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Showing UBASH3B — STS-1 is a alias.

UBASH3B

Ubiquitin-associated and SH3 domain-containing protein B · UniProt Q8TF42

Length
649 aa
Mass
72.7 kDa
Annotated
2026-06-10
31 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

UBASH3B (Sts-1/TULA-2) is a multi-domain histidine phosphatase of the PGM/acid phosphatase superfamily that acts as a negative regulator of tyrosine kinase signaling across immune, hematopoietic, and other cell types (PMID:17679096, PMID:20585042). Its catalytic C-terminal domain uses a nucleophilic histidine (His380) and general acid (Glu490) to dephosphorylate specific phosphotyrosines, with substrate selectivity defined by residues flanking the target tyrosine (PMID:24256567, PMID:20670933). Through this activity it dampens antigen- and immunoreceptor-driven signaling by dephosphorylating ZAP-70 downstream of the TCR (PMID:14738763, PMID:17679096) and Syk downstream of GPVI, FcεRI, FcγRIIA, and CLEC-2 receptors, targeting regulatory sites including Syk Y346, Y323, and Y352 (PMID:20585042, PMID:20670933, PMID:22267732, PMID:27609517); loss of the phosphatase produces hyperresponsive T cells, mast cells, osteoclasts, and a prothrombotic platelet phenotype (PMID:14738763, PMID:23149425, PMID:27765766). Independently of direct kinase dephosphorylation, UBASH3B regulates the CBL ubiquitin ligase: its SH3 domain binds Cbl while its UBA domain binds mono-ubiquitin and is recruited into activated EGFR complexes, inhibiting receptor endocytosis and degradation, and its dephosphorylation of CBL stabilizes EGFR to drive proliferative, invasive, and metastatic phenotypes in cancer (PMID:15159412, PMID:23784775). Beyond receptor signaling, UBASH3B functions as a ubiquitin receptor that recruits ubiquitylated Aurora B to mitotic microtubules to ensure faithful chromosome segregation (PMID:26766443), and it dephosphorylates additional substrates including PKCδ, controlling its proteasomal degradation (PMID:33556471), and the mitochondrial ribosomal protein MRPL12 at Y60 to regulate oxidative phosphorylation (PMID:39343960).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2004 High

    Established UBASH3B as a genetic negative regulator of TCR signaling, defining its core role in restraining immunoreceptor activation through control of ZAP-70 phosphorylation.

    Evidence Sts-1/Sts-2 double-knockout mice with T cell stimulation assays, ZAP-70 phospho-immunoblot, and an EAE autoimmunity model

    PMID:14738763

    Open questions at the time
    • Did not resolve whether ZAP-70 is a direct catalytic substrate versus an indirect target
    • Redundancy with Sts-2 obscured the individual contribution of Sts-1
  2. 2004 High

    Defined the adaptor/ubiquitin-receptor arm of UBASH3B, showing its SH3 and UBA domains couple it to Cbl, ubiquitin, and the activated EGFR to prolong mitogenic signaling.

    Evidence Co-IP, ubiquitin/EGFR-Ub chimera pulldowns, receptor internalization assays, and dominant-negative interference

    PMID:15159412

    Open questions at the time
    • Did not establish whether EGFR effects required phosphatase activity
    • Mechanism of recruitment into the EGFR complex not fully resolved
  3. 2007 High

    Identified the molecular basis of catalysis, placing UBASH3B in the PGM/AcP histidine phosphatase superfamily and tying its enzymatic activity directly to TCR suppression.

    Evidence X-ray crystallography of the C-terminal domain, in vitro phosphatase assay on ZAP-70, active-site mutagenesis, and phosphatase-dead rescue in T cells

    PMID:17348005 PMID:17679096

    Open questions at the time
    • Physiological relevance of ecdysteroid/steroid phosphate hydrolysis in mammals unclear
    • Ecdysteroid activity lacked active-site mutagenesis validation
  4. 2010 High

    Extended the phosphatase function to platelet biology and defined intrinsic substrate specificity, identifying Syk regulatory tyrosines as bona fide targets.

    Evidence Co-IP of TULA-2 with Syk, in vitro dephosphorylation, combinatorial phosphopeptide library profiling, and KO-platelet site-specific immunoblot

    PMID:20585042 PMID:20670933

    Open questions at the time
    • Did not rank which Syk site is rate-limiting in vivo (resolved later)
    • Specificity rules derived from peptides may not capture full-length substrate context
  5. 2012 High

    Generalized Syk regulation across immunoreceptor systems, showing UBASH3B restrains FcεRI signaling in mast cells and osteoclast differentiation through phosphatase-dependent control of Syk.

    Evidence Phosphopeptide pulldown/MS, siRNA knockdown with degranulation and NF-κB/NFAT readouts in mast cells; DKO mice and phosphatase-dead mutant in osteoclasts

    PMID:22267732 PMID:23149425

    Open questions at the time
    • Did not define site preference within Syk in these cell types
    • Contribution relative to other Syk phosphatases not quantified
  6. 2013 High

    Confirmed ZAP-70 as a direct active-site substrate and revealed a CBL-EGFR axis through which UBASH3B drives cancer invasion, linking its phosphatase activity to oncogenic signaling.

    Evidence Substrate-trapping His380/Glu490 mutants with vanadate competition in T cells; CBL in vitro dephosphorylation, phosphatase-dead mutant, and xenografts in TNBC cells

    PMID:23784775 PMID:24256567

    Open questions at the time
    • Whether CBL dephosphorylation and EGFR adaptor binding act synergistically not dissected
    • miR-200a regulation defined only in TNBC context
  7. 2015 Medium

    Showed UBASH3B-CBL signaling has context-dependent outputs, supporting leukemia cell growth and shaping IFN-α-induced autophagy through JAK1-STAT1.

    Evidence shRNA depletion with CBL-mutant rescue and xenografts in AML1-ETO cells; overexpression/knockdown with inhibitor epistasis in B cells

    PMID:25959715 PMID:26449661

    Open questions at the time
    • Single-lab studies without independent confirmation
    • Direct versus indirect effects on TYK2/JAK1/STAT1 not fully separated
  8. 2016 High

    Revealed a non-canonical mitotic function as a ubiquitin receptor and refined the platelet substrate map by identifying Syk Y346 as the key dephosphorylation checkpoint.

    Evidence Co-IP of ubiquitylated Aurora B, live-cell imaging, LOF/GOF chromosome segregation assays; site-specific phospho-Syk peptide phosphatase assays and FcγRIIA-transgenic KO mice in platelets

    PMID:26766443 PMID:27609517 PMID:27765766

    Open questions at the time
    • How the UBA domain selects ubiquitylated Aurora B over other substrates unknown
    • Whether the mitotic and signaling functions are coordinated unclear
  9. 2017 High

    Provided comparative structural and kinetic detail distinguishing Sts-1 from Sts-2 and mapped a phosphotyrosine-dependent ShcA interaction at the EGFR.

    Evidence X-ray structures of Sts-1/Sts-2 HP domains with sulfate, steady-state kinetics, PHPS1 inhibitor Ki, cell-based ZAP-70 assay; phosphopeptide affinity pulldown for ShcA

    PMID:28690151 PMID:28759203

    Open questions at the time
    • ShcA interaction rests on a single pulldown without reciprocal Co-IP or functional consequence
    • Functional difference between Sts-1 and Sts-2 in vivo not addressed
  10. 2024 Medium

    Broadened the substrate repertoire beyond receptor signaling to CLEC-2/HemITAM platelet signaling, endothelial VEGFR-2-driven angiogenesis, PKCδ stability, and mitochondrial metabolism via MRPL12 Y60.

    Evidence KO platelets (CLEC-2); miR-25-3p modulation with Co-IP and hindlimb ischemia (endothelium); RNAi with proteasome inhibitor (PKCδ); MS, Co-IP, Y60F mutagenesis, POLRMT interaction, and LUAD models (MRPL12)

    PMID:31249969 PMID:33201836 PMID:33556471 PMID:39343960

    Open questions at the time
    • Each substrate characterized by a single lab
    • How UBASH3B accesses a mitochondrial substrate (MRPL12) and its subcellular localization there not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how UBASH3B's three activities — phosphotyrosine catalysis, Cbl/ubiquitin adaptor function, and ubiquitin-receptor-mediated cargo recruitment — are integrated and regulated within a single cell.
  • No structural model of the full-length multidomain protein engaging substrate plus ubiquitin
  • Mechanism selecting between catalytic and adaptor modes unknown
  • Upstream signals controlling UBASH3B activity/localization largely uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 9 GO:0098772 molecular function regulator activity 4 GO:0016787 hydrolase activity 3 GO:0060090 molecular adaptor activity 2
Localization
GO:0005829 cytosol 2 GO:0005739 mitochondrion 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-168256 Immune System 5 R-HSA-109582 Hemostasis 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-1640170 Cell Cycle 1
Partners
AURKBCBLEGFRMRPL12PRKCDSHC1SYKZAP70

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 Sts-1 (UBASH3B) negatively regulates TCR signaling; T cells from Sts-1/Sts-2 double-knockout mice are hyperresponsive with increased ZAP-70 phosphorylation (including ubiquitylated forms) and hyperactivation of downstream signaling proteins, establishing Sts-1 as a critical negative regulator of ZAP-70 in the TCR signaling pathway. Genetic knockout (Sts-1/Sts-2 double-knockout mice), T cell stimulation assays, immunoblot for ZAP-70 phosphorylation, cytokine production assays, EAE autoimmunity model Immunity High 14738763
2004 Sts-1 (UBASH3B) binds to Cbl via its SH3 domain, binds mono-ubiquitin and the EGFR/Ub chimera via its UBA domain, is recruited into activated EGFR complexes upon ligand stimulation, and inhibits EGFR endocytosis and degradation, resulting in prolonged mitogenic signaling. Co-immunoprecipitation, pulldown with ubiquitin/EGFR-Ub chimera, receptor internalization assays, endocytic vesicle quantification, cell proliferation and transformation assays, dominant-negative interference The Journal of biological chemistry High 15159412
2007 Sts-1 (UBASH3B) is a phosphatase belonging to the phosphoglycerate mutase/acid phosphatase (PGM/AcP) histidine phosphatase superfamily; its C-terminal domain dephosphorylates ZAP-70 in vitro, and point mutations inactivating its phosphatase activity also impair its ability to suppress TCR signaling in T cells. X-ray crystallography of Sts-1 C-terminal domain, in vitro phosphatase assay with ZAP-70, active-site mutagenesis (key catalytic residues), TCR signaling assays in T cells with phosphatase-dead mutants Molecular cell High 17679096
2007 The C-terminal PGM-homology domain of Sts-1 (UBASH3B) catalyzes hydrolysis of ecdysteroid and steroid phosphates, confirming broad histidine phosphatase activity; the domain is structurally and functionally related to insect ecdysteroid phosphate phosphatase (EPP). Molecular modeling, cloning and expression of human Sts-1 PGM domain and Drosophila EPP, in vitro phosphatase activity assay with ecdysteroid/steroid phosphate substrates Proteins Medium 17348005
2010 TULA-2 (UBASH3B) is expressed in platelets, physically associates with Syk, dephosphorylates Syk, and negatively regulates GPVI signaling; TULA-2-knockout mice show hyperphosphorylation of Syk and PLC-γ2, enhanced GPVI-mediated platelet responses, shorter bleeding times, and a prothrombotic phenotype. Co-immunoprecipitation (TULA-2 with Syk), in vitro dephosphorylation assay, genetic knockout mice, platelet aggregation/activation assays, immunoblot for Syk/PLC-γ2 phosphorylation, bleeding time measurement Blood High 20585042
2010 TULA-2 (UBASH3B) shows defined substrate specificity for phosphotyrosyl peptides: class I substrates have Pro at pY-1 and hydrophilic residue at pY-2; class II substrates have acidic residues at pY-1 to pY-3. TULA-2 is highly active toward Syk pY323 and pY352 sites; in GPVI-stimulated TULA-2-KO platelets, Syk Y323 and Y352 phosphorylation is significantly elevated, confirming Syk as a bona fide substrate. Combinatorial phosphotyrosyl peptide library screening, kinetic analysis of representative peptides, TULA-2 knockout platelets with immunoblot for site-specific Syk phosphorylation The Journal of biological chemistry High 20670933
2012 TULA-2 (UBASH3B) is recruited to tyrosine-phosphorylated Syk C-terminal tail peptides in mast cells, is present in complexes with Syk after FcεRI activation, and siRNA-mediated knockdown of TULA-2 increases Syk activation-loop phosphorylation, PLC-γ2 phosphorylation, degranulation, and NF-κB/NFAT activation, establishing TULA-2 as a negative regulator of FcεRI signaling. Phosphopeptide pulldown from mast cell lysates, mass spectrometry identification, immunoprecipitation, far-Western blot, siRNA knockdown, degranulation assay, immunoblot The Journal of biological chemistry High 22267732
2012 TULA-2 (UBASH3B) is the only family member expressed in osteoclasts and negatively regulates osteoclast differentiation and function; its absence increases Syk phosphorylation at Y352 and Y525/526, activates PLC-γ2 downstream of ITAM signaling, and a phosphatase-dead TULA-2 mutant increases osteoclast function, confirming the mechanism requires phosphatase activity. Genetic double-knockout mice (DKO), skeletal analysis, in vitro osteoclast differentiation assays, immunoblot for Syk and PLC-γ2 phosphorylation, phosphatase-dead TULA-2 overexpression Cellular and molecular life sciences High 23149425
2013 UBASH3B dephosphorylates CBL ubiquitin ligase, inactivating it and leading to EGFR stabilization and up-regulation; this phosphatase activity is required for the invasive and metastatic phenotype of triple-negative breast cancer cells, and UBASH3B is a direct functional target of miR-200a. Knockdown/overexpression of UBASH3B in TNBC cells, in vitro phosphatase assay with CBL as substrate, immunoblot for CBL phosphorylation and EGFR levels, invasion/migration assays, xenograft models, phosphatase-dead mutant analysis Proceedings of the National Academy of Sciences of the United States of America High 23784775
2013 Substrate-trapping variants of Sts-1 (UBASH3B), generated by mutagenesis of the nucleophilic His380 and general acid Glu490 in the histidine phosphatase active site, bind with high affinity to tyrosine-phosphorylated ZAP-70 from activated T cell lysates, validating ZAP-70 as a direct substrate of the Sts-1 phosphatase active site; vanadate competition confirms substrate trapping occurs through the active site. Active-site mutagenesis (H380, E490), substrate-trapping pulldown from T cell lysates, immunoblot for phospho-ZAP-70, vanadate competition assay, T cell signaling assay with overexpressed trapping mutants The FEBS journal High 24256567
2015 UBASH3B/Sts-1 is upregulated by AML1-ETO through transcriptional and miR-9-mediated regulation; UBASH3B depletion induces aberrant CBL phosphorylation and impairs proliferation of AML1-ETO cells; this growth inhibition is rescued by CBL mutants, demonstrating that UBASH3B supports AML1-ETO leukemia cell growth partly by modulating CBL phosphorylation state. shRNA depletion of UBASH3B, ectopic expression of CBL mutants (rescue experiment), immunoblot for CBL phosphorylation, proliferation assays, xenograft model, transcriptional analysis Leukemia Medium 26449661
2015 STS-1 (UBASH3B) promotes IFN-α-induced autophagy in B cells by inhibiting CBL phosphorylation, thereby de-repressing TYK2 phosphorylation and enhancing JAK1-STAT1 signaling; JAK1 and STAT1 inhibitors block the STS-1-promoted autophagy, placing STS-1 upstream of JAK1-STAT1 in this pathway. Overexpression and knockdown of STS-1 in B cells, immunoblot for CBL/TYK2/JAK1/STAT1 phosphorylation, autophagy assays (LC3 conversion), pharmacological inhibition of JAK1/STAT1 European journal of immunology Medium 25959715
2016 UBASH3B acts as a ubiquitin receptor that interacts with ubiquitylated Aurora B and controls Aurora B subcellular localization (recruitment to mitotic microtubules prior to anaphase) without affecting Aurora B protein levels; this activity is required for timely and faithful chromosome segregation in human cells. Co-immunoprecipitation of UBASH3B with ubiquitylated Aurora B, live-cell imaging of Aurora B localization, loss-of-function (siRNA/KO), gain-of-function, chromosome segregation fidelity assays Developmental cell High 26766443
2016 TULA-2 (UBASH3B) suppresses Syk activation through GPVI-FcRγ largely by dephosphorylating Syk Tyr346 (regulatory site phosphorylated early after receptor ligation) with high efficiency; it is less efficient at other Syk regulatory sites, identifying Tyr346 dephosphorylation as a key checkpoint in the TULA-2-mediated control of Syk. In vitro phosphatase assay with site-specific phospho-Syk peptides and proteins, TULA-2-knockout platelet immunoblot for pY346-Syk, GPVI-stimulated platelet signaling assays The Journal of biological chemistry High 27609517
2016 TULA-2 (UBASH3B) negatively regulates FcγRIIA signaling in platelets; TULA-2 knockout in FcγRIIA-transgenic mice causes hyperphosphorylation of Syk, LAT, and PLC-γ2, enhanced platelet aggregation/secretion/PS exposure, aggravated thrombocytopenia, and augmented thrombin generation in a HIT model; even heterozygous (50%) reduction of TULA-2 significantly increases platelet reactivity. Genetic KO crossed with FcγRIIA-transgenic mice, immunoblot for phospho-Syk/LAT/PLCγ2, platelet functional assays, HIT mouse model (antibody-mediated thrombocytopenia), bleeding time Arteriosclerosis, thrombosis, and vascular biology High 27765766
2017 X-ray crystal structures of the histidine phosphatase domains of human Sts-1 and Sts-2 were determined (unliganded Sts-1HP at 2.5 Å, Sts-1HP/sulfate at 1.9 Å, Sts-2HP/sulfate at 2.4 Å); steady-state kinetics show Sts-1HP has significantly higher phosphatase activity than Sts-2HP; Sts-1HP kinetics mirror full-length Sts-1, confirming it is a functional surrogate; PHPS1 (SHP-1 inhibitor) inhibits Sts-1 with Ki = 1.05 μM; human Sts-1 dephosphorylates ZAP-70 in a cell-based assay. X-ray crystallography, steady-state kinetic analysis, full-length vs. isolated domain activity comparison, inhibitor Ki determination, cell-based ZAP-70 dephosphorylation assay Biochemistry High 28759203
2017 STS-1 (UBASH3B) interacts with ShcA via a phosphotyrosine-dependent interaction, and this interaction is regulated by EGF receptor activation. Phosphotyrosine-containing peptide affinity pulldown from cell lysates, immunoblot for STS-1, EGF stimulation-dependent comparison Biochemical and biophysical research communications Low 28690151
2018 TULA-2 (UBASH3B) deficiency enhances platelet aggregation, secretion, thromboxane production, and kinetics of signaling downstream of the CLEC-2 (HemITAM) receptor; TULA-2 knockout platelets show enhanced Syk Y346 phosphorylation and downstream PLCγ2/SLP-76 phosphorylation, demonstrating that TULA-2 negatively regulates CLEC-2 signaling by dephosphorylating Syk Y346. TULA-2 knockout mice, platelet aggregation/secretion assays, immunoblot for pY346-Syk/pPLCγ2/pSLP-76, thromboxane ELISA, stimulation with CLEC-2 antibody and rhodocytin TH open Medium 31249969
2020 In endothelial cells, TULA-2 (UBASH3B) interacts with SYK and suppresses SYK Y323 phosphorylation; loss of TULA-2 (via miR-25-3p targeting) leads to increased SYK Y323 phosphorylation, which elevates VEGFR-2 Y1175 phosphorylation and promotes angiogenesis. miR-25-3p overexpression/inhibition, immunoblot for TULA-2/pSYK Y323/pVEGFR-2 Y1175, co-immunoprecipitation of TULA-2 with SYK, in vitro angiogenesis assays, hindlimb ischemia mouse model Aging Medium 33201836
2021 UBASH3B (Ubash3b) is induced by TPA treatment and promotes dephosphorylation and subsequent proteasomal degradation of PKCδ protein; RNAi-mediated depletion of Ubash3b blocks TPA-induced PKCδ degradation, establishing Ubash3b as an upstream regulator of PKCδ protein stability through dephosphorylation. TPA treatment, RNAi knockdown of Ubash3b, immunoblot for PKCδ phosphorylation and protein levels, proteasome inhibition experiment (ALLN), mouse leukemia model Biochimie Medium 33556471
2024 UBASH3B directly binds MRPL12 and dephosphorylates MRPL12 at tyrosine 60 (Y60); loss of Y60 phosphorylation impedes MRPL12 binding to mitochondrial RNA polymerase (POLRMT), downregulating mitochondrial oxidative phosphorylation and inhibiting LUAD tumor progression. Mass spectrometry identification of MRPL12 Y60 phosphorylation, Co-immunoprecipitation of UBASH3B with MRPL12, in vitro dephosphorylation assay, Y60 mutation analysis (Y60F), POLRMT interaction assay, in vivo LUAD mouse model and patient-derived organoids Journal of experimental & clinical cancer research Medium 39343960

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Regulation of ZAP-70 activation and TCR signaling by two related proteins, Sts-1 and Sts-2. Immunity 153 14738763
2004 Suppressors of T-cell receptor signaling Sts-1 and Sts-2 bind to Cbl and inhibit endocytosis of receptor tyrosine kinases. The Journal of biological chemistry 120 15159412
2007 A phosphatase activity of Sts-1 contributes to the suppression of TCR signaling. Molecular cell 100 17679096
2013 Protein tyrosine phosphatase UBASH3B is overexpressed in triple-negative breast cancer and promotes invasion and metastasis. Proceedings of the National Academy of Sciences of the United States of America 64 23784775
2010 A novel histidine tyrosine phosphatase, TULA-2, associates with Syk and negatively regulates GPVI signaling in platelets. Blood 61 20585042
2015 UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO. Leukemia 49 26449661
2010 Determination of the substrate specificity of protein-tyrosine phosphatase TULA-2 and identification of Syk as a TULA-2 substrate. The Journal of biological chemistry 49 20670933
2012 Once phosphorylated, tyrosines in carboxyl terminus of protein-tyrosine kinase Syk interact with signaling proteins, including TULA-2, a negative regulator of mast cell degranulation. The Journal of biological chemistry 37 22267732
2016 Ubiquitin Receptor Protein UBASH3B Drives Aurora B Recruitment to Mitotic Microtubules. Developmental cell 35 26766443
2012 TULA-2, a novel histidine phosphatase, regulates bone remodeling by modulating osteoclast function. Cellular and molecular life sciences : CMLS 33 23149425
2015 STS-1 promotes IFN-α induced autophagy by activating the JAK1-STAT1 signaling pathway in B cells. European journal of immunology 31 25959715
1983 Medical results from STS 1-4: analysis of body fluids. Aviation, space, and environmental medicine 29 6661134
2016 TULA-2 Protein Phosphatase Suppresses Activation of Syk through the GPVI Platelet Receptor for Collagen by Dephosphorylating Tyr(P)346, a Regulatory Site of Syk. The Journal of biological chemistry 28 27609517
2016 TULA-2 (T-Cell Ubiquitin Ligand-2) Inhibits the Platelet Fc Receptor for IgG IIA (FcγRIIA) Signaling Pathway and Heparin-Induced Thrombocytopenia in Mice. Arteriosclerosis, thrombosis, and vascular biology 23 27765766
2013 Insights into the suppressor of T-cell receptor (TCR) signaling-1 (Sts-1)-mediated regulation of TCR signaling through the use of novel substrate-trapping Sts-1 phosphatase variants. The FEBS journal 21 24256567
2007 An unsuspected ecdysteroid/steroid phosphatase activity in the key T-cell regulator, Sts-1: surprising relationship to insect ecdysteroid phosphate phosphatase. Proteins 20 17348005
2020 miR-25-3p promotes endothelial cell angiogenesis in aging mice via TULA-2/SYK/VEGFR-2 downregulation. Aging 13 33201836
2017 Structural and Functional Characterization of the Histidine Phosphatase Domains of Human Sts-1 and Sts-2. Biochemistry 13 28759203
2024 UBASH3B-mediated MRPL12 Y60 dephosphorylation inhibits LUAD development by driving mitochondrial metabolism reprogramming. Journal of experimental & clinical cancer research : CR 12 39343960
2018 TULA-2 Deficiency Enhances Platelet Functional Responses to CLEC-2 Agonists. TH open : companion journal to thrombosis and haemostasis 12 31249969
2006 Crystallization and initial crystal characterization of the C-terminal phosphoglycerate mutase homology domain of Sts-1. Acta crystallographica. Section F, Structural biology and crystallization communications 12 16511305
2024 FLI1 induces erythroleukemia through opposing effects on UBASH3A and UBASH3B expression. BMC cancer 8 38461240
2017 Identification of STS-1 as a novel ShcA-binding protein. Biochemical and biophysical research communications 8 28690151
2017 UBASH3B-mediated silencing of the mitotic checkpoint: Therapeutic perspectives in cancer. Molecular & cellular oncology 8 29487893
2021 Ubash3b promotes TPA-mediated suppression of leukemogenesis through accelerated downregulation of PKCδ protein. Biochimie 7 33556471
2018 Ubiquitin Associated and SH3 Domain Containing B (UBASH3B) Gene Association with Behcet's Disease in Iranian Population. Current eye research 6 30289285
2017 UBASH3B promotes tamoxifen resistance and could be negatively regulated by ESR1. Oncotarget 6 29492198
2014 Enhanced response of T cells from murine gammaherpesvirus 68-infected mice lacking the suppressor of T cell receptor signaling molecules Sts-1 and Sts-2. PloS one 4 24587276
2023 STS-1 and STS-2, Multi-Enzyme Proteins Equipped to Mediate Protein-Protein Interactions. International journal of molecular sciences 3 37298164
1984 [Medical results from STS 1-4: analysis of body fluids]. Kosmicheskaia biologiia i aviakosmicheskaia meditsina 2 6700189
2025 Investigating the role of UBASH3B in cancer: structural relevance, physiological functions, and therapeutic possibilities. Journal of experimental & clinical cancer research : CR 0 40885971

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