Affinage

ST14

Suppressor of tumorigenicity 14 protein · UniProt Q9Y5Y6

Length
855 aa
Mass
94.8 kDa
Annotated
2026-06-10
59 papers in source corpus 22 papers cited in narrative 22 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

ST14 (matriptase/epithin/MT-SP1) is a type II transmembrane serine protease that functions as the essential initiating protease of an epidermal proteolytic cascade controlling skin barrier formation, and as a multifunctional regulator of cancer cell motility and metastasis (PMID:12032844, PMID:14638864, PMID:32493324). Its catalytic domain adopts a trypsin-like fold with an S4 cavity favoring basic P3/P4 residues, accounting for substrate cleavage at basic positions, and docks its preceding LDL-receptor-class-A domain and the inhibitor HAI-1 (PMID:11696548, PMID:16407223). In the epidermis, matriptase proteolytically activates the downstream protease prostasin to drive profilaggrin processing, cornified envelope morphogenesis, lipid matrix formation, and stratum corneum desquamation; loss of this matriptase→prostasin→profilaggrin axis produces a fatal neonatal barrier defect in mice and underlies human autosomal recessive ichthyosis with hypotrichosis, caused by hypomorphic and loss-of-function ST14 mutations (PMID:12032844, PMID:14638864, PMID:17940283, PMID:18843291). The protease is regulated by ectodomain shedding executed sequentially through PKCβII and TACE/ADAM17 and triggered by TGF-β, JNK inhibition, or environmental selenite; the membrane stub is then cleaved by the intramembrane protease SPPL2b to release an intracellular domain (EICD) that translocates to the nucleus and reprograms chemokine genes including CCL2 to promote migration, invasion, and metastasis (PMID:25245289, PMID:32493324, PMID:32241917, PMID:35950457). Extracellularly, matriptase cleaves the Tie2 receptor ectodomain, degrades fibronectin and laminin, and the shed soluble form acts as a proangiogenic factor, while in macrophages its expression is induced by IFN-γ via JAK/STAT1 to enable transendothelial migration (PMID:11573963, PMID:21097670, PMID:20652801, PMID:21295011). A mitochondrial pool binds the β subunit of F0F1-ATP synthase through its CUB and LDL-receptor motifs to sustain bioenergetics in neural stem cells, and in kidney St14 controls ENaC subunit abundance indirectly by regulating the co-protease CAP1/Prss8 rather than by direct ENaC cleavage (PMID:30566397, PMID:37830556).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2001 High

    Establishing the catalytic-domain architecture explained how matriptase achieves trypsin-like specificity and revealed how its accessory domains and the inhibitor HAI-1 engage the active site.

    Evidence High-resolution X-ray crystal structures of the catalytic domain with benzamidine and BPTI

    PMID:11696548

    Open questions at the time
    • Structure of the full-length multidomain transmembrane protease not resolved
    • Conformational basis of zymogen activation not addressed
  2. 2002 High

    Germline knockout revealed that matriptase is essential for epidermal barrier formation and demonstrated pleiotropic developmental roles, framing it as a physiologically critical protease rather than merely a cancer-associated enzyme.

    Evidence Null mouse with histological, ultrastructural, and transepidermal water loss analyses

    PMID:12032844

    Open questions at the time
    • Molecular substrates underlying barrier defect not identified in this study
    • Mechanism of thymocyte apoptosis unexplained
  3. 2003 High

    Epidermal-specific deletion identified profilaggrin processing as a key downstream pathway, placing matriptase within keratinocyte differentiation biochemistry.

    Evidence Conditional epidermal knockout mouse with epidermal proteomics and Western blotting

    PMID:14638864

    Open questions at the time
    • Direct vs indirect cleavage of profilaggrin not distinguished
    • Intermediate proteases between matriptase and filaggrin not yet defined
  4. 2007 High

    A disease-associated catalytic mutant and hypomorphic mice tied reduced enzymatic activity to defective prostasin activation, defining the matriptase→prostasin cascade and genetically validating the human disease link.

    Evidence In vitro activity assay of G827R mutant plus ST14 hypomorphic mouse phenotyping

    PMID:17940283

    Open questions at the time
    • Whether prostasin is a direct matriptase substrate not fully resolved in vivo
    • Other epidermal substrates not excluded
  5. 2008 Medium

    Human patient mutations confirmed that loss of matriptase impairs prostasin activation and profilaggrin processing, translating the murine cascade to human ichthyosis-hypotrichosis.

    Evidence Patient keratinocyte Western blots and ST14 sequencing

    PMID:18843291

    Open questions at the time
    • Single lab; biochemical readouts not reconstituted in vitro
    • Genotype-phenotype range across patients limited
  6. 2001 Medium

    Polarized basolateral localization and degradation of matrix proteins suggested a role in epithelial cell-substratum adhesion, the earliest hint of extracellular substrate function.

    Evidence Heterologous expression/immunolocalization in Caco-2 and in vitro fibronectin/laminin cleavage

    PMID:11573963

    Open questions at the time
    • In vitro cleavage not validated as physiological substrate
    • Single-lab, heterologous system
  7. 2006 Medium

    Domain-resolved interaction mapping showed the serine protease domain binds HAI-1 and the CUB domain binds TMEFF1, beginning to define matriptase's regulatory and binding partners.

    Evidence GST pull-down, qRT-PCR and homology modeling in RKO/MCF7 cells

    PMID:16407223

    Open questions at the time
    • Functional consequence of TMEFF1 interaction unclear
    • Pull-downs not reciprocally validated in vivo
  8. 2007 High

    Engineered scFv inhibitors with mapped active-site epitopes established that matriptase is druggable at the S1 substrate-binding site, providing mechanistic tools.

    Evidence Kinetic inhibition assays and alanine-scanning mutagenesis of active-site loops

    PMID:17475279

    Open questions at the time
    • Therapeutic efficacy in vivo not addressed here
    • Specificity against related proteases not detailed
  9. 2009 Medium

    Gain/loss-of-function in breast cancer cells linked ST14 to cell-cycle restraint via p27/cyclin E-CDK2, indicating context-dependent anti-proliferative effects independent of miR-27b.

    Evidence Overexpression/knockdown with flow cytometry, Western blot and luciferase reporter

    PMID:19546220

    Open questions at the time
    • Whether protease activity mediates the cell-cycle effect not resolved
    • Reconciliation with pro-metastatic roles unaddressed
  10. 2010 High

    Identification of Tie2 as a cleaved substrate and of shed soluble matriptase as a proangiogenic factor connected the protease to vascular remodeling and metastatic dissemination.

    Evidence Co-IP, in vitro cleavage, shRNA knockdown, transendothelial migration, CAM assay and in vivo metastasis

    PMID:20652801 PMID:21097670

    Open questions at the time
    • In vivo relevance of Tie2 cleavage vs other substrates not quantified
    • Identity of the proangiogenic shed substrate not pinpointed
  11. 2011 Medium

    Transcriptional induction by IFN-γ through JAK/STAT1 established a regulatory input controlling matriptase expression in immune cells and its role in macrophage transendothelial migration.

    Evidence STAT1 ChIP, JAK inhibitor, shRNA knockdown and migration assays

    PMID:21295011

    Open questions at the time
    • Macrophage substrate driving migration not identified
    • Single lab
  12. 2018 Medium

    CDX2-dependent regulation of ST14 and SPINT1 via distinct enhancers revealed transcriptional control of the protease/inhibitor balance in intestinal cells.

    Evidence CDX2 ChIP-seq, luciferase reporters, overexpression/knockdown and qRT-PCR

    PMID:30087389

    Open questions at the time
    • Functional oncogenic consequence of altered ratio not demonstrated
    • Cell-specific repressive vs enhancing logic not mechanistically explained
  13. 2018 Medium

    A mitochondrial pool binding ATP synthase β subunit via CUB/LDL motifs revealed an unexpected non-proteolytic bioenergetic function in neural stem cells.

    Evidence Fractionation, co-IP, proximity ligation, MitoTracker co-staining and Seahorse respiration with knockdown

    PMID:30566397

    Open questions at the time
    • Mechanism of mitochondrial targeting unknown
    • Whether catalytic activity is involved unresolved
    • Single lab
  14. 2020 High

    Sequential PKCβII/TACE shedding followed by SPPL2b intramembrane proteolysis releasing a nuclear EICD established a bidirectional signaling cascade coupling extracellular proteolysis to transcriptional reprogramming of chemokines driving metastasis.

    Evidence Inhibitor/siRNA/dominant-negative shedding analyses, SPPL2b loss/gain-of-function, fractionation, RNA-seq, antibody arrays and in vivo metastasis

    PMID:25245289 PMID:32241917 PMID:32493324

    Open questions at the time
    • Nuclear partners and DNA-binding mode of EICD undefined
    • Direct vs indirect chemokine promoter regulation not established
  15. 2022 Medium

    Demonstrating that environmental selenite triggers shedding and that EICD alone is sufficient to induce CCL2 secretion pinpointed the intracellular fragment as the effector of the pro-metastatic transcriptional response.

    Evidence Selenite treatment, EICD heterologous expression, shRNA knockdown, CCL2 ELISA and invasion assay in 4T1 cells

    PMID:35950457

    Open questions at the time
    • Generality of selenite trigger across tissues unknown
    • Mechanism by which EICD activates CCL2 promoter not defined
  16. 2019 Medium

    Knockdown and antibody blockade established matriptase as a metastasis-selective target whose inhibition spares primary tumor growth, supporting therapeutic targeting of the autocatalytic loop epitope.

    Evidence shRNA and mAb3F3 treatment in 4T1, E0771 and MMTV-PyMT models with migration assays

    PMID:31426843

    Open questions at the time
    • Molecular target of mAb-induced inhibition not biochemically detailed
    • Single lab
  17. 2023 Medium

    Kidney-specific and double knockouts showed St14 regulates ENaC subunit abundance indirectly through the co-protease CAP1/Prss8 rather than by direct ENaC cleavage, refining its role in renal sodium handling.

    Evidence Tissue-specific and double KO mice with Western blots, RNAscope, sodium balance and Na+-deprivation challenge

    PMID:37830556

    Open questions at the time
    • Mechanism by which St14 controls CAP1/Prss8 abundance unknown
    • Physiological significance limited as sodium balance is maintained

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the same protease reconciles anti-proliferative, pro-metastatic, mitochondrial, and barrier-forming activities, and what governs tissue-specific substrate selection and subcellular targeting, remains unresolved.
  • No unifying model integrating extracellular, intramembrane, nuclear, and mitochondrial functions
  • Tissue-specific substrate repertoire incompletely defined
  • Regulatory switch between tumor-suppressive and tumor-promoting outputs unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016787 hydrolase activity 3 GO:0140110 transcription regulator activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005634 nucleus 2 GO:0005576 extracellular region 1 GO:0005739 mitochondrion 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2 R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-168256 Immune System 1
Partners
ADAM17ATP5F1BPRSS8SPINT1SPPL2BTEKTMEFF1

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Crystal structures of the MT-SP1/matriptase catalytic domain were solved in complex with benzamidine (1.3 Å) and bovine pancreatic trypsin inhibitor (2.9 Å), revealing a trypsin-like serine proteinase fold with a unique nine-residue 60-insertion loop, a trypsin-like S1 pocket, a small hydrophobic S2 subsite, and an open negatively charged S4 cavity favoring basic P3/P4 residues. The structure also suggested a complementary charge pattern for docking of the preceding LDL receptor class A domain and served as a model for HAI-1 inhibitor interactions. X-ray crystallography (1.3 Å and 2.9 Å resolution crystal structures) with functional interpretation of active-site architecture The Journal of biological chemistry High 11696548
2002 Matriptase/MT-SP1 null mice die within 48 h of birth due to fatal dehydration caused by compromised epidermal barrier function (both inward and outward). Loss of the protease caused malformations of the stratum corneum (dysmorphic corneocytes, absence of vesicular bodies), follicular hypoplasia, absence of vibrissal hair canal formation, and dramatically increased thymocyte apoptosis with thymocyte depletion, establishing pleiotropic roles in epidermal development, hair follicle development, and thymic homeostasis. Germline knockout mouse (null mutation), histological and ultrastructural analysis, transepidermal water loss measurements Oncogene High 12032844
2003 Epidermal-specific deletion of Matriptase/MT-SP1 causes loss of proteolytically processed filaggrin monomers and the NH2-terminal filaggrin S-100 regulatory protein, with accumulation of profilaggrin and aberrant profilaggrin-processing products in the stratum corneum, identifying keratinocyte matriptase as an essential component of the profilaggrin-processing pathway. Epidermal deficiency also perturbed lipid matrix formation, cornified envelope morphogenesis, and stratum corneum desquamation. Conditional (epidermal) knockout mouse, proteomic analysis of epidermis, Western blotting The Journal of cell biology High 14638864
2007 The ARIH-associated G827R missense mutation in the matriptase serine protease domain (G216 in chymotrypsin numbering) strongly reduces proteolytic activity toward small-molecule substrates and toward the candidate epidermal substrate prostasin. ST14 hypomorphic mice (100-fold reduced epidermal matriptase mRNA) phenocopy human ARIH with ichthyosis, hypotrichosis, and tooth defects, and display reduced prostasin proteolytic activation and reduced profilaggrin processing, consistent with a matriptase→prostasin proteolytic cascade operating in the epidermis. In vitro protease activity assay with G827R recombinant protein against small-molecule and protein substrates; ST14 hypomorphic mouse strain; biochemical analysis of epidermis The Journal of biological chemistry High 17940283
2008 Mutations in ST14 (splice-site and frameshift) cause loss of matriptase protein in differentiated patient keratinocytes, reduced proteolytic activation of prostasin, and disturbed processing of profilaggrin in human ichthyosis-hypotrichosis patients, confirming the matriptase→prostasin→profilaggrin axis in human skin. Patient keratinocyte analysis (Western blot for matriptase and prostasin activation, profilaggrin processing assays), Sanger sequencing of ST14 The Journal of investigative dermatology Medium 18843291
2001 Rat MT-SP1 (ST14) expressed in Caco-2 cells localizes exclusively to the basolateral membrane surface; a secreted form of the enzyme produced in COS-1 cells degrades fibronectin and laminin in vitro, suggesting a role in regulating cell-substratum adhesion during intestinal epithelial turnover. Heterologous expression and immunolocalization (Caco-2); in vitro substrate cleavage assay (fibronectin, laminin) with secreted protease form Biochemical and biophysical research communications Medium 11573963
2006 GST pull-down assays demonstrate that the ST14 serine protease (SP) domain physically interacts with HAI-1 (hepatocyte growth factor activator inhibitor-1). The CUB domain of ST14 interacts with TMEFF1 (transmembrane protein with EGF-like and two follistatin-like domains 1), and TMEFF1 expression is dependent on ST14 transfection in RKO cells; co-expression was confirmed in MCF7 cells and normal tissues. GST fusion protein pull-down assay; quantitative RT-PCR; homology modeling The Journal of biological chemistry Medium 16407223
2007 Two scFv antibody inhibitors of MT-SP1/matriptase inhibit the protease with K(I) values in the low picomolar range by competing with substrate at the S1 site. Alanine scanning of active-site loops defined distinct three-dimensional binding epitopes for each antibody. One inhibitor acts as a standard mechanism (substrate-like) inhibitor and can be processed by MT-SP1 at low pH. Kinetic inhibition assays; alanine scanning mutagenesis of active-site loops; antibody-based mechanistic characterization Journal of molecular biology High 17475279
2009 ST14 overexpression in breast cancer cells reduces cell proliferation by upregulating p27, which results in downregulation of cyclin E-CDK2 complexes, thereby inhibiting S-phase entry. ST14 also reduces cell migration and invasion. Introduction of miR-27b into ST14-expressing cells did not suppress the cell-growth effect, indicating this cell-cycle regulatory function is independent of miR-27b regulation. Stable overexpression/knockdown; flow cytometry (cell cycle); Western blot (p27, cyclin E, CDK2); luciferase reporter assay for miR-27b target validation The Journal of biological chemistry Medium 19546220
2010 Epithin/PRSS14 (ST14) physically interacts with and proteolytically cleaves the extracellular domain of the angiopoietin receptor Tie2, degrading its ligand-binding domain. The remaining Tie2 fragment is highly phosphorylated and recruits PI3K. Knockdown of epithin in thymoma or breast cancer cells impairs transendothelial migration in vitro and reduces metastatic nodules in vivo. Co-immunoprecipitation; in vitro cleavage assay; shRNA knockdown; in vitro transendothelial migration assay; in vivo metastasis model (4T1) Blood High 21097670
2010 Soluble (shed) epithin/PRSS14 secreted from cancer cells promotes endothelial cell migration and invasion, tube formation in vitro, and neovascularization in the chicken chorioallantoic membrane assay. Shed epithin is increased under hypoxia. Knockdown of epithin abolishes the protease activity of the secreted fraction and reduces endothelial invasion and tube formation, identifying secreted epithin as a proangiogenic factor. shRNA knockdown; endothelial migration/invasion assays; tube formation assay; CAM assay; specific antibody neutralization Molecules and cells Medium 20652801
2011 PRSS14/Epithin (ST14) is induced in macrophages by IFN-γ through the JAK/STAT1 pathway; ChIP confirmed that STAT1 binds two sites in the PRSS14/Epithin promoter upon IFN-γ activation. IFN-γ-treated macrophages show enhanced transendothelial migration that is abolished by PRSS14/Epithin knockdown, despite normal expression of ICAM1, CD80, and CD40. Chromatin immunoprecipitation (ChIP) for STAT1 binding; shRNA knockdown; JAK inhibitor (tyrphostin AG490); transendothelial migration assay Biochemical and biophysical research communications Medium 21295011
2014 Ectodomain shedding of epithin/PRSS14 is induced by TGF-β through a receptor-mediated pathway and is executed by TACE (tumor necrosis factor-α converting enzyme/ADAM17). TGF-β treatment induces translocation of intracellular TACE to the plasma membrane where epithin/PRSS14 resides. TACE inhibitor TAPI-0 and TACE siRNA greatly reduce TGF-β-induced shedding. TACE inhibitor treatment; TACE siRNA knockdown; Western blot for shedding products; immunofluorescence for TACE translocation Biochemical and biophysical research communications Medium 25245289
2018 A mitochondrial fraction of matriptase (ST14) in neural stem/progenitor cells co-immunoprecipitates with the β subunit of mitochondrial F0F1-ATP synthase (ATP-β), and this interaction was confirmed by co-immunofluorescence and in situ proximity ligation assay. The interaction requires both the CUB/CLR and LDL receptor motifs of matriptase. Knockdown of matriptase impairs mitochondrial membrane potential, reduces ATP synthesis and oxygen consumption rate (especially energy reserve capacity by >50%), and renders cells unable to tolerate hydrogen peroxide stress. Subcellular fractionation; co-immunoprecipitation; in situ proximity ligation assay; MitoTracker co-staining; mitochondrial respiration assay (Seahorse); shRNA knockdown FASEB journal Medium 30566397
2018 The transcription factor CDX2 regulates both ST14 (matriptase) and SPINT1 (HAI-1) gene expression in intestinal cells through distinct genomic enhancer elements identified by ChIP-seq. CDX2 shows both repressive and enhancing regulatory activity in a cell-specific manner and affects the ST14/SPINT1 mRNA ratio, thereby potentially controlling the oncogenic balance between matriptase and its inhibitor. CDX2 ChIP-seq; promoter-reporter luciferase assays; CDX2 overexpression/knockdown; quantitative RT-PCR Scientific reports Medium 30087389
2020 After ectodomain shedding of epithin/PRSS14, the remaining membrane stub undergoes intramembrane proteolysis by signal peptide peptidase-like 2b (SPPL2b), releasing the intracellular domain (EICD) which preferentially localizes to the nucleus. Nuclear EICD enhances cancer cell migration, invasion, and metastasis and increases promoter activities of chemokines involved in cell motility (identified by RNA-seq and antibody arrays). This establishes a bidirectional signaling cascade: extracellular proteolysis by shed epithin and intracellular transcriptional reprogramming by EICD. SPPL2b knockdown/overexpression; subcellular fractionation and immunofluorescence; RNA-seq; antibody arrays; migration/invasion assays; in vivo metastasis; bioinformatics survival analysis BMC biology High 32493324
2020 JNK inhibition (SP600125) induces ectodomain shedding of Prss14/epithin via PKCβII and TACE. PKCβII is identified as a major mediator of both JNK inhibition- and PMA-induced shedding; loss-of-function using specific inhibitors, shRNA knockdown, and dominant-negative PKCβII variants all reduce shedding. SP600125 increases phosphorylation of PKCβII and TACE and induces their translocation to the plasma membrane where epithin/PRSS14 resides. MAP kinase inhibitor panel; shRNA knockdown; dominant-negative overexpression; Western blot for phosphorylation and shedding products; immunofluorescence for membrane translocation; in vitro invasion assay The Journal of biological chemistry Medium 32241917
2022 Ectodomain shedding of epithin/PRSS14 in breast cancer 4T1 cells is induced by environmental selenite and increases CCL2 secretion in an epithin-dependent manner. Heterologous expression of the intracellular domain (EICD) alone is sufficient to induce CCL2 secretion, establishing that intramembrane proteolysis-mediated EICD release is responsible for the metastatic transcriptional effect downstream of ectodomain shedding. Selenite treatment; EICD heterologous expression; shRNA knockdown; ELISA for CCL2; invasion assay Molecules and cells Medium 35950457
2023 Kidney-specific CAP3/St14 knockout mice show significantly decreased CAP1/Prss8 protein expression, altered ENaC subunit protein abundances, and decreased pNCC abundances, but maintain overall sodium balance. Double CAP1/Prss8; CAP3/St14 knockout mice restore ENaC subunit protein abundances but show reduced NCC activity under Na+ deprivation. RNAscope analysis confirmed co-expression of CAP3/St14 and CAP1/Prss8 with α-ENaC in distal tubules. The data establish that CAP3/St14 is NOT required for direct proteolytic activation of ENaC in vivo but regulates ENaC protein abundance, in part through controlling CAP1/Prss8 expression. Kidney-specific and double knockout mice; Western blot for ENaC/NCC subunit abundance; RNAscope in situ hybridization; sodium balance measurements; Na+-deprived diet challenge Cells Medium 37830556
2005 Post-translational processing of SNC19/ST14 (matriptase) in cancer cell lines produces at least two forms: a 120 kDa and a 75 kDa species. The 75 kDa form, identified using anti-His antibody after expression and purification, displays gelatinase (proteolytic) activity as assessed by gelatin zymography. Eukaryotic expression (Psectag2A-SNC19 ORF in BCAP37 cells); Western blot; gelatin zymography Zhejiang da xue xue bao. Yi xue ban Low 15693122
2019 Prss14/ST14 knockdown in mouse breast cancer cells reduces metastasis (tumor nodules in vivo) without significantly affecting primary tumor growth in two syngeneic mouse models, and monoclonal antibody mAb3F3 targeting the autocatalytic loop epitope reduces cell migration and eliminates metastasis in MMTV-PyMT mice. shRNA knockdown; in vivo orthotopic/syngeneic tumor models (4T1, E0771, MMTV-PyMT); antibody treatment; cell migration assay; immunoprecipitation; flow cytometry Journal of experimental & clinical cancer research Medium 31426843
2004 Overexpression of SNC19/ST14 in RKO colorectal cancer cells alters F-actin (cytoskeletal) organization and decreases cell adhesion to extracellular matrix, without significantly changing cell cycle, apoptosis, or proliferation at moderate expression levels. Stable transfection; rhodamine-phalloidin confocal imaging of F-actin; MTT adhesion assay; flow cytometry Zhonghua yi xue za zhi Low 15200890

Source papers

Stage 0 corpus · 59 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Matriptase/MT-SP1 is required for postnatal survival, epidermal barrier function, hair follicle development, and thymic homeostasis. Oncogene 283 12032844
2003 Loss of proteolytically processed filaggrin caused by epidermal deletion of Matriptase/MT-SP1. The Journal of cell biology 178 14638864
2007 Autosomal recessive ichthyosis with hypotrichosis caused by a mutation in ST14, encoding type II transmembrane serine protease matriptase. American journal of human genetics 144 17273967
2001 Catalytic domain structures of MT-SP1/matriptase, a matrix-degrading transmembrane serine proteinase. The Journal of biological chemistry 101 11696548
2009 ST14 (suppression of tumorigenicity 14) gene is a target for miR-27b, and the inhibitory effect of ST14 on cell growth is independent of miR-27b regulation. The Journal of biological chemistry 94 19546220
2013 Predominance of Klebsiella pneumoniae ST14 carrying CTX-M-15 causing neonatal sepsis in Tanzania. BMC infectious diseases 85 24099282
2008 Ichthyosis, follicular atrophoderma, and hypotrichosis caused by mutations in ST14 is associated with impaired profilaggrin processing. The Journal of investigative dermatology 79 18843291
2007 Autosomal ichthyosis with hypotrichosis syndrome displays low matriptase proteolytic activity and is phenocopied in ST14 hypomorphic mice. The Journal of biological chemistry 74 17940283
2001 A role for membrane-type serine protease (MT-SP1) in intestinal epithelial turnover. Biochemical and biophysical research communications 69 11573963
2003 The novel serine protease tumor-associated differentially expressed gene-15 (matriptase/MT-SP1) is highly overexpressed in cervical carcinoma. Cancer 56 14584072
2005 Expression of serine protease SNC19/matriptase and its inhibitor hepatocyte growth factor activator inhibitor type 1 in normal and malignant tissues of gastrointestinal tract. World journal of gastroenterology 46 16273651
2007 The mechanism of inhibition of antibody-based inhibitors of membrane-type serine protease 1 (MT-SP1). Journal of molecular biology 43 17475279
1987 Linkage and genetic counselling for the fragile X using DNA probes 52A, F9, DX13, and ST14. American journal of medical genetics 43 2886048
2008 MT-SP1 proteolysis and regulation of cell-microenvironment interactions. Frontiers in bioscience : a journal and virtual library 36 17981566
2013 Large oligoclonal outbreak due to Klebsiella pneumoniae ST14 and ST26 producing the FOX-7 AmpC β-lactamase in a neonatal intensive care unit. Journal of clinical microbiology 30 24088849
2003 Quantitation of membrane type serine protease 1 (MT-SP1) in transformed and normal cells. Biological chemistry 28 12675519
2020 Emergence of Transferable mcr-9 Gene-Carrying Colistin-Resistant Salmonella enterica Dessau ST14 Isolated from Retail Chicken Meat in Korea. Foodborne pathogens and disease 27 32830987
2010 Epithin/PRSS14 proteolytically regulates angiopoietin receptor Tie2 during transendothelial migration. Blood 24 21097670
1988 Linkage between the fragile X and F9, DXS52 (St14), DXS98 (4D-8) and DXS105 (cX55.7). American journal of medical genetics 22 2902797
2021 Diversity of carbapenem-resistant Klebsiella pneumoniae ST14 and emergence of a subgroup with KL64 capsular locus in the Arabian Peninsula. European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology 15 34855011
2006 Protein interaction analysis of ST14 domains and their point and deletion mutants. The Journal of biological chemistry 15 16407223
2005 Effect of SNC19/ST14 gene overexpression on invasion of colorectal cancer cells. World journal of gastroenterology 15 16237759
2016 Degradation Pathways of 2- and 4-Nitrobenzoates in Cupriavidus sp. Strain ST-14 and Construction of a Recombinant Strain, ST-14::3NBA, Capable of Degrading 3-Nitrobenzoate. Applied and environmental microbiology 14 27208126
2019 Targeting metastatic breast cancer with peptide epitopes derived from autocatalytic loop of Prss14/ST14 membrane serine protease and with monoclonal antibodies. Journal of experimental & clinical cancer research : CR 11 31426843
2014 Shedding of epithin/PRSS14 is induced by TGF-β and mediated by tumor necrosis factor-α converting enzyme. Biochemical and biophysical research communications 11 25245289
2019 Molecular characterization of carbapenem-resistant Klebsiella pneumoniae ST14 and ST512 causing bloodstream infections in ICU and surgery wards of a tertiary university hospital of Verona (northern Italy): co-production of KPC-3, OXA-48, and CTX-M-15 β-lactamases. Diagnostic microbiology and infectious disease 10 31924425
2018 Intestinal regulation of suppression of tumorigenicity 14 (ST14) and serine peptidase inhibitor, Kunitz type -1 (SPINT1) by transcription factor CDX2. Scientific reports 10 30087389
2017 A Nonsense Variant in the ST14 Gene in Akhal-Teke Horses with Naked Foal Syndrome. G3 (Bethesda, Md.) 10 28235824
2010 Soluble epithin/PRSS14 secreted from cancer cells contains active angiogenic potential. Molecules and cells 10 20652801
2018 Mutant cytoskeletal and ECM peptides sensitive to the ST14 protease are associated with a worse outcome for glioblastoma multiforme. Biochemical and biophysical research communications 9 29953855
2011 PRSS14/Epithin is induced in macrophages by the IFN-γ/JAK/STAT pathway and mediates transendothelial migration. Biochemical and biophysical research communications 9 21295011
2000 Carrier detection and prenatal diagnosis of hemophilia A in a Korean population by PCR-based analysis of the BclI/intron 18 and St14 VNTR polymorphisms. Journal of human genetics 9 10944851
2020 Intramembrane proteolysis of an extracellular serine protease, epithin/PRSS14, enables its intracellular nuclear function. BMC biology 8 32493324
2018 A disease-causing novel missense mutation in the ST14 gene underlies autosomal recessive ichthyosis with hypotrichosis syndrome in a consanguineous family. European journal of dermatology : EJD 8 29611532
2001 A novel serine protease SNC19 associated with human colorectal cancer. Chinese medical journal 7 11780337
2020 A JUN N-terminal kinase inhibitor induces ectodomain shedding of the cancer-associated membrane protease Prss14/epithin via protein kinase CβII. The Journal of biological chemistry 6 32241917
2021 Gene-associated methylation status of ST14 as a predictor of survival and hormone receptor positivity in breast Cancer. BMC cancer 5 34418985
2017 A novel mutation in ST14 at a functionally significant amino acid residue expands the spectrum of ichthyosis-hypotrichosis syndrome. Orphanet journal of rare diseases 5 29208051
2016 Prostasin and matriptase (ST14) in placenta from preeclamptic and healthy pregnant women. Journal of hypertension 5 26867056
1995 St14 (DXS52) VNTR in the Chinese population and its application to genetic diagnosis of haemophilia A. Nouvelle revue francaise d'hematologie 5 7567434
2023 Kidney-Specific Membrane-Bound Serine Proteases CAP1/Prss8 and CAP3/St14 Affect ENaC Subunit Abundances but Not Its Activity. Cells 4 37830556
1995 Rapid typing of 4 VNTR loci, 3'ApoB, MCT118,St14 and YNZ22 by the polymerase chain reaction of a Greek sample. Cellular and molecular biology (Noisy-le-Grand, France) 4 7580849
2025 Emergence of Klebsiella pneumoniae ST14 co-harboring bla NDM-1, bla OXA-232 , mcr-1.1, and a novel IncI1 tet(X4) plasmid, with evidence of ColKP3 mobilization under antibiotic pressure. Current research in microbial sciences 3 40979677
2018 Mitochondrial localization of St14-encoding transmembrane serine protease is involved in neural stem/progenitor cell bioenergetics through binding to F0F1-ATP synthase complex. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2 30566397
1991 Linkage in fragile X families of three distal flanking markers: ST14, DX13, and F8. American journal of medical genetics 2 1673308
2024 Prevalence and Subtypes Distribution (ST10, ST14, ST25, ST26) of Blastocystis spp. in Anatolian Water Buffalo (Bubalus bubalis) in Van, Türkiye. Veterinary medicine and science 1 39329238
2022 Genome sequence dataset of Bacillus altitudinis strain ST14 isolated from Tunggak River in Gebeng Industrial Park, Kuantan, Pahang. Data in brief 1 36624876
2020 Critical Adjuvant Influences on Preventive Anti-Metastasis Vaccine Using a Structural Epitope Derived from Membrane Type Protease PRSS14. Immune network 1 32895620
2019 Identification of a novel mutation in the ST14 gene in an Iranian family with ichthyosis and hypotrichosis. Dermatology online journal 1 30982314
2011 [Improvement and application of DXS52(St14) in gene diagnosis of hemophilia A]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 1 21287503
2004 [SNC19/ST14 gene transfection and expression influence the biological behavior of colorectal cancer cells]. Zhonghua yi xue za zhi 1 15200890
1998 [Polymorphism distribution of ST14(DXS52) VNTR in normal individuals in northeastern region of China and its application in gene diagnosis of hemophilia A]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 1 9456369
2025 StACS3-mediated drought stress adaptation in potato involves interactions with StPP2C2 and St14-3-3 proteins. Frontiers in plant science 0 41245441
2022 Environment-Sensitive Ectodomain Shedding of Epithin/PRSS14 Increases Metastatic Potential of Breast Cancer Cells by Producing CCL2. Molecules and cells 0 35950457
2005 [Study on post-translational processing and active forms of the novel metastasis-associated protein SNC19]. Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 0 15693122
2004 [Diagnosis of hemophilia A by a combination of St14(DXS52) VNTR polymorphism and (CA)n repeat polymorphism within FVIII gene]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 14767918
2000 [The St14 (DXS 52) VNTR in a Guangdong Han population and detection of hemophilia A carriers]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 0 11877006
1990 Study on BcII/St14 RFLPs in Chinese for DNA diagnosis for hemophilia A. Science in China. Series B, Chemistry, life sciences & earth sciences 0 1973615
1989 [The RFLPs of St14/Taq I in Chinese and its application to gene analysis and prenatal diagnosis of hemophilia A]. Yi chuan xue bao = Acta genetica Sinica 0 2577235

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