Affinage

STAP2

Signal-transducing adaptor protein 2 · UniProt Q9UGK3

Length
403 aa
Mass
44.9 kDa
Annotated
2026-04-28
43 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

STAP2 is a multidomain adaptor/scaffold protein that integrates and tunes signaling downstream of diverse receptors in immune, cancer, and metabolic cells. Its PH domain, SH2-like domain, YXXQ motif, and C-terminal proline-rich region each mediate distinct protein–protein interactions: the YXXQ motif directly binds and sustains STAT3 activation during cytokine signaling, while the PH and SH2-like domains engage STAT5, c-Fms, LMP1/TRAF3/TRADD, EGFR, BCR-ABL, and the Src-family kinase LYN, enabling context-dependent positive or negative regulation of JAK-STAT, NF-κB, MAPK/ERK, and PI3K/AKT pathways (PMID:12540842, PMID:15611091, PMID:18573890, PMID:28986450, PMID:22231445, PMID:37669828). Phosphorylation of STAP2 at Tyr250 by kinases including Brk, Jak2, Pyk2, LYN, and BCR-ABL is a convergent regulatory switch that controls its scaffolding activity—enabling STAT3 enhancement, Brk activation in breast cancer, BCR-ABL amplification in CML, and CSK-mediated negative regulation of LYN in B cells (PMID:17368569, PMID:19393627, PMID:20929863, PMID:37669828). In T cells STAP2 bridges CD3ζ ITAMs with LCK to promote proximal TCR signaling and inflammatory responses, whereas in B cells it recruits CSK to LYN to dampen BCR signaling; in adipocytes it forms a CAP/STAP2/c-Cbl complex that facilitates insulin-stimulated GLUT4 translocation and adipogenesis (PMID:35725273, PMID:37669828, PMID:38461189).

Mechanistic history

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

    Identification of STAP-2 as an adaptor protein with PH, SH2-like, and YXXQ domains resolved how late-phase IL-6/STAT3 signaling is sustained in hepatocytes, establishing STAP-2 as a STAT3-enhancing scaffold.

    Evidence STAP-2 KO mouse hepatocytes, YXXQ mutagenesis, reporter assays

    PMID:12540842

    Open questions at the time
    • Structural basis of YXXQ–STAT3 interaction unresolved
    • Upstream signals controlling STAP-2 expression unknown
  2. 2003 Medium

    Demonstration that STAP-2 associates with PLC-γ and suppresses FcεRI-mediated degranulation in mast cells revealed its first negative regulatory role, showing domain versatility beyond STAT3 enhancement.

    Evidence Co-IP and calcium/degranulation assays in RBL-2H3 mast cells

    PMID:12810085

    Open questions at the time
    • STAP-2 KO mast cell validation not performed
    • Mechanism by which STAP-2 selectively suppresses PLC-γ but not Syk phosphorylation unclear
  3. 2004 High

    Discovery that STAP-2 binds STAT5 via PH/SH2-like domains and suppresses STAT5 activation established that STAP-2 exerts opposing effects on STAT3 (positive) and STAT5 (negative) through distinct domain interfaces.

    Evidence Reciprocal co-IP, domain mutagenesis, STAP-2 KO thymocytes with IL-2-dependent growth

    PMID:15611091

    Open questions at the time
    • How phosphorylation-dependent dissociation of STAP-2–STAT5 is regulated in different cell types unclear
  4. 2007 Medium

    Identification of Tyr250 as a phosphorylation site targeted by v-Src/Jak2, required for STAT3-enhancing activity, established a central regulatory switch for STAP-2 scaffold function.

    Evidence Phospho-specific pY250 antibody, Y250F mutagenesis, LIF stimulation in multiple cell lines

    PMID:17368569

    Open questions at the time
    • Kinase hierarchy at Y250 in physiological settings undetermined
    • Phosphatase(s) that reverse Y250 phosphorylation unknown
  5. 2007 Medium

    Showing that STAP-2 PH domain binds c-Fms and suppresses M-CSF-mediated macrophage signaling and migration extended STAP-2's negative regulatory role to receptor tyrosine kinase signaling in macrophages.

    Evidence Co-IP with PH domain mapping, signaling assays, wound-healing in Raw 264.7; later confirmed in KO macrophages (2008)

    PMID:17512498 PMID:18758078

    Open questions at the time
    • Direct vs. indirect mechanism of c-Fms phosphorylation suppression not fully dissected
  6. 2008 High

    Discovery that STAP-2 binds LMP1 and suppresses both canonical and non-canonical NF-κB signaling via TRAF3/TRADD expanded STAP-2's scope to viral oncogene signaling control.

    Evidence Co-IP, domain mapping, NF-κB reporters, STAP-2 KO MEFs

    PMID:18573890

    Open questions at the time
    • Relevance to EBV-associated lymphomagenesis in vivo not tested
  7. 2009 High

    Demonstration that Brk phosphorylates STAP-2 at Y250 and that STAP-2 in turn scaffolds Brk–STAT3 activation linked STAP-2 to breast cancer proliferation, with c-Cbl-mediated ubiquitination of STAP-2 providing a degradation-based counter-regulation.

    Evidence Phospho-specific antibody, siRNA, domain mutants, Cbl overexpression/siRNA, T47D proliferation assays

    PMID:19393627 PMID:19401194 PMID:20929863

    Open questions at the time
    • Whether c-Cbl ubiquitination is K48-linked (proteasomal) not confirmed
    • In vivo breast cancer model lacking
  8. 2011 Medium

    Finding that STAP-2 also scaffolds Brk-mediated STAT5 activation in breast cancer cells revealed that STAP-2's effect on STAT5 is context-dependent—suppressive in thymocytes but activating when bridging Brk in cancer.

    Evidence Ectopic expression, siRNA, STAT5 transcriptional activity, T47D proliferation

    PMID:21205088

    Open questions at the time
    • Molecular basis for context-dependent STAT5 outcome not mechanistically resolved
  9. 2012 High

    Identification of a reciprocal activating loop between STAP-2 and BCR-ABL—BCR-ABL phosphorylates Y250, phospho-STAP-2 enhances BCR-ABL activity—provided a mechanistic basis for STAP-2's role in CML progression and imatinib resistance.

    Evidence Co-IP (SH2-like domain mapping), K562 siRNA, Ba/F3 mouse model, chemokine receptor analysis

    PMID:22231445

    Open questions at the time
    • Patient-derived CML validation limited
    • Whether STAP-2 directly affects imatinib binding or acts indirectly unclear
  10. 2017 High

    Showing that STAP-2 stabilizes EGFR by blocking c-CBL-mediated ubiquitination, and that Pyk2 phosphorylates STAP-2 Y250 to promote T-cell chemotaxis, broadened STAP-2's receptor repertoire and identified a new upstream kinase.

    Evidence Co-IP, EGFR ubiquitination assays, xenograft (EGFR); Pyk2 phosphorylation, siRNA, chemotaxis assay (Pyk2)

    PMID:28478037 PMID:28986450

    Open questions at the time
    • Structural basis of STAP-2 competition with c-CBL for EGFR binding not resolved
  11. 2022 High

    STAP-2 was established as a positive regulator of proximal TCR signaling by bridging CD3ζ ITAMs with LCK, with KO and transgenic mice showing reciprocal effects on EAE severity, directly demonstrating STAP-2's role in adaptive T-cell immunity.

    Evidence Co-IP of CD3ζ/LCK, STAP-2 KO and transgenic mice, IL-2 production, EAE model

    PMID:35725273

    Open questions at the time
    • Whether STAP-2 binds phosphorylated or unphosphorylated ITAMs preferentially not dissected
  12. 2022 Medium

    Therapeutic proof-of-concept peptides (2D5 blocking EGFR and iSP2 blocking CD3ζ binding) validated STAP-2 protein–protein interfaces as druggable nodes.

    Evidence Peptide competition, xenograft tumor suppression (2D5); peptide-ITAM binding, T-cell proliferation suppression, EAE suppression (iSP2)

    PMID:36410436 PMID:37417746

    Open questions at the time
    • Peptide pharmacokinetics, selectivity, and off-target effects not characterized
    • Efficacy in non-murine models untested
  13. 2023 High

    Discovery that STAP-2 recruits CSK to LYN in a Y250-phosphorylation-dependent manner, promoting inhibitory LYN Y508 phosphorylation to dampen BCR signaling, resolved STAP-2's role as a negative regulator of B-cell activation.

    Evidence Co-IP with phospho-dependent binding, KO B cells with signaling and antibody production readouts

    PMID:37669828

    Open questions at the time
    • Whether STAP-2 similarly regulates other Src-family kinases in B cells unknown
    • In vivo humoral immune response phenotype not fully characterized
  14. 2024 High

    Identification of STAP-2 as a bridge between CAP and c-Cbl that promotes GLUT4 translocation and adipogenesis revealed a metabolic function independent of immune signaling.

    Evidence Co-IP (proline-rich region), GLUT4 translocation assay, KO MEFs, KO mice on high-fat diet

    PMID:38461189

    Open questions at the time
    • Whether STAP-2 affects insulin receptor phosphorylation directly or acts solely at the CAP/c-Cbl node unclear
    • Tissue-specific contributions (adipose vs. muscle) not resolved
  15. 2024 Medium

    STAP-2 interaction with HSP27 and modulation of PI3K/AKT signaling in renal fibrosis suggested a role in tissue injury/repair beyond immune cells.

    Evidence Co-IP/MS identification of HSP27, STAP-2 KO mice in IRI and cisplatin renal injury models

    PMID:39533293

    Open questions at the time
    • Functional significance of STAP-2–HSP27 interaction not mechanistically resolved
    • Renal fibrosis findings from single lab, awaits independent replication

Open questions

Synthesis pass · forward-looking unresolved questions
  • No high-resolution structural information exists for STAP-2 or its complexes, the phosphatase(s) reversing Y250 phosphorylation are unknown, and the molecular rules determining whether STAP-2 activates or suppresses a given pathway in different cell types remain unresolved.
  • No crystal or cryo-EM structure of any STAP-2 domain or complex
  • Identity of Y250-targeting phosphatase(s) unknown
  • Context-dependent signaling logic (activating vs. suppressive) lacks a unifying mechanistic model

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 8
Localization
GO:0005886 plasma membrane 2 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 9 R-HSA-168256 Immune System 5 R-HSA-1643685 Disease 3
Partners
BCR-ABLBRKCBLCSKEGFRLYNSTAT3STAT5
Complex memberships
CAP/STAP-2/c-Cbl ternary complexSTAP-2/Brk/STAT3 signaling complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 STAP-2 (also known as BKS) was identified as a novel adaptor protein containing PH and SH2-like domains that modulates STAT3 activity through its YXXQ motif. In STAP-2-deficient 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. STAP-2 knockout mice, reporter assays, overexpression of domain mutants, immunoprecipitation The Journal of biological chemistry High 12540842
2004 STAP-2/BKS physically binds STAT5 through its PH and SH2-like domains interacting with the C-terminal region of STAT5. STAP-2 and STAT5 co-localize in the cytoplasm of resting cells but dissociate upon STAT5 phosphorylation. Overexpression of STAP-2 diminishes cytokine-induced STAT5 tyrosine phosphorylation and transcriptional activation, and STAP-2-deficient thymocytes show enhanced IL-2-dependent cell growth. Co-immunoprecipitation, intracellular staining, mutational analysis, STAP-2 knockout mice, overexpression assays The Journal of biological chemistry High 15611091
2003 STAP-2/BKS associates with PLC-γ in vivo and suppresses FcεRI-mediated tyrosine phosphorylation of PLC-γ (but not Syk), leading to inhibition of calcium mobilization and degranulation in RBL-2H3 mast cells. Overexpression of STAP-2/BKS and domain mutants in RBL-2H3 cells, co-immunoprecipitation, calcium flux assay, degranulation assay Biochemical and biophysical research communications Medium 12810085
2007 STAP-2 directly interacts with c-Fms/M-CSF receptor through its PH domain independently of M-CSF stimulation. Overexpression of STAP-2 suppresses M-CSF-induced c-Fms tyrosine phosphorylation, Akt and ERK activation, and impairs macrophage migration and wound-healing in Raw 264.7 cells. Co-immunoprecipitation (PH domain mapping), kinase/phosphorylation assays, overexpression in Raw 264.7 cells, wound-healing assay Biochemical and biophysical research communications Medium 17512498
2008 STAP-2 loss-of-function in knockout macrophages results in enhanced c-Fms/M-CSF receptor signaling and increased wound-healing capacity, confirming STAP-2 as an endogenous negative regulator of M-CSF receptor signaling. STAP-2 knockout mouse-derived bone marrow macrophages, signaling assays, wound-healing assay Biological & pharmaceutical bulletin Medium 18758078
2008 STAP-2 negatively regulates EBV LMP1-mediated NF-κB signaling (both canonical and non-canonical). STAP-2 associates with LMP1 through its PH and SH2-like domains, and regulates LMP1 signaling through interactions with TRAF3 and TRADD. STAP-2 knockout mouse embryonic fibroblasts show enhanced LMP1-induced cell growth. Co-immunoprecipitation, overexpression, STAP-2 KO MEFs, NF-κB reporter assays, cell growth assays Molecular and cellular biology High 18573890
2007 STAP-2 is phosphorylated at tyrosine-250 (Tyr250) by v-Src and Jak2. Phosphorylation at Tyr250 is induced by leukemia inhibitory factor (LIF) stimulation of cells and is required for STAP-2's STAT3-enhancing activity, as Tyr250 mutants fail to enhance STAT3 activation. Phospho-specific antibody against pY250, mutational analysis (Y250F), LIF stimulation of 293T, Hep3B, and M1 cells, reporter assays Biochemical and biophysical research communications Medium 17368569
2009 STAP-2 is phosphorylated at Tyr250 by Brk (breast tumor kinase). Phosphorylated STAP-2 Y250 promotes Brk-mediated STAT3 activation; the Y250F mutant and siRNA-mediated STAP-2 knockdown both decrease Brk-mediated STAT3 activation. STAP-2 YF mutant panel, phospho-specific anti-pY250 antibody, siRNA knockdown, STAT3 phosphorylation assays Biochemical and biophysical research communications High 19393627
2009 E3 ubiquitin ligase Cbl directly binds STAP-2 through its PH and SH2-like domains and controls STAP-2 protein levels via ubiquitin-mediated degradation. Cbl siRNA restores STAP-2 levels; Cbl overexpression induces STAP-2 degradation. Cbl-mediated STAP-2 degradation reduces Brk/STAP-2-induced STAT3 activation. Co-immunoprecipitation, siRNA knockdown of Cbl, Cbl overexpression, STAT3 reporter assay Biochemical and biophysical research communications Medium 19401194
2010 STAP-2 interacts with both Brk and STAT3, with its PH domain mediating Brk-STAP-2 binding and contributing to Brk activation and STAT3 tyrosine phosphorylation. STAP-2 knockdown in T47D breast cancer cells decreases Brk-mediated STAT3 activation and cell proliferation as strongly as Brk or STAT3 knockdown. A STAP-2 PH-Brk fusion protein exhibits robust kinase activity and enhanced STAT3 activation. Co-immunoprecipitation, siRNA knockdown, PH domain mutants, fusion protein kinase assays, cell proliferation assay The Journal of biological chemistry High 20929863
2011 STAP-2 promotes Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells via its PH domain. STAP-2 knockdown in T47D cells reduces proliferation equivalently to Brk or STAT5b knockdown. Ectopic expression, siRNA knockdown, STAT5 transcriptional activity assays, domain mutants, proliferation assay Cancer science Medium 21205088
2012 STAP-2 binds BCR-ABL (and BCR and ABL proteins) through its SH2-like domain. BCR-ABL phosphorylates STAP-2 at Tyr250, and phosphorylated STAP-2 in turn upregulates BCR-ABL phosphorylation, enhancing downstream ERK, STAT5, BCL-xL, and BCL-2 signaling. STAP-2 interaction with BCR-ABL also downregulates CXCR4 and upregulates CCR7 expression, and confers growth advantage and imatinib resistance. Co-immunoprecipitation (SH2-like domain mapping), phosphorylation assays, siRNA knockdown in K562 cells, Ba/F3 mouse model, chemokine receptor expression analysis Oncogene High 22231445
2017 STAP-2 interacts with EGFR and enhances EGFR stability by inhibiting c-CBL-mediated ubiquitination of EGFR. STAP-2 knockdown in DU145 prostate cancer cells reduces EGF-induced AKT, ERK, and STAT3 phosphorylation and tumor growth. Co-immunoprecipitation, EGFR ubiquitination assay, siRNA knockdown, in vivo xenograft tumor growth The Journal of biological chemistry High 28986450
2017 STAP-2 directly interacts with Pyk2 and increases Pyk2 phosphorylation. Pyk2 itself phosphorylates STAP-2 at Y250, and this phosphorylation is required for maximal STAP-2-Pyk2 interaction. STAP-2/Pyk2 interaction enhances SDF-1α-induced T-cell chemotaxis, which is inhibited by Pyk2 siRNA or the Pyk2 inhibitor AG17. Co-immunoprecipitation, phosphorylation assays, siRNA knockdown of Pyk2, pharmacological inhibition (AG17), chemotaxis assay in Jurkat cells Biochemical and biophysical research communications Medium 28478037
2019 STAP-2 positively regulates FcεRI-mediated basophil activation: STAP-2-deficient bone marrow-derived basophils show reduced degranulation, cytokine production, and phosphorylation of Lyn, PLC-γ2, and Erk after IgE/Ag stimulation. STAP-2 KO mice show significantly reduced IgE-dependent chronic allergic inflammation. STAP-2 KO mouse-derived basophils, degranulation assay, cytokine ELISA, signaling phosphorylation assay, in vivo allergic inflammation model International immunology Medium 30726917
2022 STAP-2 positively regulates TCR signaling by associating with TCR-proximal CD3ζ ITAMs and phosphorylated LCK, enhancing their interaction after TCR stimulation. STAP-2-deficient T cells show reduced TCR-mediated signaling and IL-2 production, whereas STAP-2-overexpressing T cells show enhanced signaling. STAP-2 KO mice show reduced CD4+ T-cell-mediated inflammatory disease (EAE), while STAP-2 transgenic mice show severe EAE. Co-immunoprecipitation (CD3ζ ITAM and LCK binding), STAP-2 KO and transgenic mice, IL-2 production assay, EAE model Journal of immunology High 35725273
2023 STAP-2 negatively regulates BCR-mediated B cell signaling by recruiting CSK to LYN. STAP-2 directly binds LYN depending on STAP-2 Y250 phosphorylation by LYN. Phosphorylated STAP-2 enhances LYN-CSK interactions, promoting CSK-mediated phosphorylation of LYN Y508 (inhibitory site). STAP-2 KO B cells show reduced LYN Y508 phosphorylation and increased BCR signaling, cytokine, and antibody production. Co-immunoprecipitation, phosphorylation assays (Y250, LYN Y508), STAP-2 KO mouse B cells, cytokine and antibody production assays FEBS letters High 37669828
2023 A synthetic peptide derived from STAP-2 (iSP2) directly interacts with CD3ζ ITAM sequences and blocks STAP-2-CD3ζ interactions, suppressing TCR-induced T cell proliferation and IL-2 production in human and murine T cells. iSP2 also suppresses EAE in vivo. Peptide-ITAM binding assay, cell-penetrating peptide delivery, proliferation assay, IL-2 production, EAE model Journal of immunology Medium 37417746
2024 STAP-2 binds to CAP (c-Cbl-associated protein) through its C-terminal proline-rich region and bridges CAP and c-Cbl, enhancing their complex formation. This promotes GLUT4 translocation in response to insulin. STAP-2 expression is upregulated during adipocyte differentiation; STAP-2 overexpression promotes adipogenesis of 3T3-L1 cells and MEFs, while STAP-2 KO MEFs show suppressed adipogenesis. STAP-2 KO mice gain less weight on a high-fat diet. Co-immunoprecipitation (proline-rich region mapping), GLUT4 translocation assay, retroviral overexpression, STAP-2 KO mouse MEFs and in vivo high-fat diet Scientific reports High 38461189
2024 STAP-2 interacts with HSP27 (identified by co-immunoprecipitation and mass spectrometry) and modulates the PI3K/AKT signaling pathway in renal fibrosis. STAP-2 KO in vivo reduces EMT, inflammatory cell infiltration, and collagen deposition in renal fibrosis models; STAP-2 overexpression in vitro exacerbates fibrosis markers. STAP-2 affects phosphorylated HSP27 levels. Co-immunoprecipitation, mass spectrometry, RNA-seq, STAP-2 KO mice (IRI and cisplatin models), STAP-2 overexpression in vitro, fibrosis marker quantification Journal of translational medicine Medium 39533293
2022 KGF-2 inhibits STAP-2 expression and consequently reduces STAT3 activation, leading to decreased collagen I and collagen III levels in fibroblasts and reduced hypertrophic scar formation both in vitro and in vivo. STAP-2 expression modulation, STAT3 phosphorylation assay, collagen expression analysis, in vivo scar model The Journal of investigative dermatology Medium 34999107
2022 A STAP-2-derived peptide (2D5) blocks STAP-2-EGFR interactions and suppresses EGFR-mediated proliferation, EGFR stability, and signaling in cancer cell lines and murine xenograft models of prostate and lung cancer. Peptide competition assay, EGFR signaling assays, cell proliferation assay, in vivo xenograft model The Journal of biological chemistry Medium 36410436
2015 CCR7 upregulation by STAP-2/BCR-ABL is mediated through the MAPK/ERK pathway. STAP-2 cooperates with BCR-ABL to induce CCR7 ligand (CCL19, CCL21) production, and CCR7 contributes to STAP-2-dependent enhancement of BCR-ABL-mediated cell growth in Ba/F3 cells. Chemokine receptor expression analysis, ERK pathway inhibition, CCL19/CCL21 ELISA, cell growth assay Biochemical and biophysical research communications Medium 26102025

Source papers

Stage 0 corpus · 43 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 90 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 85 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 37 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 24 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
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
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 12 34999107
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
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 5 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
2024 STAP2 promotes the progression of renal fibrosis via HSP27. Journal of translational medicine 3 39533293
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
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