Affinage

STAP2

Signal-transducing adaptor protein 2 · UniProt Q9UGK3

Length
403 aa
Mass
44.9 kDa
Annotated
2026-06-10
44 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

STAP-2/BKS is a cytoplasmic adaptor protein, built from a PH domain, an SH2-like domain, and a C-terminal YXXQ/proline-rich region, that scaffolds and tunes the output of multiple receptor and kinase signaling pathways rather than carrying intrinsic catalytic activity (PMID:12540842, PMID:15611091). Its most conserved scaffolding function is modulation of STAT transcription factors: the YXXQ motif acts as a STAT3-docking site that enhances IL-6/LIF-induced STAT3 activation and acute-phase gene expression (PMID:12540842), while direct binding of its PH and SH2-like domains to the C-terminal region of STAT5 suppresses STAT5 activation in resting cells and dissociates upon STAT5 phosphorylation (PMID:15611091). STAP-2 function is gated by phosphorylation of a single tyrosine, Tyr250, which is targeted by diverse kinases — v-Src and Jak2, Brk, BCR-ABL, Pyk2, and LYN — and is required for its STAT3-enhancing and partner-binding activities (PMID:17368569, PMID:19393627, PMID:22231445, PMID:28478037, PMID:37669828). Through these interactions STAP-2 acts as a context-dependent positive or negative regulator: it promotes oncogenic Brk-STAT3/STAT5 signaling and proliferation in breast cancer (PMID:20929863, PMID:21205088), potentiates BCR-ABL signaling and tumor formation in CML (PMID:22231445), stabilizes EGFR by blocking c-CBL-mediated ubiquitination to sustain AKT/ERK/STAT3 signaling and tumor growth (PMID:28986450), and conversely restrains FcεRI signaling in mast cells (PMID:12810085), M-CSF receptor signaling in macrophages (PMID:17512498, PMID:18758078), and BCR signaling in B cells by recruiting CSK to LYN to enforce inhibitory LYN Y508 phosphorylation (PMID:37669828). In T cells STAP-2 binds CD3ζ ITAMs and phosphorylated LCK to amplify TCR-proximal signaling and IL-2 production, shaping CD4+ T-cell-mediated autoimmune disease in vivo (PMID:35725273). STAP-2 also bridges CAP and c-Cbl to facilitate insulin-induced GLUT4 translocation and adipogenesis (PMID:38461189), and its own abundance is controlled by Cbl-mediated degradation (PMID:19401194).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2003 High

    Established STAP-2 as an adaptor that enhances STAT3 signaling through a defined YXXQ docking motif, answering how this novel PH/SH2-like protein modulates cytokine responses.

    Evidence Knockout hepatocytes with IL-6 stimulation, YXXQ mutagenesis, and acute-phase reporter assays

    PMID:12540842

    Open questions at the time
    • Structural basis of YXXQ–STAT3 docking not resolved
    • Did not address STAP-2 effects on other STAT family members
  2. 2003 Medium

    Showed STAP-2 also acts as a negative regulator in a distinct receptor context, suppressing FcεRI-mediated mast cell activation upstream of PLC-γ.

    Evidence Overexpression in RBL-2H3 mast cells with calcium flux, degranulation, and PLC-γ Co-IP/phosphorylation assays

    PMID:12810085

    Open questions at the time
    • Based on overexpression rather than endogenous loss-of-function
    • Mechanism of PLC-γ suppression not defined
  3. 2004 High

    Defined an opposing STAT-modulating role: STAP-2 binds and suppresses STAT5, establishing it as a bidirectional STAT regulator depending on the family member.

    Evidence Reciprocal Co-IP, domain-deletion mapping, co-localization in resting cells, and KO thymocyte proliferation

    PMID:15611091

    Open questions at the time
    • How STAP-2 discriminates STAT3 versus STAT5 outcomes unresolved
    • Cytokine specificity of STAT5 suppression not mapped
  4. 2007 Medium

    Extended STAP-2's negative regulatory function to the M-CSF receptor, showing direct PH-domain binding to c-Fms dampens receptor signaling and macrophage migration.

    Evidence Domain-mapped Co-IP and overexpression in Raw 264.7 macrophages with Akt/ERK and wound-healing assays

    PMID:17512498

    Open questions at the time
    • Overexpression-based; endogenous role addressed only in later work
  5. 2007 Medium

    Identified Tyr250 as the major regulatory phosphosite (by v-Src and Jak2) required for STAP-2's STAT3-enhancing activity, providing the switch that gates adaptor function.

    Evidence Y250F mutagenesis, phospho-specific antibody, kinase assays, and endogenous LIF-induced phosphorylation in multiple lines

    PMID:17368569

    Open questions at the time
    • Single lab
    • Which interactions are gained or lost upon Tyr250 phosphorylation not comprehensively mapped
  6. 2008 High

    Confirmed endogenous negative regulation of M-CSF receptor signaling in primary cells and revealed a parallel role in restraining EBV LMP1/NF-κB signaling via TRAF3/TRADD.

    Evidence KO bone marrow macrophages with M-CSF stimulation; KO MEFs and EBV+ B cells with NF-κB reporters and LMP1 Co-IP

    PMID:18573890 PMID:18758078

    Open questions at the time
    • Mechanism by which STAP-2 inhibits LMP1/TRAF3 signaling not detailed
  7. 2009 High

    Connected STAP-2 to the oncogenic Brk kinase by mapping Tyr250 as a Brk substrate site required for Brk-driven STAT3 activation, and showed Cbl controls STAP-2 abundance.

    Evidence YF mutant panel, phospho-specific antibody, Brk kinase assays, siRNA knockdown; reciprocal Cbl gain/loss-of-function with domain-mapped Co-IP

    PMID:19393627 PMID:19401194

    Open questions at the time
    • Whether Cbl ubiquitinates STAP-2 directly versus indirectly not established
  8. 2010 High

    Established STAP-2 as a required cofactor for Brk-STAT3 signaling and proliferation in breast cancer, with the PH domain driving Brk activation, then extended this to Brk-STAT5.

    Evidence Domain deletion/fusion constructs, PH-Brk fusion kinase activity, siRNA knockdown and proliferation assays in T47D cells; STAT5 transcriptional and proliferation readouts

    PMID:20929863 PMID:21205088

    Open questions at the time
    • Structural mechanism of PH-domain-mediated Brk activation unresolved
  9. 2012 High

    Demonstrated a feed-forward oncogenic loop in CML where STAP-2 binds BCR-ABL via its SH2-like domain, is phosphorylated at Tyr250, and amplifies BCR-ABL and downstream survival signaling required for tumor formation.

    Evidence Domain-mapped Co-IP, phospho-site analysis, downstream signaling immunoblots, siRNA knockdown, and K562 xenografts

    PMID:22231445

    Open questions at the time
    • Mechanism of reciprocal BCR-ABL phosphorylation enhancement not detailed
  10. 2015 Low

    Linked the STAP-2/BCR-ABL axis to chemokine signaling by showing cooperative CCR7/CCL19/CCL21 induction via ERK contributes to growth.

    Evidence BCR-ABL/STAP-2 co-expression in Ba/F3 cells with ERK inhibitors and chemokine expression assays

    PMID:26102025

    Open questions at the time
    • Overexpression in a single cell line without endogenous validation
    • Causal role of CCR7 axis in vivo not tested
  11. 2017 High

    Revealed a stabilizing role for STAP-2 in EGFR-driven cancer by antagonizing c-CBL-mediated EGFR ubiquitination, and identified Pyk2 as another Tyr250 kinase coupling STAP-2 to T-cell chemotaxis.

    Evidence EGFR Co-IP/ubiquitination assays and siRNA knockdown with tumor model in DU145; Pyk2 Co-IP, knockdown, AG17 inhibition, and SDF-1α chemotaxis

    PMID:28478037 PMID:28986450

    Open questions at the time
    • Whether STAP-2 sterically blocks CBL or competes for EGFR not defined
    • Pyk2 work is single-lab Medium confidence
  12. 2019 High

    Showed STAP-2 can be a positive regulator of innate effector signaling, promoting FcεRI-mediated basophil activation via Lyn/PLC-γ2/ERK and driving chronic allergic inflammation.

    Evidence KO basophils with degranulation, cytokine, and phosphorylation readouts plus in vivo allergic inflammation model

    PMID:30726917

    Open questions at the time
    • Contrast with negative FcεRI regulation in mast cells not mechanistically reconciled
  13. 2022 High

    Established STAP-2 as a positive amplifier of TCR-proximal signaling by binding CD3ζ ITAMs and phospho-LCK, with reciprocal KO/transgenic mice defining its role in CD4+ T-cell autoimmunity, and validated the interaction as druggable with the iSP2 peptide.

    Evidence Co-IP of CD3ζ ITAM/LCK, KO and transgenic mouse T-cell assays, EAE models; iSP2 peptide blocking with proliferation, IL-2, and EAE readouts

    PMID:35725273 PMID:37417746

    Open questions at the time
    • Structural basis of STAP-2–ITAM recognition not resolved
    • iSP2 study is Medium confidence single-lab
  14. 2023 High

    Defined the molecular basis of STAP-2's negative regulation of BCR signaling: LYN-dependent Tyr250 phosphorylation enables STAP-2 to recruit CSK to LYN and enforce inhibitory LYN Y508 phosphorylation.

    Evidence KO B cells, Y250F mutant analysis, CSK-LYN Co-IP, LYN Y508 immunoblot, and antibody/cytokine production assays

    PMID:37669828

    Open questions at the time
    • How STAP-2 simultaneously engages LYN and CSK structurally not defined
  15. 2024 Medium

    Expanded STAP-2's adaptor repertoire to metabolic and fibrotic contexts: it bridges CAP–c-Cbl to enable insulin-induced GLUT4 translocation and adipogenesis, and promotes renal fibrosis through HSP27 binding and PI3K/AKT modulation.

    Evidence Proline-rich domain Co-IP and GLUT4 translocation assays with KO MEF/mouse metabolic phenotypes; KO fibrosis models with Co-IP/MS identification of HSP27 and RNA-seq

    PMID:38461189 PMID:39533293

    Open questions at the time
    • Single-lab studies
    • Direct versus scaffold-mediated control of PI3K/AKT in fibrosis not separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How STAP-2 selects between positive and negative regulatory outcomes across receptors, and the structural determinants of its PH/SH2-like/YXXQ domains, remain the central unresolved questions.
  • No three-dimensional structure of STAP-2 or its complexes reported
  • Rules governing context-dependent positive versus negative signaling not established
  • Tissue-specific kinase usage at Tyr250 not systematically mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 5 GO:0098772 molecular function regulator activity 4 GO:0140110 transcription regulator activity 2
Localization
GO:0005829 cytosol 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-74160 Gene expression (Transcription) 2
Partners
BCR-ABLBRKCBLEGFRLYNPLCGSTAT3STAT5

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 STAP-2/BKS was identified as a novel adaptor protein containing PH and SH2-like domains and a YXXQ motif. It is tyrosine-phosphorylated and translocates to the plasma membrane in response to EGF. In STAP-2 knockout hepatocytes, IL-6-induced STAT3 tyrosine phosphorylation and acute-phase gene expression were reduced at the late phase (6-24 h). Overexpression of wild-type STAP-2 but not YXXQ-motif mutants enhanced acute-phase response element reporter activity, establishing the YXXQ motif as the STAT3-binding element responsible for STAP-2's modulatory function. Knockout mouse generation, IL-6 stimulation of hepatocytes, reporter assays, co-immunoprecipitation, site-directed mutagenesis The Journal of biological chemistry High 12540842
2004 STAP-2/BKS directly binds STAT5 through its PH and SH2-like domains interacting with the C-terminal region of STAT5. STAP-2/BKS and STAT5 constitutively co-localize in the cytoplasm of resting cells, but STAP-2/BKS dissociates upon STAT5 phosphorylation. Overexpression of STAP-2/BKS diminished cytokine-induced STAT5 tyrosine phosphorylation and transcriptional activation. STAP-2-deficient thymocytes showed enhanced IL-2-dependent cell growth. Co-immunoprecipitation, intracellular staining, domain-deletion mutational analysis, STAP-2 KO mouse thymocyte proliferation assay The Journal of biological chemistry High 15611091
2003 STAP-2/BKS overexpression in RBL-2H3 mast cells suppresses FcεRI-mediated calcium mobilization and degranulation. STAP-2/BKS associates with PLC-γ in vivo and significantly suppresses FcεRI-induced tyrosine phosphorylation of PLC-γ (but not Syk), establishing STAP-2 as a negative regulator of FcεRI signaling upstream of PLC-γ. Overexpression in RBL-2H3 cells, co-immunoprecipitation, calcium flux assay, degranulation assay, phosphotyrosine immunoblotting Biochemical and biophysical research communications Medium 12810085
2008 STAP-2 negatively regulates EBV LMP1-mediated NF-κB signaling. STAP-2 associates with LMP1 through its PH and SH2-like domains and interacts with TRAF3 and TRADD. STAP-2 knockout mouse embryonic fibroblasts showed enhanced LMP1-induced cell growth. STAP-2 overexpression in EBV-positive human B cells decreased cell growth. Co-immunoprecipitation, overexpression in EBV+ B cells, STAP-2 KO MEFs, NF-κB reporter assays Molecular and cellular biology High 18573890
2007 STAP-2 directly interacts with c-Fms/M-CSF receptor through its PH domain independently of M-CSF stimulation. Overexpression of STAP-2 in Raw 264.7 macrophages markedly suppressed M-CSF-induced tyrosine phosphorylation of c-Fms and activation of Akt and ERK, and impaired M-CSF-induced macrophage migration and wound healing. Co-immunoprecipitation with domain mapping, overexpression in Raw 264.7 cells, Akt/ERK phosphorylation assay, wound-healing migration assay Biochemical and biophysical research communications Medium 17512498
2008 Loss of STAP-2 in bone marrow-derived macrophages from STAP-2 knockout mice results in markedly enhanced c-Fms/M-CSF receptor signaling (ERK and Akt activation) and enhanced wound-healing/migration process, confirming STAP-2 as an endogenous negative regulator of M-CSF receptor signaling in primary macrophages. STAP-2 KO mouse-derived bone marrow macrophages, M-CSF stimulation, ERK/Akt phosphorylation assay, wound-healing assay Biological & pharmaceutical bulletin Medium 18758078
2007 STAP-2 Tyr250 is a major phosphorylation site by v-Src and Jak2, identified using a phospho-specific anti-pTyr250 antibody and mutagenesis. Tyr250 phosphorylation is required for STAP-2's STAT3-enhancing activity. Endogenous STAP-2 is phosphorylated at Tyr250 following LIF stimulation in 293T, Hep3B, and murine M1 cells. Site-directed mutagenesis (Y250F), phospho-specific antibody, kinase assay, LIF stimulation of cell lines including M1 cells Biochemical and biophysical research communications Medium 17368569
2009 STAP-2 Tyr250 is phosphorylated by Brk (breast tumor kinase), identified using a series of YF mutants and an anti-phospho-STAP-2 Tyr250 antibody. A STAP-2 Y250F mutant impaired Brk-mediated STAT3 activation. siRNA-mediated knockdown of endogenous STAP-2 decreased Brk-mediated STAT3 activation. Site-directed mutagenesis (YF series), phospho-specific antibody, in vitro/cell-based kinase assay with Brk, siRNA knockdown, STAT3 activation reporter/immunoblot Biochemical and biophysical research communications High 19393627
2009 E3 ubiquitin ligase Cbl directly controls STAP-2 protein levels. STAP-2 physically interacts with Cbl through its PH and SH2-like domains. siRNA knockdown of endogenous Cbl restored STAP-2 protein levels; overexpression of Cbl induced STAP-2 degradation. Cbl-mediated regulation of STAP-2 protein levels affected Brk/STAP-2-induced STAT3 activation. Co-immunoprecipitation with domain mapping, siRNA knockdown of Cbl, Cbl overexpression, immunoblot for STAP-2 protein levels, STAT3 activation assay Biochemical and biophysical research communications Medium 19401194
2010 STAP-2 interacts with both Brk and STAT3 in breast cancer cells. The PH domain of STAP-2 is required for Brk-STAP-2 binding, Brk kinase activation, and STAT3 tyrosine phosphorylation. A STAP-2 PH-Brk fusion protein exhibited robust kinase activity and enhanced STAT3 activation. siRNA knockdown of STAP-2 in T47D cells decreased Brk-mediated STAT3 activation and strongly reduced proliferation. Co-immunoprecipitation, domain deletion/fusion constructs, siRNA knockdown, STAT3 phosphorylation assay, cell proliferation assay The Journal of biological chemistry High 20929863
2011 STAP-2 is involved in Brk-mediated STAT5 activation in breast cancer cells. The PH domain of STAP-2 participates in Brk-mediated phosphorylation of STAT5. STAP-2 knockdown in T47D cells reduced proliferation as strongly as Brk or STAT5b knockdown. Ectopic expression, domain analysis, STAT5 transcriptional activity assay, siRNA knockdown, cell proliferation assay Cancer science Medium 21205088
2012 STAP-2 binds to BCR-ABL, BCR, and ABL proteins via its SH2-like domain. BCR-ABL phosphorylates STAP-2 at Tyr250, and phosphorylated STAP-2 in turn upregulates BCR-ABL phosphorylation and downstream ERK, STAT5, BCL-xL, and BCL-2 activation. STAP-2 interaction with BCR-ABL also alters chemokine receptor expression (down-regulates CXCR4, up-regulates CCR7). STAP-2 knockdown in K562 CML cells abolished tumor formation in mice. Co-immunoprecipitation with domain mapping, phosphorylation assays, signaling pathway immunoblots, siRNA knockdown, in vivo xenograft Oncogene High 22231445
2017 STAP-2 interacts with EGFR and enhances EGFR stability by inhibiting c-CBL-mediated EGFR ubiquitination. STAP-2 knockdown in DU145 prostate cancer cells reduced EGF-induced phosphorylation of AKT, ERK, and STAT3, and strongly decreased tumor growth. Co-immunoprecipitation, EGFR ubiquitination assay, STAP-2 siRNA knockdown, signaling phosphorylation assays, in vivo tumor growth assay The Journal of biological chemistry High 28986450
2017 STAP-2 directly interacts with Pyk2 in T cells, increasing Pyk2 phosphorylation. Pyk2 itself phosphorylates STAP-2 at Y250, and this phosphorylation is critical for maximal STAP-2–Pyk2 interactions. STAP-2-enhanced SDF-1α-induced T-cell chemotaxis is inhibited by Pyk2 siRNA or the Pyk2 inhibitor AG17. Co-immunoprecipitation, phosphorylation assay, siRNA knockdown of Pyk2, pharmacological inhibition with AG17, T-cell chemotaxis assay Biochemical and biophysical research communications Medium 28478037
2019 STAP-2 positively regulates FcεRI-mediated basophil activation. STAP-2-deficient bone marrow-derived basophils showed reduced degranulation, cytokine production, and reduced phosphorylation of Lyn, PLC-γ2, and ERK after IgE/Ag stimulation. STAP-2-deficient mice showed significantly inhibited IgE-dependent chronic allergic inflammation in vivo. STAP-2 KO mouse-derived basophil culture, degranulation assay, cytokine ELISA, phosphorylation immunoblot, in vivo allergic inflammation model International immunology High 30726917
2022 STAP-2 positively regulates TCR signaling by associating with TCR-proximal CD3ζ ITAMs and phosphorylated LCK. STAP-2-deficient T cells showed reduced TCR-mediated signaling and IL-2 production; STAP-2-overexpressing T cells showed enhanced signaling. STAP-2-deficient mice exhibited reduced CD4+ T-cell-mediated EAE disease severity, while STAP-2-overexpressing transgenic mice showed severe EAE. Co-immunoprecipitation (STAP-2 with CD3ζ ITAM and LCK), STAP-2 KO and transgenic mouse T-cell assays, IL-2 production, TCR signaling phosphorylation, EAE model Journal of immunology High 35725273
2022 KGF-2 inhibits STAP-2 expression and STAT3 activation in fibroblasts, leading to reduced collagen I and collagen III levels and attenuated scar formation. This places STAP-2 downstream of KGF-2 signaling and upstream of STAT3-mediated collagen production in skin fibroblasts. KGF-2 treatment of fibroblasts and in vivo scar model, STAP-2 expression measurement, STAT3 activation assay, collagen I/III quantification The Journal of investigative dermatology Medium 34999107
2023 STAP-2 negatively regulates BCR-mediated B cell signaling by recruiting CSK to LYN. STAP-2 directly binds LYN dependently on STAP-2 Y250 phosphorylation by LYN. Phosphorylated STAP-2 enhances interactions between LYN and CSK, resulting in enhanced CSK-mediated LYN Y508 phosphorylation (inhibitory). STAP-2 KO B cells showed increased LYN activity, BCR-mediated signals, cytokine production, and antibody production. STAP-2 KO mouse B cells, Co-immunoprecipitation, Y250F mutant analysis, LYN Y508 phosphorylation immunoblot, cytokine and antibody production assays FEBS letters High 37669828
2023 A STAP-2-derived synthetic peptide (iSP2) directly interacts with CD3ζ ITAM sequences and blocks STAP-2–CD3ζ interactions, suppressing T cell proliferation and TCR-induced IL-2 production in human and murine T cells, and inhibiting TCR-mediated EAE in vivo. Peptide binding assay, Co-IP blocking experiment, T-cell proliferation assay, IL-2 production, in vivo EAE model with cell-penetrating peptide Journal of immunology Medium 37417746
2024 STAP-2 binds to CAP (c-Cbl associated protein) through its C-terminal proline-rich region, bridges CAP and c-Cbl to enhance their complex formation, and facilitates GLUT4 translocation after insulin treatment. STAP-2 KO MEFs showed suppressed adipogenesis, and STAP-2 KO mice showed reduced weight gain on a high-fat diet. Co-immunoprecipitation, domain mapping (proline-rich region), GLUT4 translocation assay in Hep3B cells, STAP-2 KO MEF adipogenesis assay, in vivo high-fat diet model Scientific reports Medium 38461189
2024 STAP2 promotes renal fibrosis. STAP2 knockout in mice mitigated EMT, reduced inflammatory cell infiltration, and reduced collagen deposition in renal fibrosis models. Mechanistically, STAP2 interacts with HSP27 (identified by co-immunoprecipitation and mass spectrometry) and modulates the PI3K/AKT signaling pathway. STAP2 KO mouse fibrosis models (IRI and cisplatin), co-immunoprecipitation, mass spectrometry, RNA-seq, STAP2 overexpression in cells, fibrosis marker quantification Journal of translational medicine Medium 39533293
2022 A STAP-2-derived peptide (2D5) blocks STAP-2–EGFR interactions and suppresses EGFR-mediated proliferation in prostate and lung cancer cell lines, and inhibits tumor growth of DU145 and A549 xenografts, confirming that the STAP-2–EGFR interaction is required for full EGFR signaling and stability. STAP-2-derived peptide competitive inhibition assay, cell proliferation assay, EGFR stability/signaling immunoblot, murine xenograft model The Journal of biological chemistry Medium 36410436
2015 STAP-2 cooperates with BCR-ABL to upregulate CCR7 expression in Ba/F3 hematopoietic cells via the MAPK/ERK pathway. STAP-2 and BCR-ABL together induce production of CCR7 ligands CCL19 and CCL21, contributing to cell growth. BCR-ABL/STAP-2 co-expression in Ba/F3 cells, ERK pathway inhibitor studies, CCR7/CCL19/CCL21 expression assays, cell growth assay Biochemical and biophysical research communications Low 26102025

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Transcriptional profiling of diabetic neuropathy in the BKS db/db mouse: a model of type 2 diabetes. Diabetes 91 21617178
2020 Human adipose-derived mesenchymal stem cell-conditioned medium ameliorates polyneuropathy and foot ulceration in diabetic BKS db/db mice. Stem cell research & therapy 86 32357914
2003 STAP-2/BKS, an adaptor/docking protein, modulates STAT3 activation in acute-phase response through its YXXQ motif. The Journal of biological chemistry 70 12540842
2004 Physical and functional interactions between STAP-2/BKS and STAT5. The Journal of biological chemistry 50 15611091
2009 STAP-2 is phosphorylated at tyrosine-250 by Brk and modulates Brk-mediated STAT3 activation. Biochemical and biophysical research communications 44 19393627
2010 Interactions of STAP-2 with Brk and STAT3 participate in cell growth of human breast cancer cells. The Journal of biological chemistry 41 20929863
2011 Reduced proliferation and a high apoptotic frequency of pancreatic beta cells contribute to genetically-determined diabetes susceptibility of db/db BKS mice. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 39 21412687
2017 Markers of Islet Endothelial Dysfunction Occur in Male B6.BKS(D)-Leprdb/J Mice and May Contribute to Reduced Insulin Release. Endocrinology 38 27870582
2011 Involvement of STAP-2 in Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells. Cancer science 31 21205088
2008 STAP-2 negatively regulates both canonical and noncanonical NF-kappaB activation induced by Epstein-Barr virus-derived latent membrane protein 1. Molecular and cellular biology 31 18573890
2003 Altering dietary protein type and quantity reduces urinary albumin excretion without affecting plasma glucose concentrations in BKS.cg-m +Lepr db/+Lepr db (db/db) mice. The Journal of nutrition 30 12612136
2017 STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization. The Journal of biological chemistry 25 28986450
2012 STAP-2 interacts with and modulates BCR-ABL-mediated tumorigenesis. Oncogene 25 22231445
2003 Regulation of FcepsilonRI-mediated signaling by an adaptor protein STAP-2/BSK in rat basophilic leukemia RBL-2H3 cells. Biochemical and biophysical research communications 22 12810085
1999 CpG oligodeoxynucleotides rescue BKS-2 immature B cell lymphoma from anti-IgM-mediated growth inhibition by up-regulation of egr-1. International immunology 22 10360960
2021 Identification of StAP2/ERF genes of potato (Solanum tuberosum) and their multiple functions in detoxification and accumulation of cadmium in yest: Implication for Genetic-based phytoremediation. The Science of the total environment 21 34902403
2007 STAP-2 regulates c-Fms/M-CSF receptor signaling in murine macrophage Raw 264.7 cells. Biochemical and biophysical research communications 19 17512498
2007 Leukemia inhibitory factor-induced phosphorylation of STAP-2 on tyrosine-250 is involved in its STAT3-enhancing activity. Biochemical and biophysical research communications 15 17368569
2021 STAP-2 Adaptor Protein Regulates Multiple Steps of Immune and Inflammatory Responses. Biological & pharmaceutical bulletin 14 34193686
2008 Enhanced c-Fms/M-CSF receptor signaling and wound-healing process in bone marrow-derived macrophages of signal-transducing adaptor protein-2 (STAP-2) deficient mice. Biological & pharmaceutical bulletin 14 18758078
1991 Cyclosporin A blocks surface IgM-mediated growth inhibition in an immature B lymphoma, BKS-2. European journal of immunology 14 1915562
2022 KGF-2 Regulates STAP-2-Mediated Signal Transducer and Activator of Transcription 3 Signaling and Reduces Skin Scar Formation. The Journal of investigative dermatology 13 34999107
2014 Oral administration of Nitraria retusa ethanolic extract enhances hepatic lipid metabolism in db/db mice model 'BKS.Cg-Dock7(m)+/+ Lepr(db/)J' through the modulation of lipogenesis-lipolysis balance. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 13 25086370
2017 STAP-2 interacts with Pyk2 and enhances Pyk2 activity in T-cells. Biochemical and biophysical research communications 12 28478037
2022 STAP-2 Is a Novel Positive Regulator of TCR-Proximal Signals. Journal of immunology (Baltimore, Md. : 1950) 11 35725273
2020 Immunolocalization of Keratan Sulfate in Rat Spinal Tissues Using the Keratanase Generated BKS-1(+) Neoepitope: Correlation of Expression Patterns with the Class II SLRPs, Lumican and Keratocan. Cells 11 32235499
2019 STAP-2 positively regulates FcεRI-mediated basophil activation and basophil-dependent allergic inflammatory reactions. International immunology 10 30726917
2009 The protein content of an adaptor protein, STAP-2 is controlled by E3 ubiquitin ligase Cbl. Biochemical and biophysical research communications 10 19401194
2014 Adaptor protein STAP-2 modulates cellular signaling in immune systems. Biological & pharmaceutical bulletin 8 24492713
2024 STAP2 promotes the progression of renal fibrosis via HSP27. Journal of translational medicine 7 39533293
2022 A peptide derived from adaptor protein STAP-2 inhibits tumor progression by downregulating epidermal growth factor receptor signaling. The Journal of biological chemistry 7 36410436
2015 CCR7 is involved in BCR-ABL/STAP-2-mediated cell growth in hematopoietic Ba/F3 cells. Biochemical and biophysical research communications 7 26102025
2019 Highly Selective Protein Tyrosine Phosphatase Inhibitor, 2,2',3,3'-Tetrabromo-4,4',5,5'-tetrahydroxydiphenylmethane, Ameliorates Type 2 Diabetes Mellitus in BKS db Mice. Molecular pharmaceutics 6 30974944
2023 STAP-2-Derived Peptide Suppresses TCR-Mediated Signals to Initiate Immune Responses. Journal of immunology (Baltimore, Md. : 1950) 4 37417746
2024 STAP-2 facilitates insulin signaling through binding to CAP/c-Cbl and regulates adipocyte differentiation. Scientific reports 3 38461189
2023 STAP-2 negatively regulates BCR-mediated B cell activation by recruiting tyrosine-protein kinase CSK to LYN. FEBS letters 3 37669828
2013 Draft Genome Sequence of Rhodococcus triatomae Strain BKS 15-14. Genome announcements 3 23538907
2013 Draft Genome Sequence of Streptomyces gancidicus Strain BKS 13-15. Genome announcements 3 23599292
2025 BKS-112, a Selective Histone Deacetylase 6 Inhibitor, Suppresses Triple-Negative Breast Cancer Cells via AKT/mTOR Pathway. Antioxidants (Basel, Switzerland) 2 41300448
2022 Verification of the folkloric and anecdotal antidiabetic effects of Hypoxis hemerocallidea (Fisch., C.A. Mey. & Avé-Lall) and isolated, β-sitosterol using early-stage type II spontaneous diabetic mutant BKS-Leprdb mice. BMC complementary medicine and therapies 2 35725532
2013 Draft Genome Sequence of Rhodococcus ruber Strain BKS 20-38. Genome announcements 2 23558535
2010 [Novel adaptor protein, STAP-2 functions as a signal modulator in immune system]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 2 20519854
2026 Functional potential of the APETALA2 transcription factors StAP2-13/18 in modulating tuberization under long-day (LD) conditions in potato. BMC genomics 0 42204454
2017 Effects of GW002, a novel recombinant human glucagon-like peptide-1 (GLP-1) analog fusion protein, on CHO recombinant cells and BKS-db mice. Acta diabetologica 0 28424924

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