 also localizes to the sperm postacrosomal sheath and can activate oocytes upon injection (PMID:30010725).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2004 Medium

    Established an early function for WBP-2 as a protein-interaction adaptor by showing it binds a transcription factor outside its canonical WW-ligand context, raising the question of whether it is always a co-activator.

    Evidence GST pulldown and Co-IP of WBP-2 with Pax8, with a negative transcription co-activation result

    PMID:14531730

    Open questions at the time
    • Co-activation was explicitly negative in this context
    • single lab, no in vivo validation
    • non-WW-domain interaction mode not generalized
  2. 2010 High

    Defined WBP2 as a required effector of TAZ oncogenicity, answering whether the TAZ WW domain–WBP2 interaction is functionally necessary rather than incidental.

    Evidence Reciprocal Co-IP, WW-domain point mutagenesis, forced-fusion rescue, transformation and reporter assays

    PMID:20972459

    Open questions at the time
    • Mechanism of how WBP2 augments transcription not fully resolved
    • scope limited to TAZ/ITGB2 readout
  3. 2011 High

    Placed WBP2 genetically within the Hippo pathway and established evolutionary conservation by showing the fly ortholog enhances Yorkie and modifies warts phenotypes.

    Evidence Co-IP, genetic epistasis with warts loss-of-function, in vivo wing growth and reporter assays in Drosophila

    PMID:21311569

    Open questions at the time
    • Mammalian pathway placement inferred from orthology
    • molecular step enhanced by Wbp2 not defined
  4. 2011 High

    Characterized the biophysical determinants of WBP2 recognition, answering which WW domains and PPXY consensus features govern binding.

    Evidence ITC, CD, molecular modeling, and MD simulation of YAP2 WW1/WW2 binding WBP1/WBP2 PPXY motifs

    PMID:21981024

    Open questions at the time
    • Promiscuous binding leaves in-cell selectivity unexplained
    • no cellular functional readout
  5. 2012 High

    Extended WBP2 PPXY recognition to the WWOX tumor suppressor and resolved the structural basis of WW1 versus WW2 differential affinity.

    Evidence ITC, CD, modeling, and E66R/Y85W gain-of-function mutagenesis of WWOX WW domains

    PMID:22634283

    Open questions at the time
    • Functional consequence of WWOX-WBP2 binding in cells not addressed
    • no in vivo validation
  6. 2016 High

    Defined the regulatory logic controlling WBP2 abundance, showing ITCH degrades WBP2 while Wnt/EGFR phosphorylation and TAZ/YAP competition stabilize it to drive β-catenin/TCF transcription.

    Evidence Reciprocal Co-IP, RNAi, proteasome inhibition, tyrosine phosphorylation analysis, transformation and xenograft assays

    PMID:27578003

    Open questions at the time
    • Phosphosites mediating ITCH dissociation not fully mapped
    • interplay with Hippo-derived stabilization not quantified
  7. 2016 Medium

    Revealed an in vivo physiological role distinct from cancer, linking WBP2 ERα/PGR co-activation to cochlear synapse maintenance and hearing.

    Evidence Wbp2-knockout mice, auditory testing, electron microscopy of inner hair cell synapses

    PMID:26881968

    Open questions at the time
    • Molecular link between WBP2/ESR1/PGR and synapse biology not dissected
    • target genes in cochlea unidentified
  8. 2017 High

    Demonstrated that WBP2 is a YAP co-factor governing epidermal stem cell proliferation under adhesion control rather than canonical Hippo signaling.

    Evidence Genome-wide RNAi screen, conditional mouse KO, TEAD reporter, reconstituted epidermis

    PMID:28332498

    Open questions at the time
    • Adhesion-to-WBP2/YAP signaling intermediates undefined
    • context-dependence relative to LATS not resolved
  9. 2018 Medium

    Mapped how WBP2 itself is transcriptionally induced, identifying USF-1 and AKT-dependent phosphorylation as upstream drivers.

    Evidence Yeast one-hybrid, promoter reporter, ChIP, MS, AKT inhibition, E-box mutagenesis

    PMID:30183375

    Open questions at the time
    • Single-lab transcriptional model
    • physiological contexts of USF-1-driven induction not surveyed
  10. 2018 High

    Established WBP2 as a co-activator for ERα at the MDR1 promoter, connecting it directly to chemoresistance.

    Evidence Reciprocal Co-IP, ChIP at MDR1 promoter, RNAi, viability/flow assays, xenograft

    PMID:29937544

    Open questions at the time
    • Generality across ER target genes untested
    • co-activation mechanism at chromatin not detailed
  11. 2018 Medium

    Defined a Wnt-priming circuit in TNBC where WBP2 upregulates GPS1/TNIK to sustain JNK/Jun feedback and AXIN2 expression.

    Evidence RNAi with RNA-Seq and MS, functional rescue, inhibitor and migration/growth assays

    PMID:30442712

    Open questions at the time
    • Direct versus indirect regulation of GPS1/TNIK unclear
    • single-lab pathway model
  12. 2018 Medium

    Identified a reproductive role, localizing WBP2 to the sperm postacrosomal sheath and showing it can activate oocytes.

    Evidence Immunoblot/IF/IHC localization and recombinant protein microinjection into MII oocytes

    PMID:30010725

    Open questions at the time
    • Physiological requirement during natural fertilization untested
    • activation mechanism in oocyte unknown
  13. 2020 Medium

    Generalized the ITCH–WBP2 degradation axis to immune cells, linking WBP2 stability to CD4 T-cell proliferation.

    Evidence Itch-KO CD4 T-cell proteomics, stability assays, Co-IP, RNAi, in vitro/in vivo proliferation

    PMID:32459862

    Open questions at the time
    • Transcriptional effectors of WBP2 in T cells unidentified
    • single-lab study
  14. 2021 Medium

    Showed WBP2 directly suppresses Hippo kinases, both inhibiting LATS2 and displacing LATS1 from WWC3 to promote YAP activation.

    Evidence Phosphoproteomics, Co-IP, phosphorylation/competitive-binding assays, RNAi epistasis, xenografts

    PMID:33475198 PMID:33837178

    Open questions at the time
    • Whether LATS inhibition is direct enzymatic or steric not fully resolved
    • relative contribution of LATS1 vs LATS2 axes context-dependent
  15. 2021 Medium

    Uncovered non-transcriptional functions: WBP2 stabilizes BTRC mRNA to activate NF-κB and blocks microprocessor assembly to suppress miRNA biogenesis.

    Evidence mRNA stability and pri-miRNA processing assays, Co-IP of microprocessor components, NF-κB reporter, epistasis

    PMID:34117091 PMID:34197030

    Open questions at the time
    • Mechanism of BTRC mRNA stabilization (RNA-binding direct or indirect) undefined
    • structural basis of microprocessor blockade unknown
  16. 2023 Medium

    Revealed a metabolic/redox role, showing WBP2 protects GPX4 from chaperone-mediated autophagy by competing with HSC70 to suppress ferroptosis.

    Evidence Co-IP, competitive binding assay, lysosomal inhibition, ferroptosis assays, cisplatin AKI model

    PMID:37516014

    Open questions at the time
    • Whether WBP2 broadly regulates CMA substrates untested
    • single-lab mechanism
  17. 2024 Medium

    Broadened the ubiquitin-regulator network of WBP2, implicating Dyrk1b-driven degradation in hepatic glucose homeostasis and reaffirming ITCH-driven degradation in chemoresistance via AMOTL2/c-JUN.

    Evidence Quantitative proteomics, in vivo rescue, ubiquitylation assays, ITCH C830A ligase-dead mutant, MG132 rescue, xenografts

    PMID:39296215 PMID:39709035

    Open questions at the time
    • Whether Dyrk1b directly phosphorylates WBP2 to flag degradation unproven
    • convergence of multiple E3/kinase inputs on WBP2 not integrated
  18. 2026 Medium

    Identified WWP1 as an additional WW-domain E3 ligase partner of WBP2 in cardiac tissue and mapped the interacting domains.

    Evidence Yeast two-hybrid (human heart library), proximity ligation assay, co-localization, domain-deletion mapping

    PMID:41891541

    Open questions at the time
    • Functional consequence of WWP1-mediated WBP2 regulation in heart untested
    • ubiquitination of WBP2 by WWP1 not directly demonstrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many parallel WBP2 functions (transcriptional co-activation, Hippo kinase inhibition, mRNA stabilization, microprocessor blockade, CMA competition) are coordinated within a cell and which dominate in each tissue context remains unresolved.
  • No unified structural or stoichiometric model integrating nuclear and cytoplasmic WBP2 roles
  • tissue-specific dominance of each function unmapped
  • post-translational code linking phosphorylation, ubiquitination, and partner choice undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0140110 transcription regulator activity 4 GO:0060090 molecular adaptor activity 3 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-392499 Metabolism of proteins 5 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-8953854 Metabolism of RNA 2

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 The WW domain of TAZ binds WBP2 through interaction with the PPXY-containing C-terminal region of WBP2. Point mutations in the WW domain of TAZ abolished interaction with WBP2 and abolished TAZ-driven transformation and transcriptional activation of ITGB2. Forced fusion of WBP2 (or its TAZ-interacting C-terminal domain) to WW-mutant TAZ rescued transforming and transcription-promoting ability, establishing that WW domain–WBP2 interaction is required for TAZ oncogenic activity. Proteomic interaction screen, co-immunoprecipitation, WW domain point mutagenesis, cell transformation assay, transcription reporter assay, RNAi knockdown, overexpression Oncogene High 20972459
2011 Drosophila Wbp2 interacts with Yorkie (the fly ortholog of YAP/TAZ) in a WW domain- and PY motif-dependent manner, enhances Yorkie's transcriptional co-activator properties, is required for normal wing growth, and genetically suppresses overgrowth caused by loss of the warts tumor suppressor gene, placing Wbp2 as a downstream component of the Salvador-Warts-Hippo pathway. Co-immunoprecipitation, genetic epistasis (warts loss-of-function suppression), in vivo tissue growth assay, transcription reporter assay in Drosophila Cell death and differentiation High 21311569
2012 The WW1 domain of WWOX tumor suppressor binds PPXY motifs within WBP2 in a physiologically relevant manner; the WW2 domain shows no affinity for these motifs due to chemically distinct residues (E66/Y85 vs. R25/W44). Introduction of E66R/Y85W double substitution into WW2 confers gain-of-function binding to WBP2, stronger than wild-type WW1. WW1 is structurally disordered and folds upon ligand binding, while WW2 is pre-structured and acts as a chaperone to stabilize and augment WW1 ligand binding. Isothermal titration calorimetry, circular dichroism, molecular modeling, site-directed mutagenesis (E66R/Y85W gain-of-function) Journal of molecular biology High 22634283
2011 The WW1 and WW2 domains of YAP2 both recognize PPXY motifs within WBP1 and WBP2 in a promiscuous manner; both WW domains strictly require the consensus PPXY sequence; a PPXYXG motif (glycine one residue C-terminal of the consensus tyrosine) is bound with highest affinity by both domains. Binding interactions are highly dynamic with rapid nanosecond-scale conformational fluctuations. Isothermal titration calorimetry, circular dichroism, molecular modeling, molecular dynamics simulation Biochemistry High 21981024
2016 WBP2 protein stability is controlled by the E3 ubiquitin ligase ITCH, which binds WBP2 and targets it for ubiquitin-dependent proteasomal degradation. Wnt3A signaling stabilizes WBP2 by disrupting ITCH–WBP2 interaction via EGFR-mediated tyrosine phosphorylation of WBP2 and competitive binding of TAZ/YAP. Stabilized nuclear WBP2 interacts with β-catenin and activates TCF-mediated transcription. ITCH silencing elevates WBP2 levels; ITCH-mediated WBP2 degradation inhibits TCF/β-catenin transcription, in vitro transformation, and in vivo tumorigenesis. Co-immunoprecipitation, RNAi knockdown, proteasome inhibitor treatment, in vitro transformation assay, in vivo xenograft, tyrosine phosphorylation analysis, somatic mutation analysis of ITCH Cancer research High 27578003
2016 WBP2 acts as a transcriptional coactivator for estrogen receptor α (ESR1) and progesterone receptor (PGR) in the cochlea; loss of Wbp2 expression in mice leads to progressive high-frequency hearing loss with a primary defect at inner hair cell afferent (glutamatergic) synapses. Mouse knockout (Wbp2-deficient), auditory function testing, electron microscopy of cochlear synapses, histology EMBO molecular medicine Medium 26881968
2017 WBP2 functions as a co-factor of YAP that enhances YAP/TEAD-mediated gene transcription in epidermal stem cells. WBP2 deletion in mouse skin reduces proliferation in neonatal and wounded adult epidermis. In reconstituted epidermis, YAP/WBP2 activity is controlled by intercellular adhesion rather than canonical Hippo signaling. Genome-wide pooled RNAi screen, mouse conditional knockout, immunofluorescence, TEAD reporter assay, reconstituted epidermis model Nature communications High 28332498
2004 WBP-2 binds Pax8 (a thyroid-specific transcription factor) in vitro via pulldown and in vivo via co-immunoprecipitation; the interaction is mediated by a novel protein-interacting domain in the C-terminal portion of Pax8 (not a WW domain). WBP-2 does not act as a transcriptional co-activator of Pax8 but behaves as an adaptor molecule in this context. Immunological/yeast screening, GST pulldown, co-immunoprecipitation, transcription assay (negative result for co-activation) The Biochemical journal Medium 14531730
2018 WBP2 interacts with ERα (estrogen receptor α) and directly modulates MDR1 (ABCB1) transcription through binding to ERα; chromatin immunoprecipitation confirmed ERα occupancy at the MDR1 promoter is WBP2-dependent, increasing chemoresistance to doxorubicin. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), RNAi knockdown, overexpression, MTT cell viability, flow cytometry, in vivo xenograft British journal of cancer High 29937544
2018 WBP2 primes TNBC cells for Wnt responses by upregulating GPS1 and TNIK; GPS1 activates the JNK/Jun pathway, which forms a positive feedback loop with TNIK to mediate Wnt-induced AXIN2 expression. WBP2 is required for expression of core Wnt target genes including AXIN2, which is essential for Wnt/WBP2-driven cancer growth and migration. RNAi coupled with RNA-Seq and mass spectrometry, functional rescue, migration and growth assays, pathway inhibitor studies The Journal of biological chemistry Medium 30442712
2018 USF-1 (upstream stimulatory factor 1) is a key transcription factor that directly drives WBP2 transcription via an E-box motif in the WBP2 minimal promoter; AKT-mediated phosphorylation of USF-1 (stimulated by insulin/PI3K signaling) enhances USF-1 binding to the WBP2 promoter and activates WBP2 transcription. Yeast one-hybrid, promoter reporter assay, chromatin immunoprecipitation, tandem mass spectrometry, AKT inhibitor treatment, mutational analysis of E-box FASEB journal Medium 30183375
2018 WBP2 is localized to the postacrosomal sheath (PAS) and perforatorium of the sperm perinuclear theca in mice, with highest expression in round spermatids during spermatogenesis. Microinjection of recombinant WBP2 into metaphase II mouse oocytes activates oocytes at comparable rates to WBP2NL (PAWP), identifying WBP2 as a candidate sperm-borne oocyte-activating factor. Immunoblotting, immunofluorescence, immunohistochemistry, recombinant protein microinjection into MII oocytes Biology of reproduction Medium 30010725
2020 ITCH (E3 ubiquitin ligase) attenuates CD4 T-cell proliferation by promoting WBP2 proteasomal degradation; Itch-deficient CD4 T cells show increased WBP2 protein stability and hyperproliferation. Itch and WBP2 physically interact in CD4 T cells. WBP2 knockdown reduces CD4 T-cell proliferation. Whole-cell proteomics of primary mouse Itch-KO CD4 T cells, protein stability assay, co-immunoprecipitation, RNAi knockdown, in vitro and in vivo proliferation assays European journal of immunology Medium 32459862
2021 WBP2 competitively binds to the WW domain of WWC3 via its PPxY motifs, displacing LATS1 from the WWC3-LATS1 complex, thereby reducing LATS1 phosphorylation, suppressing Hippo pathway activity, and ultimately promoting YAP nuclear translocation and NSCLC progression. Co-immunoprecipitation, phosphorylation assays, nuclear/cytoplasmic fractionation, gain- and loss-of-function experiments in lung cancer cells, in vivo xenograft Cell death & disease Medium 33837178
2021 WBP2 physically interacts with LATS2 kinase and inhibits LATS2 phosphorylation and activity; WBP2 knockdown increases p-LATS2 with concomitant increase in p-YAP, causing cytoplasmic YAP retention and inhibition of YAP/TEAD target genes (CTGF, CYR61). Loss of LATS2 reverses Hippo pathway activation caused by WBP2 knockdown, establishing LATS2 as the functional effector downstream of WBP2 in this context. Mass spectrometry-based phosphoproteomics, co-immunoprecipitation, phosphorylation assay, RNAi epistasis (LATS2 rescue), reporter assay, migration assay FASEB journal Medium 33475198
2021 WBP2 suppresses microRNA biogenesis by blocking processing of pri-miRNAs to pre-miRNAs; mechanistically, WBP2 physically interacts with components of the microprocessor complex (DGCR8, DDX5, DDX17) and negatively regulates assembly of this complex. WBP2 blocks the tumor-suppressive properties of DGCR8. Co-immunoprecipitation of microprocessor components, pri-miRNA processing assay, 2D and 3D in vitro proliferation assays, RNAi Life science alliance Medium 34117091
2021 WBP2 promotes TNBC cell migration and invasion via TNF-α-stimulated NF-κB activation; mechanistically, WBP2 enhances mRNA stability of BTRC (β-TrCP), the E3 ligase that ubiquitinates IκBα, leading to IκBα degradation and NF-κB nuclear translocation. IκBα overexpression rescues the WBP2-driven invasive phenotype; BTRC loss blocks WBP2-driven migration. Proteogenomic analysis (TCGA), RNAi knockdown, mRNA stability assay, NF-κB reporter assay, nuclear fractionation, migration/invasion assays, epistasis (IκBα rescue, BTRC knockdown) Molecular oncology Medium 34197030
2023 WBP2 interacts with GPX4 via its PPXY1 motif and inhibits ferroptosis by competing with HSC70 for binding to KFERQ-like motifs on GPX4, thereby decelerating chaperone-mediated autophagy (CMA) and lysosomal degradation of GPX4. WBP2 downregulation in cisplatin-induced AKI accelerates GPX4 degradation and ferroptosis. Co-immunoprecipitation (WBP2-GPX4, WBP2-HSC70), competitive binding assay, lysosomal inhibitor experiments, ferroptosis assays, in vivo cisplatin AKI model, bioinformatics Redox biology Medium 37516014
2024 Dyrk1b kinase promotes ubiquitylation and proteasomal degradation of Wbp2 in a kinase activity-dependent manner in hepatocytes; restoration of hepatic Wbp2 partially rescues impaired glucose homeostasis caused by Dyrk1b overexpression, placing Wbp2 downstream of Dyrk1b in hepatic glucose regulation. Quantitative proteomics, in vivo mouse overexpression/knockout, ubiquitylation assay, kinase-dead mutant (Dyrk1b kinase inhibitor AZ191), Wbp2 restoration rescue experiment Heliyon Medium 39296215
2024 E3 ubiquitin ligase ITCH mediates proteasomal degradation of WBP2 (ligase-dead ITCH C830A mutant loses this activity); WBP2 overexpression drives chemoresistance via activation of the AMOTL2/c-JUN axis; exogenous ITCH suppresses WBP2-mediated chemoresistance and AMOTL2/c-JUN activation in a proteasome-dependent manner. RNA sequencing, co-immunoprecipitation, proteasome inhibitor (MG132) rescue, ITCH C830A ligase-dead mutagenesis, in vivo xenograft, AMOTL2 knockdown, c-JUN antagonist Biochemical pharmacology Medium 39709035
2026 E3 ubiquitin ligase WWP1 interacts with WBP2 in human heart tissue; co-localization and proximity ligation assays confirmed endogenous interaction. Using yeast two-hybrid, the interaction was mapped to WW domains 1 and 3 of WWP1 and PY (PPXY) domains 2 and 3 of WBP2. Yeast two-hybrid screen (human heart library), immunofluorescence, proximity ligation assay, domain-deletion mapping Biology open Medium 41891541

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 WW domain-mediated interaction with Wbp2 is important for the oncogenic property of TAZ. Oncogene 93 20972459
2017 A genome-wide screen identifies YAP/WBP2 interplay conferring growth advantage on human epidermal stem cells. Nature communications 83 28332498
2016 Wnt Signaling Promotes Breast Cancer by Blocking ITCH-Mediated Degradation of YAP/TAZ Transcriptional Coactivator WBP2. Cancer research 70 27578003
2011 Wbp2 cooperates with Yorkie to drive tissue growth downstream of the Salvador-Warts-Hippo pathway. Cell death and differentiation 59 21311569
2023 WBP2 restrains the lysosomal degradation of GPX4 to inhibit ferroptosis in cisplatin-induced acute kidney injury. Redox biology 41 37516014
2022 EIF4A3-mediated circPRKCI expression promotes triple-negative breast cancer progression by regulating WBP2 and PI3K/AKT signaling pathway. Cell death discovery 37 35236829
2012 Biophysical basis of the binding of WWOX tumor suppressor to WBP1 and WBP2 adaptors. Journal of molecular biology 37 22634283
2016 Wbp2 is required for normal glutamatergic synapses in the cochlea and is crucial for hearing. EMBO molecular medicine 36 26881968
2011 Biophysical analysis of binding of WW domains of the YAP2 transcriptional regulator to PPXY motifs within WBP1 and WBP2 adaptors. Biochemistry 35 21981024
2019 microRNA-485-5p inhibits the progression of hepatocellular carcinoma through blocking the WBP2/Wnt signaling pathway. Cellular signalling 30 31706018
2018 Interaction of WBP2 with ERα increases doxorubicin resistance of breast cancer cells by modulating MDR1 transcription. British journal of cancer 30 29937544
2018 WBP2 Downregulation Inhibits Proliferation by Blocking YAP Transcription and the EGFR/PI3K/Akt Signaling Pathway in Triple Negative Breast Cancer. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 30 30092563
2017 WBP2 modulates G1/S transition in ER+ breast cancer cells and is a direct target of miR-206. Cancer chemotherapy and pharmacology 27 28391353
2020 The emerging roles of WBP2 oncogene in human cancers. Oncogene 25 32393834
2004 WBP-2, a WW domain binding protein, interacts with the thyroid-specific transcription factor Pax8. The Biochemical journal 25 14531730
2018 WBP2 shares a common location in mouse spermatozoa with WBP2NL/PAWP and like its descendent is a candidate mouse oocyte-activating factor. Biology of reproduction 23 30010725
2018 The transcriptional coactivator WBP2 primes triple-negative breast cancer cells for responses to Wnt signaling via the JNK/Jun kinase pathway. The Journal of biological chemistry 23 30442712
2021 WBP2 promotes BTRC mRNA stability to drive migration and invasion in triple-negative breast cancer via NF-κB activation. Molecular oncology 21 34197030
2021 WBP2 negatively regulates the Hippo pathway by competitively binding to WWC3 with LATS1 to promote non-small cell lung cancer progression. Cell death & disease 17 33837178
2018 Phosphorylation of E-box binding USF-1 by PI3K/AKT enhances its transcriptional activation of the WBP2 oncogene in breast cancer cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 17 30183375
2018 Elevated WBP2 Expression in HER2-positive Breast Cancers Correlates with Sensitivity to Trastuzumab-based Neoadjuvant Therapy: A Retrospective and Multicentric Study. Clinical cancer research : an official journal of the American Association for Cancer Research 15 30593516
2019 Localisation of phospholipase Cζ1 (PLCZ1) and postacrosomal WW-binding protein (WBP2 N-terminal like) on equine spermatozoa and flow cytometry quantification of PLCZ1 and association with cleavage in vitro. Reproduction, fertility, and development 12 31597592
2021 WBP2 promotes gastric cancer cell migration via novel targeting of LATS2 kinase in the Hippo tumor suppressor pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 11 33475198
2024 E3 ubiquitin ligase ITCH-mediated proteasomal degradation of WBP2 sensitizes breast cancer cells to chemotherapy through restraining AMOTL2/c-JUN axis. Biochemical pharmacology 8 39709035
2022 WW domain binding protein 2 (WBP2) as an oncogene in breast cancer: mechanisms and therapeutic prospects-a narrative review. Gland surgery 8 36654949
2020 Itch attenuates CD4 T-cell proliferation in mice by limiting WBP2 protein stability. European journal of immunology 8 32459862
2021 WBP2 inhibits microRNA biogenesis via interaction with the microprocessor complex. Life science alliance 6 34117091
2021 Reciprocal Regulation of Hippo and WBP2 Signalling-Implications in Cancer Therapy. Cells 5 34831354
2025 WBP2 and its network of transcription coregulators in an expanding repertoire of human cancers. International journal of cancer 1 40958198
2024 Hepatic Dyrk1b impairs systemic glucose homeostasis by modulating Wbp2 expression in a kinase activity-dependent manner. Heliyon 1 39296215
2026 WBP2 Attenuates Metformin Response in HER2-Positive Breast Cancer Cells by Repressing AMPK Activation and Inducing a Lower AMP:ATP Ratio State Through Enhanced ATP Production. Cells 0 41744824
2026 Identification and validation of an interaction between the E3 ubiquitin ligase WWP1 and the Transcriptional Co-Activator WBP2 in the human heart. Biology open 0 41891541
2024 Evaluating the involvement and mutual interaction of wbp2 and yap in embryogenesis with an emphasis on liver function in zebrafish embryos. Tissue & cell 0 39486132

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