Affinage

ADAM15

Disintegrin and metalloproteinase domain-containing protein 15 · UniProt Q13444

Length
863 aa
Mass
93.0 kDa
Annotated
2026-04-28
96 papers in source corpus 41 papers cited in narrative 41 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ADAM15 is a membrane-anchored metalloprotease-disintegrin that integrates catalytic ectodomain shedding with non-catalytic cytoplasmic scaffolding to regulate cell adhesion, vascular permeability, neovascularization, tissue remodeling, and cell death decisions. Its extracellular disintegrin domain binds integrins αvβ3 and α5β1 in an RGD-dependent manner to modulate cell adhesion and migration (PMID:9516430, PMID:9914169), while its metalloprotease domain cleaves substrates including E-cadherin, N-cadherin, FGFR2iiib, CD23, and TRIF, with TIMP-3-sensitive but phorbol-ester-insensitive catalytic properties (PMID:19207106, PMID:18434311, PMID:23365087); notably, pathological retinal neovascularization requires ADAM15 but not its catalytic activity, establishing a protease-independent scaffolding role in angiogenesis (PMID:25249606, PMID:20189953). The cytoplasmic domain undergoes extensive alternative splicing generating isoform-specific interactions with Src family kinases, Grb2, FAK, calmodulin, Nck, nephrocystin, SNX33, and PABP, thereby activating FAK/Src, ERK, PI3K/Akt, and calcineurin/NFAT pathways to govern endothelial barrier function, chondrocyte survival, cardiac remodeling after injury, synovial fibroblast mechanosensing, and necroptosis competence (PMID:11741929, PMID:22544741, PMID:30003689, PMID:36330793, PMID:41340056).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1998 High

    Establishing that ADAM15 is an RGD-dependent integrin ligand resolved how a membrane metalloprotease could directly mediate cell adhesion: the disintegrin domain binds αvβ3 via a specific RPTRGD motif, and furin processes the pro-domain in the Golgi, with mature ADAM15 accumulating primarily in a perinuclear/TGN compartment rather than at the cell surface.

    Evidence Recombinant GST-disintegrin binding assays with RGD→SGA mutagenesis; pulse-chase, furin cleavage, and immunolocalization in COS-7 cells

    PMID:9516430 PMID:9748307

    Open questions at the time
    • Crystal structure of ADAM15 disintegrin–integrin complex not determined
    • Mechanism controlling ADAM15 surface trafficking vs perinuclear retention unresolved
  2. 1999 High

    Demonstrating that ADAM15 engages both αvβ3 and α5β1 on haemopoietic cells and that its cytoplasmic domain interacts with SH3-domain proteins (endophilin I, SH3PX1) established ADAM15 as a dual-function molecule coupling extracellular adhesion with intracellular signaling scaffolds.

    Evidence Solid-phase adhesion assays with Fc-fusion protein and antibody blocking; yeast two-hybrid screen confirmed by co-IP from COS-7 cells

    PMID:10531379 PMID:9914169

    Open questions at the time
    • Functional consequence of endophilin/SH3PX1 binding on ADAM15 biology not established
    • Whether pro-domain-preferential interaction reflects trafficking regulation is unknown
  3. 2001 High

    Identification of Src family kinases (Hck, Lck) as cytoplasmic-domain kinases and Grb2 as an adaptor partner, together with evidence that ADAM15 overexpression strengthens cell–cell contacts and suppresses migration, defined ADAM15 as a signaling-competent adhesion molecule at cell junctions.

    Evidence SH3 pulldowns, co-IP from hematopoietic lines, in vitro kinase assays with Tyr715/735 mutagenesis; overexpression in NIH3T3 with permeability, adhesion, and migration assays

    PMID:11697891 PMID:11741929

    Open questions at the time
    • Which downstream pathways are activated by Hck/Lck-mediated ADAM15 phosphorylation was not yet mapped
    • Endogenous stoichiometry of ADAM15–kinase complexes not determined
  4. 2002 Medium

    Localizing ADAM15 to VE-cadherin-positive adherens junctions in endothelial cells, with VE-cadherin co-expression driving ADAM15 surface translocation, positioned ADAM15 within the junctional machinery controlling vascular integrity.

    Evidence Immunofluorescence colocalization and GFP-ADAM15 imaging in endothelial cells and CHO cells co-expressing VE-cadherin

    PMID:12243749

    Open questions at the time
    • Direct molecular interaction between ADAM15 and VE-cadherin not demonstrated
    • Whether VE-cadherin-driven surface translocation involves specific sorting signals is unknown
  5. 2003 High

    Knockout mice revealed ADAM15 is required for pathological but not developmental neovascularization and tumor angiogenesis, while in vitro studies established ADAM15 as a bona fide sheddase for CD23, defining its first validated in vivo function and catalytic substrate.

    Evidence Adam15−/− mice in retinopathy of prematurity and B16F0 tumor models; recombinant ADAM15 peptide substrate profiling and CD23 shedding assay with catalytic-dead mutant control

    PMID:12777399 PMID:12897135

    Open questions at the time
    • Whether CD23 shedding is relevant in vivo not tested
    • Catalytic vs non-catalytic contribution to neovascularization not yet resolved
  6. 2005 High

    ADAM15 knockout mice developing accelerated osteoarthritis, coupled with ADAM15 overexpression enhancing chondrocyte adhesion to cartilage collagens and viability, established a chondroprotective homeostatic role, while RGD-dependent suppression of αvβ3-mediated adhesion in cancer cells clarified the disintegrin domain's anti-migratory mechanism.

    Evidence Adam15−/− joint histomorphometry; chondrocyte overexpression with collagen adhesion and viability assays; cancer cell adhesion/motility with RGD→SGA mutant

    PMID:15618016 PMID:15818704

    Open questions at the time
    • Molecular basis of ADAM15–collagen II/VI interaction unknown
    • Whether chondroprotection is catalytic or scaffolding-dependent not determined
  7. 2007 Medium

    Characterization of 13 cytoplasmic splice variants from a TATA-less CpG-island promoter explained the molecular basis for isoform-specific signaling diversity observed in subsequent functional studies.

    Evidence Genomic analysis, RT-PCR across human tissues, luciferase reporter assays for promoter

    PMID:17937806

    Open questions at the time
    • Regulatory mechanisms governing tissue-specific splicing not identified
    • Epigenetic regulation of the CpG-island promoter not explored
  8. 2008 High

    Multiple studies resolved ADAM15's dual catalytic and scaffolding outputs: E-cadherin shedding activates HER2/HER3–ERK signaling in breast cancer; N-cadherin cleavage promotes prostate cancer transendothelial migration and bone metastasis; isoform-specific cytoplasmic domains differentially recruit Src, Nck, and Brk to control migration and invasion; and a VEGF–ADAM15 amplification loop drives ischemic retinal neovascularization.

    Evidence shRNA/overexpression with catalytic mutant in breast and prostate cancer cells; isoform-specific pulldowns; SCID mouse metastasis model; Adam15−/− mice in OIR and CNV models with VEGF pathway analysis

    PMID:18281484 PMID:18296648 PMID:18381816 PMID:18434311

    Open questions at the time
    • Whether E-cadherin and N-cadherin are cleaved at the same or different sites unknown
    • In vivo relevance of isoform-specific signaling not tested in genetic models
  9. 2009 High

    Defining FGFR2iiib as a TIMP-3-sensitive, PMA-insensitive ADAM15 substrate with Src-dependent enhancement in the ADAM15B isoform established a paradigm in which cytoplasmic splice variation controls extracellular catalytic output, while nephrocystin and SNX33 were mapped as isoform-selective SH3-domain partners.

    Evidence Cell-based FGFR2iiib shedding with catalytic mutant, inhibitor panel, Src−/− cells with rescue; co-precipitation with proline-cluster mutations for nephrocystin/SNX33

    PMID:19207106 PMID:19487280 PMID:19718658

    Open questions at the time
    • Physiological consequence of FGFR2iiib shedding in vivo not demonstrated
    • Whether nephrocystin interaction links ADAM15 to ciliopathy pathways untested
  10. 2010 High

    Demonstrating that catalytically dead ADAM15 still increases endothelial permeability and ERK phosphorylation via Src definitively separated the protease-independent scaffolding function from ectodomain shedding in vascular biology.

    Evidence Wild-type and catalytically dead ADAM15 overexpression in HUVECs; transendothelial resistance, albumin flux, neutrophil migration; Src/ERK inhibitors

    PMID:20189953

    Open questions at the time
    • Structural basis of protease-independent Src/ERK activation unknown
    • Whether scaffolding and catalytic functions are spatially segregated at junctions not resolved
  11. 2012 High

    Three parallel advances solidified ADAM15's physiological roles: Adam15−/− endothelial rescue experiments confirmed its requirement for LPS-induced lung injury permeability; FAK was identified as a direct cytoplasmic-tail binding partner mediating anti-apoptotic Src activation; and exosomal ADAM15 release revealed a paracrine RGD-dependent mechanism suppressing cancer cell adhesion.

    Evidence Adam15−/− mice in LPS acute lung injury with rescue expression; mammalian two-hybrid, pulldown, Far Western for FAK binding with chimeric construct; exosome isolation with RGD mutant controls and tumor models

    PMID:22505472 PMID:22544741 PMID:23161886

    Open questions at the time
    • Whether exosomal ADAM15 operates in non-cancer physiological contexts unknown
    • FAK binding site on ADAM15 cytoplasmic tail not mapped to specific residues
  12. 2013 High

    ADAM15 was found to cleave TRIF and suppress TLR3/TLR4-mediated NF-κB/IFN-β signaling, expanding its substrate repertoire to innate immune adaptors, while parallel work showed it confers apoptosis resistance in synovial fibroblasts via Src/FAK/PI3K/NF-κB signaling.

    Evidence LC-MS identification of TRIF interaction, co-IP, TRIF cleavage assay, NF-κB/IFN-β reporters with ADAM15 knockdown; RASF siRNA with caspase assays and FAK/Src/NF-κB pathway inhibitors

    PMID:23365087 PMID:23918525

    Open questions at the time
    • TRIF cleavage site not identified
    • Whether TRIF cleavage is relevant in vivo during infection not tested
  13. 2014 High

    Adam15 catalytic-dead knock-in mice definitively showed that pathological retinal neovascularization is protease-independent while tumor suppression requires catalytic activity, parsing the in vivo contributions of ADAM15's two functional arms.

    Evidence Adam15E>A knock-in mice in OIR and tumor implantation models; cell-based shedding panel for angiogenesis receptors

    PMID:25249606

    Open questions at the time
    • Identity of the non-catalytic mechanism driving neovascularization (which integrin or signaling partner) not defined
    • Limited substrate panel tested in cell-based assays
  14. 2018 High

    Calmodulin was identified as the calcium-sensing mediator linking FasL/Fas death signals to ADAM15-dependent prosurvival Src/FAK activation in synovial fibroblasts, while PABP recruitment to ADAM15's cytoplasmic tail during cell adhesion revealed an unexpected role in local mRNA translation at the membrane.

    Evidence CaM-Sepharose pulldown, co-IP, recombinant CaM binding, CRAC/Orai1 inhibitor, CaM inhibitor, cytoplasmic-tail deletion; co-IP/domain-mapping for PABP with puromycin incorporation assay

    PMID:30003689 PMID:30265671

    Open questions at the time
    • Which mRNAs are locally translated at ADAM15/PABP sites unknown
    • Whether CaM–ADAM15 interaction is isoform-specific not tested
  15. 2019 Medium

    ADAM15 was placed downstream of shear-stress-induced KLF2 in endothelial cells to promote survival, and shown to upregulate Claudin-1 via PI3K/Akt/mTOR in an isoform- and catalysis-dependent manner while forming complexes with ZO1/ZO2 at tight junctions, broadening its junctional repertoire beyond adherens junctions.

    Evidence KLF2 overexpression/siRNA with ADAM15 readout under flow; isogenic ADAM15 isoform panel with PI3K/Akt/mTOR pathway analysis and ZO1/ZO2 co-IP

    PMID:31271758 PMID:31467400

    Open questions at the time
    • Direct KLF2 binding to ADAM15 promoter not shown by ChIP
    • Functional consequence of ZO1/ZO2–ADAM15 complex on barrier integrity not tested
  16. 2021 Medium

    ADAM15 was identified as a mechanosensory scaffold in synovial fibroblasts promoting TRPV4 membrane density and Src-dependent pannexin-1 ATP release, and independently as a host factor required for tick-borne encephalitis virus replication and membrane reorganization.

    Evidence ADAM15 loss-of-function in synovial fibroblasts with TRPV4/pannexin-1/JNK pathway assays; CRISPR KO and siRNA in TBEV-infected cells with replication and assembly readouts

    PMID:33208450 PMID:34685689

    Open questions at the time
    • Mechanism by which ADAM15 regulates TRPV4 surface density unclear
    • Whether ADAM15's role in TBEV replication involves its protease or scaffolding function not resolved
  17. 2022 High

    In vivo cardiac studies revealed ADAM15 is required for post-MI scar integrity through PAK1-dependent collagen cross-linking and for restraining calcineurin/NFAT-driven eccentric hypertrophy during pressure overload, establishing ADAM15 as a cardiac remodeling regulator.

    Evidence Adam15−/− mice in LAD ligation and TAC models; SHG imaging, collagen fractionation, LOX-1/PAK1 analysis; calcineurin activity assay with cyclosporin-A rescue

    PMID:34995785 PMID:36330793

    Open questions at the time
    • Whether ADAM15's cardiac role is cell-autonomous to fibroblasts vs cardiomyocytes not resolved
    • Direct ADAM15–calcineurin interaction or intermediate not identified
  18. 2025 Medium

    ADAM15 was found essential for necroptosis competence: its loss enhances basal caspase-8 activity, partially degrades RIPK1, and increases TNF-R1 surface expression, while in synovial fibroblasts ADAM15 co-localizes with N-cadherin at adherens junctions to transduce mechanical strain via PAK2/Nck into epigenetic regulation of invasion.

    Evidence CRISPR KO in U937/Jurkat with necroptosis assays, caspase-8 activity, RIPK1 blots, TNF-R1 flow cytometry; co-IP of ADAM15/NCAD complex with PAK2/Nck recruitment and lncRNA H19/miR-130a-3p expression

    PMID:40118917 PMID:41340056

    Open questions at the time
    • TNF-R1 as direct ADAM15 substrate not conclusively demonstrated
    • Whether RIPK1 degradation is a direct consequence of altered ADAM15-dependent trafficking unknown
    • In vivo validation of ADAM15 in necroptosis regulation lacking

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for ADAM15 substrate selectivity; the in vivo relevance of most identified substrates beyond genetic models; how isoform-specific cytoplasmic splicing is regulated in disease; whether ADAM15's necroptosis role is relevant in inflammatory pathologies; and the molecular mechanism linking ADAM15 scaffolding to calcineurin/NFAT restraint in the heart.
  • No crystal or cryo-EM structure of full-length ADAM15 available
  • Isoform-specific knockout mice not generated
  • In vivo substrate trapping has not been performed

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0060090 molecular adaptor activity 4 GO:0098631 cell adhesion mediator activity 3
Localization
GO:0005886 plasma membrane 5 GO:0005764 lysosome 1 GO:0005794 Golgi apparatus 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-1500931 Cell-Cell communication 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-168256 Immune System 2 R-HSA-1474244 Extracellular matrix organization 1
Partners
CALM1FAKGRB2ITGAVLCKNCK1PABPC1SRC
Complex memberships
ADAM15–FAK–Src complexADAM15–N-cadherin junctional complexADAM15–ZO1/ZO2 complex

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 The recombinant disintegrin-like domain of ADAM15 specifically binds integrin αvβ3 in an RGD-dependent manner; mutation of RGD to SGA abolishes binding, and the flanking sequence RPTRGD determines receptor specificity (αvβ3 vs αIIbβ3). GST fusion protein binding assay with recombinant integrins expressed in mammalian cells; site-directed mutagenesis of RGD motif The Journal of biological chemistry High 9516430
1999 The extracellular domain of ADAM15 (metargidin) mediates cell adhesion to haemopoietic cells via integrin αvβ3 on U937 monocytic cells and integrin α5β1 on MOLT-4 T cells, in an RGD-dependent, divalent cation-dependent manner. Solid-phase cell-adhesion assays with chimeric ADAM15-Fc protein; anti-integrin antibody blocking; purified recombinant integrins Journal of cell science High 9914169
1998 Mouse MDC15/ADAM15 pro-domain is removed by a pro-protein convertase (furin) in a late Golgi compartment; processed mature ADAM15 is endoglycosidase H-resistant, and the majority accumulates in a perinuclear/trans-Golgi network/endosomal compartment rather than at the cell surface. Pulse-chase experiments; brefeldin A/monensin treatment; in vitro furin cleavage assay; cell-surface trypsinization; immunolocalization in COS-7 cells The Journal of biological chemistry High 9748307
1999 The cytoplasmic domains of ADAM15 (MDC15) and MDC9 interact with the SH3 domain-containing proteins endophilin I (SH3GL2) and a novel SH3-PX domain protein (SH3PX1); these interactions are preferential for the precursor (pro-domain-containing) forms and were identified by yeast two-hybrid, bacterial fusion pulldown, and co-immunoprecipitation from eukaryotic cells. Yeast two-hybrid screen; bacterial GST fusion pulldown; co-immunoprecipitation from COS-7 cells The Journal of biological chemistry High 10531379
2001 The cytoplasmic domain of ADAM15 interacts with Src family kinases (Lck, Fyn, Abl, Src, Hck) via SH3 domain binding to proline-rich motifs, and with adaptor protein Grb2; interactions are phosphorylation-dependent (enhanced by tyrosine phosphorylation); Hck and Lck phosphorylate the ADAM15 cytoplasmic domain in vitro; Tyr715 and Tyr735 are regulatory residues. SH3 domain pulldowns; co-immunoprecipitation from hematopoietic cell lines; in vitro immune complex kinase assays; Far Western analysis; deletion and point mutation analysis; PMA stimulation and PP1 inhibitor treatment The Journal of biological chemistry High 11741929
2001 ADAM15 overexpression in NIH3T3 cells enhances cell-cell interactions: it localizes to cell-cell contacts in epithelial cells, decreases monolayer permeability, and increases cell adhesion to ADAM15-expressing monolayers by 45%, while inhibiting cell migration on fibronectin. Tetracycline-regulated overexpression; Boyden chamber migration assay; scratch wound model; monolayer permeability assay; cell adhesion assay; epitope-tagged ADAM15 immunolocalization Experimental cell research Medium 11697891
2002 ADAM15 localizes to adherens junctions in endothelial cells, colocalizing with VE-cadherin; VE-cadherin coexpression drives ADAM15 surface expression and translocation to the cell periphery in CHO cells. Immunofluorescence colocalization; ADAM15-GFP fusion protein imaging; flow cytometry for cell surface levels; co-expression of VE-cadherin and ADAM15 in CHO cells Experimental cell research Medium 12243749
2003 ADAM15-deficient (adam15-/-) mice show major reduction in pathological retinal neovascularization in a retinopathy of prematurity model, and reduced tumor growth of implanted B16F0 melanoma cells, demonstrating ADAM15 is required for pathological but not developmental neovascularization. Targeted gene deletion (knockout mice); mouse model of retinopathy of prematurity; heterotopic tumor implantation model; mRNA in situ hybridization for expression pattern Molecular and cellular biology High 12897135
2003 Recombinant soluble ADAM15, ADAM8, and ADAM28 (MDC-L) cleave synthetic peptide substrates with distinct specificities from ADAM17, and catalyze ectodomain shedding of CD23 (low-affinity IgE receptor); shedding requires proteolytically active enzyme and is inhibited by hydroxamic acid metalloprotease inhibitor. Peptide substrate library screening with purified recombinant enzymes; ectodomain shedding assay; catalytically inactive mutant control; metalloprotease inhibitor treatment The Journal of biological chemistry High 12777399
2005 ADAM15 deficiency in aging mice leads to accelerated osteoarthritic lesions; overexpression of ADAM15 in chondrocytes enhances adhesion to cartilage collagens (type II and VI) and promotes cell viability under serum starvation, indicating a chondroprotective/homeostatic role. ADAM15 knockout mice joint morphology analysis; stable transfection of T/C28a4 chondrocyte cell line; cell adhesion assays on fibronectin and collagens; cell viability under serum starvation Arthritis and rheumatism High 15818704
2005 ADAM15 overexpression in cancer cells suppresses integrin αvβ3-mediated adhesion to vitronectin and reduces cell motility in an RGD-dependent manner; mutation of RGD to SGA abrogates these effects. Stable overexpression of ADAM15 and RGD→SGA mutant in OV-MZ-6 ovarian cancer cells; cell adhesion assay on vitronectin; cell motility assay The international journal of biochemistry & cell biology Medium 15618016
2007 ADAM15 gene contains 23 exons; alternative splicing of cytoplasmic-domain-encoding exons 19, 20a/b, and 21a/b generates at least 13 splice variants in normal human tissues with different combinations of regulatory protein interaction motifs; a GC-rich, TATA-less promoter with functional activity located within a CpG island proximal to the translation start was confirmed by reporter assays. Genomic characterization; RT-PCR splice variant analysis in human tissues; luciferase reporter expression experiments BMC molecular biology Medium 17937806
2008 ADAM15 catalytically cleaves E-cadherin ectodomain; the soluble E-cadherin fragment binds to and stabilizes HER2/HER3 heterodimerization, activating ERK signaling and promoting breast cancer cell migration and proliferation. ADAM15 overexpression and shRNA knockdown in breast cancer cells; metalloprotease inhibitor treatment; catalytically inactive ADAM15 mutant; co-immunoprecipitation of sE-cad with HER2/HER3; ERK pathway activation assays The Journal of biological chemistry High 18434311
2008 ADAM15 knockdown in PC-3 prostate cancer cells reduces N-cadherin cleavage at the cell surface, decreases αv integrin and CD44 surface expression, abrogates MMP9 secretion/activity, reduces adhesion and migration through vascular endothelial monolayers, and attenuates bone metastasis in SCID mice. Lentiviral shRNA knockdown; FACS for surface markers; MMP9 activity assay; transendothelial migration assay; SCID mouse bone metastasis model Cancer research High 18281484
2008 ADAM15 splice variants differ only in their cytoplasmic domains; ADAM15A and ADAM15B variants show differential isoform-specific association with Nck, Src, and Brk tyrosine kinases (but equivalent binding to ERK, Grb2, and Tks5/Fish), leading to different effects on cell morphology, adhesion, migration, and invasion in breast cancer cells. Cloning and characterization of four alternatively spliced ADAM15 forms; GST pulldown assays; expression in MDA-MB-435 cells; adhesion, migration, invasion assays Molecular cancer research : MCR Medium 18296648
2008 ADAM15 suppresses cell motility by driving increased cell surface expression of integrin α5 (without directly interacting with α5β1) via downregulation of ERK1/2 phosphorylation; MEK inhibitor or ERK siRNA mimics this effect, and ADAM15 overexpression reduces lung metastatic nodules in a B16F10 model. CHO cell transfection with ADAM15; immunoprecipitation and immunofluorescence; MEK inhibitor PD98059; ERK1/2 siRNA; flow cytometry for integrin surface expression; B16F10 pulmonary metastasis model The international journal of biochemistry & cell biology Medium 18387333
2008 VEGF upregulates ADAM15 expression in retinal vascular endothelial cells in ischemic retina; ADAM15 and VEGF participate in an amplification loop, with ADAM15 increasing VEGF, VEGFR1, and VEGFR2 expression; ADAM15-deficient mice show reduced ischemia-induced retinal neovascularization and choroidal neovascularization. ADAM15 knockout mice; oxygen-induced retinopathy model; choroidal neovascularization model; VEGF knockdown in ischemic retina; VEGF overexpression in non-ischemic retina; mRNA quantification FASEB journal High 18381816
2009 Membrane-anchored ADAM15 sheds the ectodomain of fibroblast growth factor receptor 2iiib (FGFR2iiib) in cell-based assays; catalytically inactive ADAM15E→A mutant does not shed FGFR2iiib; shedding is inhibited by hydroxamate inhibitors (marimastat, TAPI-2, GM6001) and TIMP-3 (50 nM) but not TIMP-1 or TIMP-2; ADAM15 is not stimulated by phorbol esters or calcium ionophores. Overexpression of ADAM15 and catalytically inactive ADAM15E→A in cells; cell-based shedding assay; metalloprotease inhibitor panel; TIMP inhibitor panel The Biochemical journal High 19207106
2009 ADAM15 splice variant ADAM15B (containing a Src-binding cytoplasmic site) has enhanced catalytic activity (FGFR2iiib shedding) compared to ADAM15A; this enhanced activity depends on Src kinase, as it is abolished by Src kinase inhibitors and in Src-/- cells but restored by Src rescue. Cell-based shedding assay; Src kinase inhibitors; Src-/- cells and rescue; comparison of ADAM15A vs ADAM15B splice variants Cancer research High 19487280
2009 Alternative splicing of ADAM15 cytoplasmic exons profoundly influences selection of SH3-containing binding partners; isoforms containing exons 20 and/or 21 (with RxLPxxP motif) specifically bind nephrocystin; isoforms with the C-terminal proline cluster bind SNX33; these interactions were abolished by specific proline-cluster mutations. Co-precipitation from cell lysates; isoform-specific pull-downs; proline-cluster point mutations Journal of cellular biochemistry Medium 19718658
2010 ADAM15 promotes endothelial hyperpermeability and neutrophil transendothelial migration via Src/ERK1/2 signaling, independent of junction molecule (VE-cadherin) shedding; both wild-type and catalytically dead ADAM15 increase ERK1/2 phosphorylation and permeability; Src or ERK inhibition reverses ADAM15-induced effects. siRNA knockdown; overexpression of wild-type and catalytically dead ADAM15 in HUVECs; transendothelial electric resistance and albumin flux assays; neutrophil migration assay; pharmacological Src/ERK inhibitors; ERK1/2 phosphorylation by Western blot Cardiovascular research High 20189953
2010 An ADAM15 metalloprotease domain-derived peptide (ADoPep1 containing HWRR sequence) activates GRP78 on endothelial cell membranes under hypoxia, inducing angiogenesis via Akt phosphorylation and ERK1/2 activation (VEGF-independent); GRP78 siRNA blocks this effect. Synthetic peptide derived from ADAM15 sequence; cell proliferation, migration, tube formation assays; mouse hind limb ischemia model; siRNA against GRP78; Western blot for Akt/ERK phosphorylation; VEGFR2 phosphorylation assay Journal of vascular research Medium 20145413
2011 Loss of ADAM15 in osteoblasts leads to increased nuclear β-catenin translocation (with increased cytoplasmic/membrane degradation), upregulation of cyclin D1 and c-Jun (downstream Wnt targets), and increased osteoblast proliferation, alkaline phosphatase activity, nodule deposition, and mineralization, resulting in higher trabecular and cortical bone mass in ADAM15-/- mice. ADAM15-/- mice bone analysis; primary ADAM15-/- osteoblast cultures; β-catenin immunoreactivity (nuclear vs cytoplasmic); cyclin D1 and c-Jun Western blot Biological chemistry Medium 21801086
2012 ADAM15 is released from cells as an exosomal component in response to PKC activation; exosomal ADAM15 binds integrin αvβ3 in an RGD-dependent manner and suppresses vitronectin/fibronectin-induced cancer cell adhesion, growth, migration, and in vivo tumor growth; macrophage-derived ADAM15 exosomes have tumor inhibitory effects. Exosome isolation; phorbol ester (PMA/PKC activator) treatment; integrin αvβ3 binding assay; RGD mutation control; in vitro cancer cell adhesion, growth, migration assays; in vivo tumor growth model FASEB journal Medium 22505472
2012 ADAM15 deficiency attenuates LPS-induced acute lung injury: loss of ADAM15 in endothelial cells reduces hyperpermeability response to LPS and decreases neutrophil chemotactic transmigration; rescue expression of ADAM15 in Adam15-/- ECs restores neutrophil transendothelial migration. Adam15-/- mice; LPS-induced acute lung injury model; primary mouse lung endothelial cell culture; albumin flux and TER assays; neutrophil transmigration assay; ADAM15 rescue expression American journal of physiology. Lung cellular and molecular physiology High 23161886
2012 ADAM15 cytoplasmic domain directly binds the C-terminus of FAK; genotoxic stress (camptothecin) in ADAM15-transfected chondrocytes causes enhanced FAK phosphorylation at Tyr-397, Tyr-576, and Tyr-861 and concomitant Src activation; ADAM15 lacking its cytoplasmic tail loses this anti-apoptotic/FAK-activating property; Src binds FAK but not directly ADAM15, placing FAK as critical adaptor. Mammalian two-hybrid; pulldown; Far Western studies; chimeric IL-2Rα/ADAM15-cytoplasmic-tail construct; Western blot for phospho-FAK and phospho-Src; FAK/Src inhibitors The Journal of biological chemistry High 22544741
2013 ADAM15 interacts with TRIF (TLR adaptor) following TLR3/TLR4 stimulation; ADAM15 acts as a negative regulator of TRIF-mediated NF-κB and IFN-β signaling, and mediates proteolytic cleavage of TRIF; ADAM15 suppression enhances proinflammatory cytokine production in response to poly I:C, LPS, rhinovirus 16, and VSV. Co-immunoprecipitation of TRIF signaling complex; LC-MS protein identification; ADAM15 knockdown; NF-κB and IFN-β reporter assays; cytokine production measurement; TRIF cleavage assay Journal of immunology High 23365087
2013 ADAM15 adds to apoptosis resistance of rheumatoid arthritis synovial fibroblasts (RASFs) by activating Src/FAK signaling upon FasL stimulation; ADAM15 knockdown by siRNA increases caspase 3/7 activity and apoptosis upon camptothecin and FasL treatment; FasL-induced FAK/Src activation, PI3K activation, and NF-κB activity are ADAM15-dependent. siRNA knockdown of ADAM15 in RASFs; caspase 3/7 enzyme assays; annexin V staining; immunoblotting for phospho-FAK, phospho-Src, NF-κB; FAK inhibitor 14 and dasatinib treatment Arthritis and rheumatism Medium 23918525
2014 Catalytic activity of ADAM15 is NOT required for pathological retinal neovascularization in the OIR model (Adam15E>A knock-in mice show WT-equivalent neovascularization), but catalytic activity contributes to suppression of tumor implantation; ADAM15 can process FGFR2iiib but not several angiogenesis-related receptors in cell-based assays. Adam15E>A catalytic point-mutation knock-in mice; OIR model; heterotopic melanoma tumor implantation; cell-based shedding assays for multiple angiogenesis receptors Investigative ophthalmology & visual science High 25249606
2015 ADAM15 proteolytically cleaves and activates pro-MMP9 in vitro; ADAM15 interacts with MMP9 in vivo; ADAM15 upregulates MMP9 expression via MEK-ERK pathway activation; MMP9 knockdown attenuates ADAM15-driven lung cancer cell invasion. In vitro pro-MMP9 cleavage assay; co-immunoprecipitation (in vivo interaction); MMP9 Western blot; MEK-ERK pathway analysis; shRNA knockdown; invasion assay Oncology reports Medium 26323669
2018 ADAM15 converts FasL/Fas-death signals into prosurvival Src/FAK activation in RASFs via calmodulin (CaM) recruitment: FasL triggers CRAC/Orai1-dependent Ca2+ release, leading to CaM recruitment to Fas/CD95 and ADAM15 at the membrane, followed by Src-CaM engagement in the ADAM15/FAK complex; cytoplasmic ADAM15 domain is required for this prosurvival scaffolding. CaM-Sepharose pulldown; co-immunoprecipitation with anti-ADAM15 and anti-CD95 antibodies; recombinant CaM protein binding assay; immunofluorescence colocalization; CRAC/Orai1 inhibitor BTP-2; CaM inhibitor trifluoperazine; ADAM15 cytoplasmic domain deletion construct; caspase 3/7 assays; annexin V staining Arthritis & rheumatology High 30003689
2018 ADAM15 cytoplasmic domain transiently interacts with poly(A) binding protein 1 (PABP) via the PABP proline-rich linker during cell adhesion; this interaction recruits PABP to the cell membrane and promotes local mRNA translation (detected by puromycin-terminated polypeptides); loss of ADAM15 or its cytoplasmic tail reduces cell membrane-associated protein neosynthesis during adhesion. Co-immunoprecipitation; domain-mapping pulldown; immunostaining for PABP and puromycin-incorporated nascent proteins; ADAM15 siRNA and cytoplasmic-tail deletion mutant PloS one Medium 30265671
2019 ADAM15 isoform-specific, catalytic-function-dependent upregulation of Claudin-1 in breast cancer cells; ADAM15A (and to lesser extent C, E isoforms) increase Claudin-1 expression via PI3K/Akt/mTOR pathway; ADAM15 co-localizes with Claudin-1 and ZO1 at cell-cell junctions; ADAM15 forms a complex with ZO1/ZO2 as shown by co-immunoprecipitation. Isogenic cell panels expressing five ADAM15 variants (WT and catalytically inactive); shRNA knockdown; PI3K/Akt/mTOR pathway analysis; immunofluorescence; co-immunoprecipitation of ADAM15 with ZO1/ZO2 Scientific reports Medium 31467400
2019 KLF2 transcription factor (induced by laminar shear stress) drives ADAM15 expression in endothelial cells; physiologic shear stress upregulates ADAM15 (~4-fold mRNA, 5.6-fold protein); ADAM15 promotes endothelial cell survival under growth factor depletion or TNF stimulation; KLF2 siRNA prevents shear-stress-induced ADAM15 upregulation. Flow culture of primary endothelial cells; transcriptomic analysis; KLF2 overexpression and siRNA; simvastatin induction; ADAM15 shRNA knockdown; endothelial survival assays Journal of molecular and cellular cardiology Medium 31271758
2021 ADAM15 promotes a pro-inflammatory mechanosensing pathway in synovial fibroblasts: ADAM15 promotes cell membrane density of mechanosensitive TRPV4 calcium channels and reinforces Src-mediated pannexin-1 channel activation for ATP release; loss of ADAM15 abolishes Ca2+-dependent JNK activation, HOTAIR lncRNA downregulation, and sirtuin-1 upregulation in response to mechanical stimulation. ADAM15 loss-of-function in synovial fibroblasts; TRPV4 membrane density assay; pannexin-1 channel activity; JNK phosphorylation; HOTAIR and sirtuin-1 expression; Ca2+ signaling measurements Cells Medium 34685689
2021 ADAM15 participates in tick-borne encephalitis virus (TBEV) replication and assembly; ADAM15 subcellular localization changes during TBEV infection contributing to membrane reorganization and replication organelle formation; ADAM15 knockdown/knockout causes TBEV replication and assembly defects. siRNA knockdown; CRISPR knockout; RNA-seq; subcellular localization imaging; virus production and replication assays Journal of virology Medium 33208450
2022 ADAM15 is required for optimal collagen cross-linking and scar formation after myocardial infarction: Adam15-/- mice show higher rate of LV rupture post-MI, reduced fibrillar collagen density, lower insoluble collagen, reduced lysyl oxidase-1 (LOX-1) and fibronectin; ADAM15 loss reduces PAK1 levels in cardiac fibroblasts; PAK1 regulates fibronectin and LOX-1 expression. Adam15-/- mice; LAD ligation MI model; second harmonic generation imaging; soluble/insoluble collagen fractionation; LOX-1, fibronectin, PAK1 Western blot; primary cardiac fibroblast ischemia model; echocardiography Matrix biology High 34995785
2022 Loss of ADAM15 in pressure-overload cardiomyopathy (TAC) exacerbates eccentric hypertrophy and dilation through increased calcineurin/NFAT pathway activity; integrin-α7 expression increases more in Adam15-/- TAC hearts while integrin-laminin interaction decreases; calcineurin inhibition (cyclosporin-A) blocks excess hypertrophy in Adam15-/- TAC mice. Adam15-/- mice; TAC model; calcineurin activity assay; NFAT phosphorylation; integrin-α7 and laminin interaction; cyclosporin-A treatment; proteome profiling; echocardiography Hypertension High 36330793
2022 ADAM15 promotes FAK and EGFR signaling in lung cancer through interactions with integrins; integrin αV mediates ADAM15-FAK signaling; ADAM15 cooperates with CD151 to modulate integrin α3/α6-related EGFR signaling; miR-204-5p directly targets and suppresses ADAM15. Co-IP between ADAM15 and integrins; CD151 co-expression studies; FAK/EGFR signaling pathway assays; luciferase reporter assay for miR-204-5p targeting; nude mouse xenograft Cell death & disease Medium 35597804
2025 ADAM15 loss abrogates necroptosis induced by death ligands (TNF, TRAIL, FasL, TL1a) and a BH3 mimetic; loss of ADAM15 results in enhanced basal caspase-8 activity (non-cytotoxic) and partial RIPK1 degradation; ADAM15 is found in intracellular lysosomal compartments and enhanced TNF-R1 surface expression in ADAM15-KO cells suggests TNF-R1 as a potential substrate. CRISPR/Cas9 adam15 knockout in U937 and Jurkat cells; necroptosis/apoptosis assays; caspase-8 enzyme assay; Western blot for RIPK1; flow cytometry for TNF-R1 surface expression; immuno-magnetic fractionation for subcellular localization; bottom-up proteome analysis Cell communication and signaling Medium 41340056
2025 ADAM15 and N-cadherin (NCAD) co-localize in adherens junctions of synovial fibroblasts; mechanical strain triggers a pathway through this complex involving PAK2 phosphorylation and co-recruitment of Nck; this leads to downregulation of lncRNA H19 and miR-130a-3p, upregulation of cadherin-11, and enhanced cell invasion. Immunofluorescence co-localization; co-immunoprecipitation of ADAM15/NCAD complex; PAK2 phosphorylation assay; Nck recruitment assay; lncRNA H19 and miR-130a-3p expression; invasion assay Scientific reports Medium 40118917

Source papers

Stage 0 corpus · 96 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Specific interaction of the recombinant disintegrin-like domain of MDC-15 (metargidin, ADAM-15) with integrin alphavbeta3. The Journal of biological chemistry 196 9516430
1999 Interaction of metargidin (ADAM-15) with alphavbeta3 and alpha5beta1 integrins on different haemopoietic cells. Journal of cell science 177 9914169
2008 The ectodomain shedding of E-cadherin by ADAM15 supports ErbB receptor activation. The Journal of biological chemistry 160 18434311
2003 Potential role for ADAM15 in pathological neovascularization in mice. Molecular and cellular biology 154 12897135
1999 Interaction of the metalloprotease disintegrins MDC9 and MDC15 with two SH3 domain-containing proteins, endophilin I and SH3PX1. The Journal of biological chemistry 149 10531379
2005 The disintegrin-metalloproteinases ADAM9, ADAM12, and ADAM15 are upregulated in gastric cancer. International journal of oncology 147 15586220
2003 Catalytic activity of ADAM8, ADAM15, and MDC-L (ADAM28) on synthetic peptide substrates and in ectodomain cleavage of CD23. The Journal of biological chemistry 147 12777399
1998 Intracellular maturation of the mouse metalloprotease disintegrin MDC15. The Journal of biological chemistry 137 9748307
2001 Phosphorylation-dependent interactions between ADAM15 cytoplasmic domain and Src family protein-tyrosine kinases. The Journal of biological chemistry 94 11741929
2006 ADAM15 disintegrin is associated with aggressive prostate and breast cancer disease. Neoplasia (New York, N.Y.) 86 16756724
2008 ADAM15 supports prostate cancer metastasis by modulating tumor cell-endothelial cell interaction. Cancer research 74 18281484
2009 ADAM-9, ADAM-15, and ADAM-17 are upregulated in macrophages in advanced human atherosclerotic plaques in aorta and carotid and femoral arteries--Tampere vascular study. Annals of medicine 68 19253070
2010 ADAM15 regulates endothelial permeability and neutrophil migration via Src/ERK1/2 signalling. Cardiovascular research 65 20189953
2007 ADAM-15: a metalloprotease that mediates inflammation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 59 17905725
2001 ADAM15 overexpression in NIH3T3 cells enhances cell-cell interactions. Experimental cell research 56 11697891
2003 Increased expression of disintegrin-metalloproteinases ADAM-15 and ADAM-9 following upregulation of integrins alpha5beta1 and alphavbeta3 in atherosclerosis. Journal of cellular biochemistry 55 12858346
2012 Exosome release of ADAM15 and the functional implications of human macrophage-derived ADAM15 exosomes. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 53 22505472
2005 Homeostatic effects of the metalloproteinase disintegrin ADAM15 in degenerative cartilage remodeling. Arthritis and rheumatism 53 15818704
2008 Distinct functions of natural ADAM-15 cytoplasmic domain variants in human mammary carcinoma. Molecular cancer research : MCR 51 18296648
2005 ADAM15 decreases integrin alphavbeta3/vitronectin-mediated ovarian cancer cell adhesion and motility in an RGD-dependent fashion. The international journal of biochemistry & cell biology 50 15618016
2002 ADAM15 is an adherens junction molecule whose surface expression can be driven by VE-cadherin. Experimental cell research 48 12243749
2009 Characterization of the catalytic activity of the membrane-anchored metalloproteinase ADAM15 in cell-based assays. The Biochemical journal 43 19207106
2004 ADAM-15 inhibits wound healing in human intestinal epithelial cell monolayers. American journal of physiology. Gastrointestinal and liver physiology 42 15358598
2005 Expression of ADAM15 in lung carcinomas. Virchows Archiv : an international journal of pathology 41 15756594
2014 MicroRNA-147b regulates vascular endothelial barrier function by targeting ADAM15 expression. PloS one 40 25333931
1999 Up-regulation of MDC15 (metargidin) messenger RNA in human osteoarthritic cartilage. Arthritis and rheumatism 39 10513811
2005 Expression of ADAM15 in rheumatoid synovium: up-regulation by vascular endothelial growth factor and possible implications for angiogenesis. Arthritis research & therapy 36 16277668
2001 Highly enhanced expression of the disintegrin metalloproteinase MDC15 (metargidin) in rheumatoid synovial tissue. Arthritis and rheumatism 34 11592366
2010 Activation of GRP78 on endothelial cell membranes by an ADAM15-derived peptide induces angiogenesis. Journal of vascular research 33 20145413
2013 TRIF-mediated TLR3 and TLR4 signaling is negatively regulated by ADAM15. Journal of immunology (Baltimore, Md. : 1950) 32 23365087
2006 ADAM15 upregulation and interaction with multiple binding partners in inflammatory bowel disease. Laboratory investigation; a journal of technical methods and pathology 30 16894352
2015 ADAM15 targets MMP9 activity to promote lung cancer cell invasion. Oncology reports 29 26323669
2012 ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice. American journal of physiology. Lung cellular and molecular physiology 28 23161886
2009 The role of the disintegrin metalloproteinase ADAM15 in prostate cancer progression. Journal of cellular biochemistry 28 19229865
2008 ADAM15 suppresses cell motility by driving integrin alpha5beta1 cell surface expression via Erk inactivation. The international journal of biochemistry & cell biology 28 18387333
2016 ADAM15 Is Functionally Associated with the Metastatic Progression of Human Bladder Cancer. PloS one 27 26930657
2009 Src stimulates fibroblast growth factor receptor-2 shedding by an ADAM15 splice variant linked to breast cancer. Cancer research 27 19487280
2008 An Adam15 amplification loop promotes vascular endothelial growth factor-induced ocular neovascularization. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 27 18381816
2010 ADAM15 exerts an antiapoptotic effect on osteoarthritic chondrocytes via up-regulation of the X-linked inhibitor of apoptosis. Arthritis and rheumatism 26 20213810
2007 ADAM15 gene structure and differential alternative exon use in human tissues. BMC molecular biology 25 17937806
2004 Aberrant alternative exon use and increased copy number of human metalloprotease-disintegrin ADAM15 gene in breast cancer cells. Genes, chromosomes & cancer 25 15384173
2022 Integrin α3/α6 and αV are implicated in ADAM15-activated FAK and EGFR signalling pathway individually and promote non-small-cell lung cancer progression. Cell death & disease 24 35597804
2019 ADAM15 mediates upregulation of Claudin-1 expression in breast cancer cells. Scientific reports 24 31467400
2019 The metalloproteinase ADAM15 is upregulated by shear stress and promotes survival of endothelial cells. Journal of molecular and cellular cardiology 23 31271758
2008 Presence, processing, and localization of mouse ADAM15 during sperm maturation and the role of its disintegrin domain during sperm-egg binding. Reproduction (Cambridge, England) 22 18390692
2007 Inhibition of airway smooth muscle adhesion and migration by the disintegrin domain of ADAM-15. American journal of respiratory cell and molecular biology 22 17575078
2013 ADAM15 adds to apoptosis resistance of synovial fibroblasts by modulating focal adhesion kinase signaling. Arthritis and rheumatism 21 23918525
2009 Alternative splicing of ADAM15 regulates its interactions with cellular SH3 proteins. Journal of cellular biochemistry 18 19718658
2020 The microRNA miR-3174 Suppresses the Expression of ADAM15 and Inhibits the Proliferation of Patient-Derived Bladder Cancer Cells. OncoTargets and therapy 17 32547057
2017 Overexpression of the A Disintegrin and Metalloproteinase ADAM15 is linked to a Small but Highly Aggressive Subset of Prostate Cancers. Neoplasia (New York, N.Y.) 16 28282546
2013 Molecular implication of ADAM-15 and -17 in intrauterine adhesions. European journal of obstetrics, gynecology, and reproductive biology 16 23910172
2009 The therapeutic potential of ADAM15. Current pharmaceutical design 16 19601833
2005 ADAM9, ADAM10, and ADAM15 mRNA levels in the rat brain after kainic acid-induced status epilepticus. Brain research. Molecular brain research 16 15950787
2022 ADAM15 is required for optimal collagen cross-linking and scar formation following myocardial infarction. Matrix biology : journal of the International Society for Matrix Biology 15 34995785
2012 Differential expression of ADAM15 and ADAM17 metalloproteases in the rat brain after severe hypobaric hypoxia and hypoxic preconditioning. Neuroscience research 15 22230263
2012 ADAM15 protein amplifies focal adhesion kinase phosphorylation under genotoxic stress conditions. The Journal of biological chemistry 15 22544741
2010 ADAM-15 disintegrin-like domain structure and function. Toxins 15 22069559
2020 ADAM15 expression is increased in lung CD8+ T cells, macrophages, and bronchial epithelial cells in patients with COPD and is inversely related to airflow obstruction. Respiratory research 14 32677970
2013 Recombinant disintegrin domain of ADAM15 inhibits the proliferation and migration of Bel-7402 cells. Biochemical and biophysical research communications 14 23688428
2020 Interleukin 13 (IL-13)-regulated expression of the chondroprotective metalloproteinase ADAM15 is reduced in aging cartilage. Osteoarthritis and cartilage open 13 33381768
2014 Characterization of oxygen-induced retinopathy in mice carrying an inactivating point mutation in the catalytic site of ADAM15. Investigative ophthalmology & visual science 13 25249606
2010 ADAM15 expression is downregulated in melanoma metastasis compared to primary melanoma. Biochemical and biophysical research communications 13 20851104
2006 Integrin binding characteristics of the disintegrin-like domain of ADAM-15. Thrombosis and haemostasis 13 17080222
2018 ADAM15 in Apoptosis Resistance of Synovial Fibroblasts: Converting Fas/CD95 Death Signals Into the Activation of Prosurvival Pathways by Calmodulin Recruitment. Arthritis & rheumatology (Hoboken, N.J.) 12 30003689
2009 ADAM15 modulates outside-in signalling in chondrocyte-matrix interactions. Journal of cellular and molecular medicine 12 18774960
2021 ADAM15 Participates in Tick-Borne Encephalitis Virus Replication. Journal of virology 11 33208450
2013 ADAM15 is involved in MICB shedding and mediates the effects of gemcitabine on MICB shedding in PANC-1 pancreatic cancer cells. Molecular medicine reports 11 23314034
2021 NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis. Cancer cell international 10 34247598
2015 The ADAM15 ectodomain is shed from secretory exosomes. BMB reports 10 25208722
2004 Expression of splice variants of the human ADAM15 gene and strong interaction between the cytoplasmic domain of one variant and Src family proteins Lck and Hck. Pathobiology : journal of immunopathology, molecular and cellular biology 10 15263807
2011 Lack of ADAM15 in mice is associated with increased osteoblast function and bone mass. Biological chemistry 9 21801086
2006 Novel function of human ADAM15 disintegrin-like domain and its derivatives in platelet aggregation. Thrombosis research 9 16797059
2019 Endothelin 1, NF-κB, and ADAM-15 expression in diabetic foot wounds. Bratislavske lekarske listy 8 30685994
2012 Role of ADAM-15 in wound healing and melanoma development. Experimental dermatology 8 22621184
2022 Quantitative Proteomics Reveals That ADAM15 Can Have Proteolytic-Independent Functions in the Steady State. Membranes 7 35736286
2009 Expression of ADAM-15 in rat myocardial infarction. International journal of experimental pathology 7 19563617
2022 Loss of ADAM15 Exacerbates Transition to Decompensated Myocardial Hypertrophy and Dilation Through Activation of the Calcineurin Pathway. Hypertension (Dallas, Tex. : 1979) 6 36330793
2013 Helping Eve overcome ADAM: G-quadruplexes in the ADAM-15 promoter as new molecular targets for breast cancer therapeutics. Molecules (Basel, Switzerland) 6 24317528
2023 Identification of membrane proteins regulated by ADAM15 by SUSPECS proteomics. Frontiers in molecular biosciences 5 37388246
2014 ADAM15 participates in fertilization through a physical interaction with acrogranin. Reproduction (Cambridge, England) 5 25392190
2025 Mechanical forces trigger invasive behavior in synovial fibroblasts through N-cadherin/ADAM15 -dependent modulation of LncRNA H19. Scientific reports 4 40118917
2023 Loss of cancer cell-derived ADAM15 alters the tumor microenvironment in colorectal tumors. International journal of cancer 4 37602921
2021 A Novel Pro-Inflammatory Mechanosensing Pathway Orchestrated by the Disintegrin Metalloproteinase ADAM15 in Synovial Fibroblasts. Cells 4 34685689
2009 Identification of binding peptides of the ADAM15 disintegrin domain using phage display. Journal of biosciences 4 19550037
2008 Screening cellular proteins involved in the anti-proliferative effect of the ADAM15 disintegrin domain in murine melanoma cells. Oncology reports 4 18695922
2022 Detection of ADAM15 in urine from patients with bladder cancer. Analytical biochemistry 3 35810783
2010 Characterisation of the human ADAM15 promoter. Nephron. Experimental nephrology 3 21196774
2024 Digital spatial profiling of segmental outflow regions in trabecular meshwork reveals a role for ADAM15. PloS one 2 38394161
2018 Cell adhesion-induced transient interaction of ADAM15 with poly(A) binding protein at the cell membrane colocalizes with mRNA translation. PloS one 2 30265671
2008 [Improving production and bioactivity of recombinant human disintegrin domain of ADAM15 (rhADAM15) in Escherichia coli]. Wei sheng wu xue bao = Acta microbiologica Sinica 2 18956757
2025 Loss of ADAM15 prevents necroptosis induction by partial RIPK1 degradation due to enhanced TNF-R1 surface expression and basal caspase-8 activation. Cell communication and signaling : CCS 1 41340056
2024 ADAM15 in Fibroblasts: Improving the Matrix Remodeling by Blocking the Action of Transforming Growth Factor-β1. Annals of clinical and laboratory science 1 39048163
2026 ADAM15 promotes the progression and metastasis of hepatocellular carcinoma by activating the JNK/p38 pathway. Scientific reports 0 41986445
2025 TFDP1 overexpression promotes apoptosis of nucleus pulposus cells in intervertebral disc degeneration through regulating ADAM15/MMP9 axis. General physiology and biophysics 0 39815900
2025 A Disintegrin and Metalloprotease 15 (ADAM15) as a Potential Predictor of Distant Metastasis in Colorectal Cancer (CRC). Journal of clinical medicine 0 40725774
2024 Loss of ADAM15 in female mice does not worsen pressure overload cardiomyopathy, independent of ovarian hormones. American journal of physiology. Heart and circulatory physiology 0 38607341