Affinage

TSPAN15

Tetraspanin-15 · UniProt O95858

Length
294 aa
Mass
33.2 kDa
Annotated
2026-06-10
50 papers in source corpus 22 papers cited in narrative 22 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

TSPAN15 is a TspanC8-subfamily tetraspanin that functions as a dedicated regulatory partner of the transmembrane metalloprotease ADAM10, controlling its maturation, surface stability, and substrate selectivity (PMID:22446748, PMID:23035126). It directly binds ADAM10 and accelerates exit of the complex from the endoplasmic reticulum, stabilizing the active/mature enzyme at the plasma membrane by slowing its endocytosis; ADAM10 reciprocally stabilizes TSPAN15, and endogenous TSPAN15 is unstable in the absence of ADAM10 (PMID:22446748, PMID:31792032, PMID:32111735). The interaction is mediated by the TSPAN15 large extracellular loop (LEL) contacting the membrane-proximal stalk, cysteine-rich, and disintegrin domains of ADAM10; crystallographic and cryo-EM structures show that TSPAN15 binding relieves ADAM10 autoinhibition and acts as a 'molecular measuring stick', positioning the catalytic active site approximately 20 Å above the membrane to dictate membrane-proximal cleavage-site selection (PMID:26668317, PMID:34739841, PMID:37516108). Through this mechanism TSPAN15 confers substrate specificity distinct from other TspanC8/ADAM10 pairs, preferentially directing ADAM10 toward N-cadherin, cellular prion protein, and GPVI rather than APP or Notch targets, as confirmed in knockout mice (PMID:29520422, PMID:35269584). Beyond the canonical protease axis, TSPAN15 has been implicated in cancer signaling—interacting with the BTRC E3 ligase to promote IκBα and PDCD4 degradation (PMID:29650964, PMID:40398082) and with integrin-β1 to sustain FAK/AKT/mTOR signaling (PMID:40505345)—and is required at the surface of neuronal extracellular vesicles for their docking at target neurons (PMID:38938373).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2000 Low

    Before any functional role was known, TSPAN15 had to be defined as a distinct gene; its identification as the tetraspanin NET-7 established the four-transmembrane architecture and conserved residues that place it in the tetraspanin family.

    Evidence EST sequencing, sequence analysis, and RT-PCR expression profiling across human cell lines

    PMID:10719184

    Open questions at the time
    • No functional mechanism established
    • Differential expression not linked to any pathway
  2. 2012 High

    The central question of what TSPAN15 does was answered by showing it directly binds ADAM10, accelerates ER exit of the complex, stabilizes mature surface ADAM10, and increases shedding of N-cadherin and APP—establishing TSPAN15 as an ADAM10 trafficking and maturation regulator.

    Evidence Split-ubiquitin Y2H, co-IP, ER-retention mutant pulse-chase, RNAi, and substrate shedding assays in mammalian cells; reciprocal Co-IP and maturation assays establishing the broader TspanC8 family role and Notch regulation

    PMID:22446748 PMID:23035126 PMID:23091066

    Open questions at the time
    • Did not resolve whether substrate preference differs among TspanC8 members
    • Structural basis of the interaction not defined
  3. 2015 High

    To explain why different TspanC8s yield different ADAM10 outputs, studies mapped the interaction interface and demonstrated compartment-specific and substrate-specific effects, showing TSPAN15 uniquely promotes N-cadherin cleavage and places ADAM10 in a distinct membrane environment.

    Evidence Chimeric ADAM10/TspanC8 constructs, sucrose gradient fractionation, single-molecule tracking, quantitative MS co-IP, and substrate cleavage/Notch reporter assays

    PMID:26668317 PMID:26686862

    Open questions at the time
    • Mechanism of how compartmentalization selects substrates not structurally defined
    • In vivo relevance not yet tested
  4. 2018 High

    Genetic knockout in mice resolved whether TSPAN15 substrate selectivity operates in vivo, showing loss of mature ADAM10 in brain and age-dependent loss of N-cadherin and PrP shedding but not APP or Notch readouts—proving physiological substrate steering.

    Evidence Tspan15 knockout mouse brain analyzed by western blotting for ADAM10 maturation and substrate-specific shedding and Notch target gene expression

    PMID:29520422

    Open questions at the time
    • Molecular basis for in vivo substrate discrimination not addressed
    • Phenotypic consequences for brain physiology not characterized
  5. 2019 High

    The mechanism of surface stabilization was clarified by showing TSPAN15 slows ADAM10 endocytosis (in contrast to Tspan5), with the cytoplasmic domain—not the C-terminal palmitoylation site—governing trafficking and Notch outcomes.

    Evidence Endocytosis assays, cell surface biotinylation, flow cytometry, chimeric cytoplasmic-domain constructs, and palmitoylation-site mutagenesis

    PMID:31792032

    Open questions at the time
    • Endocytic adaptor recognizing the cytoplasmic domain not identified
    • Quantitative contribution of trafficking versus stability to net activity unresolved
  6. 2020 High

    To confirm physiological relevance and therapeutic tractability, work on endogenous proteins showed ADAM10 is the principal TSPAN15 partner, TSPAN15 is unstable without ADAM10, a synthetic fusion is a functional scissor, and antibodies can inhibit the complex.

    Evidence Monoclonal antibody generation, endogenous co-localization and co-IP, ADAM10-KO cell lines, synthetic fusion protein, and antibody inhibition of substrate cleavage

    PMID:32111735

    Open questions at the time
    • Epitopes of inhibitory antibodies not mapped
    • Therapeutic specificity against other TspanC8/ADAM10 complexes not established
  7. 2023 High

    The structural logic of substrate selection was resolved when crystal and cryo-EM structures showed the TSPAN15 LEL binding site relieves ADAM10 autoinhibition and acts as a molecular measuring stick positioning the active site ~20 Å above the membrane to dictate cleavage-site choice.

    Evidence X-ray crystallography of the TSPAN15 LEL with mutagenesis and N-cadherin cleavage assays; cryo-EM of a vFab-ADAM10-Tspan15 complex with interface mutagenesis and cell-based shedding assays

    PMID:34739841 PMID:37516108

    Open questions at the time
    • Structures of complexes with other TspanC8s for comparison not available
    • Dynamics of substrate engagement not captured
  8. 2022 High

    Substrate-selectivity rules were extended by showing TSPAN15 and Tspan33 act compensatorily in ADAM10-mediated GPVI cleavage, with TSPAN15 dominant and its extracellular region setting the cleavage distance.

    Evidence CRISPR/Cas9 knockout cell lines with TSPAN15 and GPVI mutant constructs and GPVI cleavage assays

    PMID:35269584

    Open questions at the time
    • Mechanism of TSPAN15/Tspan33 compensation not defined
    • Platelet-physiological consequences not tested here
  9. 2018 Medium

    A non-protease cancer role was opened by showing TSPAN15 binds the BTRC E3 ligase to drive phospho-IκBα ubiquitination and NF-κB activation of metastasis genes, later paralleled by BTRC-dependent PDCD4 degradation driving autophagy and EMT.

    Evidence Co-IP, ubiquitination assays, NF-κB reporter, and target gene analysis in oesophageal carcinoma; co-IP, ubiquitination, autophagic flux, PDCD4 rescue, and xenograft in hepatocellular carcinoma

    PMID:29650964 PMID:40398082

    Open questions at the time
    • Direct versus ADAM10-dependent nature of these effects not separated
    • How a tetraspanin engages a cytosolic E3 ligase mechanistically unclear
    • Independent replication of BTRC axis limited
  10. 2023 Medium

    TSPAN15 was assigned a function distinct from ADAM10 in neuronal extracellular vesicle biology, where it is required at the EV surface for docking at target neurons rather than at the recipient membrane.

    Evidence EV fractionation and marker analysis, fluorescent fusion tracking, and Tspan15-knockout cortical neuron EV target-cell docking assays

    PMID:38938373

    Open questions at the time
    • Docking receptor/ligand on target neurons not identified
    • Whether ADAM10 is involved not resolved
    • Single lab
  11. 2025 Medium

    An ADAM10-independent oncogenic axis was proposed in which TSPAN15 binds integrin-β1, blocks its ubiquitination, and sustains FAK/AKT/mTOR/GPX4 signaling to suppress ferroptosis and confer chemoresistance.

    Evidence Co-IP, ubiquitination assay, phospho-signaling and GPX4 westerns, knockdown in vitro and in vivo xenograft, and ferroptosis assays in pancreatic cancer cells

    PMID:40505345

    Open questions at the time
    • Direct binding interface with ITGB1 not mapped
    • Independence from ADAM10 not formally tested
    • Single lab, novel interaction
  12. 2025 Medium

    Disease-tissue context was extended by identifying a THSD7A/ADAM10/TSPAN15 tricomponent complex at podocyte foot processes that regulates ADAM10 substrate usage and surface protein stability.

    Evidence Co-localization and Co-IP, ADAM10-deficient mice, ADAM10-inhibited pig glomeruli, in vitro shedding assays, and biochemical fractionation

    PMID:40339751

    Open questions at the time
    • Whether THSD7A binds TSPAN15 directly not resolved
    • Pathophysiological link to membranous nephropathy not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the canonical ADAM10-scaffolding role of TSPAN15 mechanistically relates to its reported ADAM10-independent activities (BTRC/E3-ligase coupling, integrin-β1 stabilization, EV docking), and whether these reflect distinct molecular interfaces of the same protein.
  • No structural or interface data for the cytosolic/cancer interactions
  • No demonstration that protease-independent roles occur without ADAM10 present
  • In vivo physiological weighting of the multiple roles unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 2
Pathway
GO:0140096 catalytic activity, acting on a protein 3
Partners
ADAM10BTRCITGB1THSD7A
Complex memberships
ADAM10-TSPAN15 sheddase complexTHSD7A/ADAM10/TSPAN15 complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 TSPAN15 directly interacts with ADAM10 (identified by split-ubiquitin yeast two-hybrid screen and co-immunoprecipitation in mammalian cells), accelerates ER exit of the ADAM10-TSPAN15 complex (shown by pulse-chase experiments with an ER-retention mutant), stabilizes the active/mature form of ADAM10 at the cell surface, and increases ADAM10-mediated shedding of N-cadherin and amyloid precursor protein. Split-ubiquitin yeast two-hybrid, co-immunoprecipitation, ER-retention mutant overexpression, RNAi knockdown, pulse-chase experiments, N-cadherin/APP shedding assays Cellular and molecular life sciences : CMLS High 22446748
2012 TSPAN15 (along with all TspanC8 members: Tspan5, Tspan10, Tspan14, Tspan17, Tspan33) co-immunoprecipitates with ADAM10 and promotes ADAM10 maturation (prodomain processing) and trafficking to the cell surface, establishing TspanC8 tetraspanins as essential regulators of ADAM10 maturation. Co-immunoprecipitation, cell surface expression assays, maturation assays in multiple cell lines The Journal of biological chemistry High 23035126
2012 TspanC8 tetraspanins including TSPAN15 directly interact with ADAM10, regulate its exit from the endoplasmic reticulum, and promote Notch activation; two TspanC8 genes were identified as Notch regulators in an independent Drosophila RNAi screen, and human Tspan5 and Tspan14 positively regulated ligand-induced ADAM10-dependent Notch1 signaling (TSPAN15 interaction with ADAM10 confirmed but its specific effect on Notch was not separately quantified in this paper). Co-immunoprecipitation, RNAi screen in Drosophila, Notch reporter assays, overexpression in mammalian cells The Journal of cell biology High 23091066
2015 TSPAN15 (and Tspan5, Tspan14, Tspan33) positively regulates ADAM10 surface expression levels and differentially impacts ADAM10-dependent cleavage of APP, N-cadherin, and CD44, as well as Notch activation, by differentially regulating ADAM10 membrane compartmentalization; sucrose gradient fractionation, single molecule tracking, and quantitative mass-spectrometry showed that Tspan5 and Tspan15 place ADAM10 in distinct membrane compartments with different molecular environments. Sucrose gradient fractionation, single molecule tracking, quantitative mass-spectrometry co-immunoprecipitation, Notch reporter assays, substrate shedding assays Cellular and molecular life sciences : CMLS High 26686862
2015 The large extracellular loop (LEL) of Tspan14 mediates co-immunoprecipitation with ADAM10 and promotes ADAM10 maturation and trafficking; chimeric ADAM10 constructs showed that the membrane-proximal stalk, cysteine-rich, and disintegrin domains of ADAM10 mediate its interaction with TspanC8s including Tspan15, and this region is required for ADAM10 ER exit. Tspan15 was the only TspanC8 to promote cleavage of N-cadherin, whereas Tspan14 uniquely reduced cleavage of GPVI, indicating distinct substrate selectivity depending on the associated TspanC8. Chimeric protein constructs, co-immunoprecipitation, substrate cleavage assays, antibody development to endogenous Tspan14 The Journal of biological chemistry High 26668317
2018 In Tspan15 knockout mice, the active/mature form of ADAM10 is substantially decreased in brain tissue, and this is accompanied by age-dependent reduced shedding of N-cadherin and cellular prion protein, but not APP alpha-secretase cleavage or Notch-dependent gene expression, demonstrating that Tspan15 in vivo preferentially directs ADAM10 toward specific substrates (N-cadherin, PrP) rather than others (APP, Notch targets). Tspan15 knockout mouse model, western blotting for ADAM10 maturation, substrate shedding assays (N-cadherin, PrP, APP), Notch target gene expression analysis Cellular and molecular life sciences : CMLS High 29520422
2019 ADAM10 undergoes faster endocytosis in the presence of Tspan5 than Tspan15; Tspan15 stabilizes ADAM10 at the cell surface yielding high surface expression levels, and reciprocally ADAM10 stabilizes Tspan15 at the cell surface (the Tspan15/ADAM10 complex is retained at the plasma membrane). The cytoplasmic domains of Tspan5 and Tspan15 contribute to their opposite effects on ADAM10 trafficking and Notch signaling, while an unusual C-terminal palmitoylation site of Tspan15 is dispensable for these functions. Endocytosis assays, cell surface biotinylation, flow cytometry, chimeric cytoplasmic domain constructs, palmitoylation site mutagenesis Life science alliance High 31792032
2020 Endogenous Tspan15 and ADAM10 co-localize on the cell surface; ADAM10 is the principal Tspan15-interacting protein; endogenous Tspan15 expression requires ADAM10 in cell lines and primary cells (Tspan15 is unstable without ADAM10); a synthetic ADAM10/Tspan15 fusion protein is a functional scissor complex; two of four anti-Tspan15 monoclonal antibodies impaired ADAM10/Tspan15 activity. Monoclonal antibody generation, co-localization by immunofluorescence, co-immunoprecipitation of endogenous proteins, ADAM10-knockout cell lines, synthetic fusion protein assay, substrate cleavage inhibition assay The Journal of biological chemistry High 32111735
2021 Crystal structure of the Tspan15 large extracellular loop (LEL) was solved, revealing a core helical framework with a variable region; a site on the Tspan15 LEL required for both ADAM10 binding and promoting N-cadherin substrate cleavage was identified by co-immunoprecipitation and cellular cleavage assay. X-ray crystallography, co-immunoprecipitation, N-cadherin cellular cleavage assay, mutagenesis of LEL binding site Structure (London, England : 1993) High 34739841
2023 Cryo-EM structure of a vFab-ADAM10-Tspan15 complex shows that Tspan15 binding relieves ADAM10 autoinhibition and acts as a molecular measuring stick, positioning the ADAM10 enzyme active site approximately 20 Å from the plasma membrane for membrane-proximal substrate cleavage. Cell-based N-cadherin shedding assays confirmed that the positioning of the active site by the ADAM10-Tspan15 interface influences preferred cleavage site selection. Cryo-EM structure determination, cell-based N-cadherin shedding assays, interface mutagenesis Cell High 37516108
2018 TSPAN15 specifically interacts with BTRC (beta-TrCP) E3 ubiquitin ligase to promote ubiquitination and proteasomal degradation of phospho-IκBα, thereby triggering NF-κB nuclear translocation and activation of metastasis-related genes (ICAM1, VCAM1, uPA, MMP9, TNFα, CCL2) in oesophageal squamous cell carcinoma cells. Co-immunoprecipitation, ubiquitination assay, NF-κB reporter assay, western blotting for IκBα degradation and p65 nuclear translocation, target gene expression analysis Nature communications Medium 29650964
2022 CRISPR/Cas9 knockout of Tspan15 (and Tspan33) in human cell lines demonstrated that Tspan15 and Tspan33 play compensatory roles in GPVI cleavage by ADAM10, with Tspan15 bearing the more important role. The Tspan15 extracellular region was found critical for promoting GPVI cleavage, enabling ADAM10 access to the cleavage site at a particular distance above the membrane. CRISPR/Cas9 knockout cell lines, Tspan15 and GPVI mutant expression constructs, GPVI cleavage assays International journal of molecular sciences High 35269584
2023 Tspan15 is a component of TSG101- and CD81-positive extracellular vesicle (EV) fractions in neurons. Tspan15 is dispensable at target neuron plasma membranes but is required at the EV surface to promote EV docking at target neurons, as EVs from Tspan15 knockout cortical neurons showed significantly impaired association with target cells compared to wild-type EVs. EV fractionation and marker analysis, fluorescent fusion protein tracking, Tspan15 knockout mouse cortical neuron EVs, target cell docking assays Journal of extracellular biology Medium 38938373
2019 In oral squamous cell carcinoma cells, knockdown of Tspan15 reduced ADAM10 expression, decreased soluble N-cadherin shedding, reduced nuclear β-catenin immunoreactivity, and suppressed tumor invasion and migration, placing Tspan15 upstream of ADAM10-mediated N-cadherin shedding and downstream Wnt/β-catenin signaling in OSCC metastasis. siRNA knockdown, N-cadherin shedding ELISA, immunofluorescence for β-catenin localization, Transwell invasion/migration assays Experimental cell research Medium 31518558
2019 Tspan15 overexpression in the hepatoma cell line HepG2 increases ERK1/2 phosphorylation, leading to increased CTGF expression and secretion; proteomic profiling of Tspan15 complexes identified multiple membrane proteins including growth factor receptors as interaction partners. Overexpression, western blotting for p-ERK1/2, quantitative secretome proteomics (MS), Tspan15 complex immunoprecipitation/MS Proteomics Medium 31390680
2025 TSPAN15 directly interacts with integrin-β1 (ITGB1) and maintains ITGB1 stability by inhibiting its ubiquitination; this interaction activates downstream p-FAK/p-AKT/p-mTOR signaling and promotes GPX4 expression, thereby attenuating gemcitabine-induced ferroptosis in pancreatic ductal adenocarcinoma cells. Co-immunoprecipitation, ubiquitination assay, western blotting for FAK/AKT/mTOR phosphorylation and GPX4, TSPAN15 knockdown in vitro and in vivo xenograft, ferroptosis assays Redox biology Medium 40505345
2025 TSPAN15 physically interacts with BTRC to promote proteasomal degradation of tumor suppressor PDCD4 via ubiquitination, thereby activating autophagy and autophagy-mediated EMT and metastasis in hepatocellular carcinoma cells. Co-immunoprecipitation, ubiquitination assay, autophagic flux analysis, TSPAN15 silencing, PDCD4 rescue experiments, xenograft mouse model Molecular immunology Medium 40398082
2023 In intrahepatic cholangiocarcinoma (ICC) cells, Tspan15 mediates translocation of activated mature ADAM10 from the cytoplasm to the cell membrane surface, which cleaves the Notch1 intracellular domain from its extracellular domain, activating Notch1 signaling and enhancing cancer stem cell-like properties, EMT, and chemoresistance against gemcitabine and cisplatin. Western blotting, flow cytometry, immunohistochemistry, RT-PCR, Tspan15/ADAM10 knockdown, Notch1 activation assays, chemoresistance functional assays Liver international : official journal of the International Association for the Study of the Liver Medium 37545390
2024 In invasive bladder cancer cells, Tspan15 is required for ADAM10-mediated selective cleavage of N-cadherin; the PPARβ/δ agonist GW501516 decreases Tspan15 expression and prevents N-cadherin cleavage (NTF generation) without modifying ADAM10 expression levels, demonstrating that pharmacological targeting of Tspan15 can selectively block ADAM10 substrate cleavage. siRNA knockdown of Tspan15, western blotting for N-cadherin fragments (NTF/CTF1), GW501516 treatment, ADAM10 expression analysis Cells Medium 38667323
2025 A tricomponent complex of THSD7A/ADAM10/Tspan15 was found in podocytes; Tspan15 regulates ADAM10 substrate usage and the stability of podocyte cell surface proteins (THSD7A, PLA2R1, β-dystroglycan), where THSD7A acts as both an ADAM10 substrate and regulator of the complex; Tspan15 is present at podocyte foot processes. Co-localization and Co-IP, ADAM10-deficient mice, ADAM10-inhibited pig glomeruli, in vitro shedding assays, biochemical fractionation Kidney international Medium 40339751
2025 Silencing of Tspan15 (and Tspan10) in astrocytoma cells reduced Venezuelan equine encephalitis virus (VEEV) genome replication without affecting viral entry; silencing of the ADAM10 substrate N-cadherin also reduced VEEV infectivity, suggesting Tspan15/ADAM10 and downstream substrates modulate VEEV replication. siRNA silencing, pharmacological ADAM10 inhibition, VEEV infection assays, viral entry vs. replication discrimination assays Molecular biology of the cell Low 39878649
2000 TSPAN15 (identified as NET-7) was identified and sequenced as a new tetraspanin family member with the characteristic structure of four transmembrane domains, two extracellular regions, and conserved tetraspanin amino acid residues; it shows differential expression across human cell lines. EST sequencing, sequence analysis, RT-PCR expression profiling Biochimica et biophysica acta Low 10719184

Source papers

Stage 0 corpus · 50 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 TspanC8 tetraspanins regulate ADAM10/Kuzbanian trafficking and promote Notch activation in flies and mammals. The Journal of cell biology 157 23091066
2012 The TspanC8 subgroup of tetraspanins interacts with A disintegrin and metalloprotease 10 (ADAM10) and regulates its maturation and cell surface expression. The Journal of biological chemistry 136 23035126
2015 TspanC8 tetraspanins differentially regulate the cleavage of ADAM10 substrates, Notch activation and ADAM10 membrane compartmentalization. Cellular and molecular life sciences : CMLS 107 26686862
2012 Tetraspanin15 regulates cellular trafficking and activity of the ectodomain sheddase ADAM10. Cellular and molecular life sciences : CMLS 93 22446748
2000 Sequence and expression of seven new tetraspans. Biochimica et biophysica acta 84 10719184
2015 Genetics of Venous Thrombosis: update in 2015. Thrombosis and haemostasis 83 26354877
2015 TspanC8 Tetraspanins and A Disintegrin and Metalloprotease 10 (ADAM10) Interact via Their Extracellular Regions: EVIDENCE FOR DISTINCT BINDING MECHANISMS FOR DIFFERENT TspanC8 PROTEINS. The Journal of biological chemistry 82 26668317
2018 TSPAN15 interacts with BTRC to promote oesophageal squamous cell carcinoma metastasis via activating NF-κB signaling. Nature communications 78 29650964
2017 Regulation of the trafficking and the function of the metalloprotease ADAM10 by tetraspanins. Biochemical Society transactions 51 28687716
2023 Structural basis for membrane-proximal proteolysis of substrates by ADAM10. Cell 44 37516108
2016 The Emerging Role of Tetraspanins in the Proteolytic Processing of the Amyloid Precursor Protein. Frontiers in molecular neuroscience 43 28066176
2018 In vivo regulation of the A disintegrin and metalloproteinase 10 (ADAM10) by the tetraspanin 15. Cellular and molecular life sciences : CMLS 40 29520422
2021 Regulation of ADAM10 by the TspanC8 Family of Tetraspanins and Their Therapeutic Potential. International journal of molecular sciences 39 34201472
2022 The role of tetraspanins pan-cancer. iScience 38 35992081
2024 High-dimensional phenotyping to define the genetic basis of cellular morphology. Nature communications 37 38184653
2020 The tetraspanin Tspan15 is an essential subunit of an ADAM10 scissor complex. The Journal of biological chemistry 37 32111735
2019 TspanC8 tetraspanins differentially regulate ADAM10 endocytosis and half-life. Life science alliance 37 31792032
2005 Identification of two molecular groups of seminomas by using expression and tissue microarrays. Clinical cancer research : an official journal of the American Association for Cancer Research 29 16115909
1986 Primary hyperparathyroidism: evaluated by 47calcium kinetics, calcium balance and serum bone-Gla-protein. European journal of clinical investigation 29 3093240
2017 New insights into the tetraspanin Tspan5 using novel monoclonal antibodies. The Journal of biological chemistry 27 28428248
2018 Regulation of Leukocytes by TspanC8 Tetraspanins and the "Molecular Scissor" ADAM10. Frontiers in immunology 26 30013551
1985 Do sodium and potassium forms of Na,K-ATPase differ in their secondary structure? The Journal of biological chemistry 25 2989261
2019 Tspan15 Is a New Stemness-Related Marker in Hepatocellular Carcinoma. Proteomics 23 31390680
2021 Role of Tetraspanins in Hepatocellular Carcinoma. Frontiers in oncology 22 34540692
2021 Crystal structure of the Tspan15 LEL domain reveals a conserved ADAM10 binding site. Structure (London, England : 1993) 20 34739841
2021 Clinical Assessment of 177Lu-DOTATATE Quantification by Comparison of SUV-Based Parameters Measured on Both Post-PRRT SPECT/CT and 68Ga-DOTATOC PET/CT in Patients With Neuroendocrine Tumors: A Feasibility Study. Clinical nuclear medicine 19 33234927
2020 The synthetic progestin norethindrone causes thyroid endocrine disruption in adult zebrafish. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 17 32512198
2019 Tspan15 plays a crucial role in metastasis in oral squamous cell carcinoma. Experimental cell research 15 31518558
2018 Whole Exome Sequencing Identifies New Host Genomic Susceptibility Factors in Empyema Caused by Streptococcus pneumoniae in Children: A Pilot Study. Genes 15 29751582
2025 Safety and dosimetry of [177Lu]Lu-DOTA-TATE in adolescent patients with somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumours, or pheochromocytomas and paragangliomas: Primary analysis of the Phase II NETTER-P study. European journal of nuclear medicine and molecular imaging 14 40198358
2010 Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine. Biological research 14 20140304
1985 Characteristics of the formation and membrane transport of 7-hydroxymethotrexate in freshly isolated rabbit hepatocytes. Cancer research 14 2578871
2022 The Platelet Collagen Receptor GPVI Is Cleaved by Tspan15/ADAM10 and Tspan33/ADAM10 Molecular Scissors. International journal of molecular sciences 13 35269584
2024 The role of Tetraspanins in digestive system tumor development: update and emerging evidence. Frontiers in cell and developmental biology 12 38389703
2023 Tetraspanin 15 depletion impairs extracellular vesicle docking at target neurons. Journal of extracellular biology 11 38938373
2023 Next Generation of Ovarian Cancer Detection Using Aptamers. International journal of molecular sciences 10 37047289
2025 A real-world study on the characteristics of autoimmune gastritis: A single-center retrospective cohort in China. Clinics and research in hepatology and gastroenterology 9 39961485
2023 Tspan15-ADAM10 signalling enhances cancer stem cell-like properties and induces chemoresistance via Notch1 activation in ICC. Liver international : official journal of the International Association for the Study of the Liver 8 37545390
2023 Classifying tetraspanins: A universal system for numbering residues and a proposal for naming structural motifs and subfamilies. Biochimica et biophysica acta. Biomembranes 6 38154528
2025 Regulation of podocyte surface proteins by the enzyme A Disintegrin And Metalloproteinase 10 (ADAM10). Kidney international 5 40339751
2020 [microRNA-16-5p targeted tetraspanin 15 gene to inhibit the proliferation, migration and invasion of osteosarcoma cell through phospoinositide 3-kinase/protein kinase B signaling pathway]. Zhonghua yi xue za zhi 4 32486604
2025 Tetraspanins 10 and 15 support Venezuelan equine encephalitis virus replication in astrocytoma cells. Molecular biology of the cell 3 39878649
2024 GW501516-Mediated Targeting of Tetraspanin 15 Regulates ADAM10-Dependent N-Cadherin Cleavage in Invasive Bladder Cancer Cells. Cells 3 38667323
2021 Enhancement of Mast Cell Degranulation Mediated by Purinergic Receptors' Activation and PI3K Type δ. Journal of immunology (Baltimore, Md. : 1950) 3 34330752
2025 TSPAN15 sustains ITGB1 stability to block gemcitabine-induced ferroptosis in pancreatic ductal adenocarcinoma through the FAK/AKT/Mtor-gpx4 cascade. Redox biology 2 40505345
2025 TSPAN15 enhances EMT-mediated metastasis of HCC by promoting autophagy through BTRC-mediated PDCD4 degradation. Molecular immunology 1 40398082
2025 Multipopulation GWAS for venous thromboembolism identifies novel loci followed by experimental validation in zebrafish. Blood advances 1 40554366
2026 EchoVisuALL: From Echocardiography to Gene Discovery. bioRxiv : the preprint server for biology 0 41756822
2026 Signaling and transcriptional networks governing late synovial joint development. Developmental biology 0 42248342
2024 A molecular docking exploration of the large extracellular loop of tetraspanin CD81 with small molecules. In silico pharmacology 0 38584777

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