Affinage

ADAM19

Disintegrin and metalloproteinase domain-containing protein 19 · UniProt Q9H013

Length
955 aa
Mass
105.0 kDa
Annotated
2026-04-28
58 papers in source corpus 24 papers cited in narrative 24 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ADAM19 is a membrane-anchored zinc-dependent metalloprotease of the ADAM family that cleaves diverse substrates—including neuregulin-1 beta (NRG-β1), amyloid precursor protein (APP), parathyroid hormone receptor (PTHR1), and the (pro)renin receptor—primarily within the Golgi apparatus and lipid rafts, and also performs non-proteolytic functions through protein–protein interactions (PMID:11116142, PMID:15030395, PMID:17352738, PMID:38331475, PMID:21270819, PMID:17112471). Its catalytic maturation involves furin-mediated prodomain removal followed by disulfide-bond-regulated autolytic processing within the cysteine-rich domain, and its activity is sensitive to hydroxamic acid metalloprotease inhibitors but resistant to TIMPs 1–3 (PMID:15242783, PMID:12682046). Independent of its protease activity, ADAM19 interacts with EphA4 to block ephrin-A5 endocytosis at neuromuscular junctions and stabilizes ADAM13 to sustain canonical Wnt signaling during neural crest specification (PMID:18830404, PMID:29540504). Loss-of-function studies in mice establish causal roles in Schwann cell remyelination via Akt/Krox-20 signaling, pulmonary mechanics and inflammatory responses, and metabolic regulation including insulin sensitivity (PMID:19049978, PMID:39153120, PMID:28265178).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2000 High

    Identifying ADAM19 as a NRG-β1 sheddase established its first defined substrate and showed it acts intracellularly rather than at the cell surface, distinguishing it from other ADAMs.

    Evidence Overexpression/dominant-negative mutants in L929 cells with secretory pathway inhibitors and NRG isoform comparisons

    PMID:11116142

    Open questions at the time
    • Intracellular compartment of cleavage not yet identified
    • Endogenous validation in neuronal tissue lacking
  2. 2001 Medium

    Demonstration that ADAM19 cleaves α2-macroglobulin and is blocked by chelating agents but not TIMPs began to define its inhibitor profile and broad substrate range.

    Evidence Recombinant ADAM19 with co-immunoprecipitation and metalloprotease inhibitor panel

    PMID:11162584

    Open questions at the time
    • α2-macroglobulin cleavage not confirmed in vivo
    • Physiological relevance of this substrate unclear
  3. 2002 Medium

    Identification of ArgBP1 as a cytoplasmic tail interactor via SH3-ligand sites, plus discovery of a truncated isoform (meltrin β mini) that induces neurite outgrowth, revealed that ADAM19 signals through its intracellular domain and possesses isoform-specific non-proteolytic functions.

    Evidence Yeast two-hybrid/GST-pulldown for ArgBP1; RT-PCR cloning and overexpression of meltrin β mini in neuronal cells

    PMID:12463424 PMID:12482604

    Open questions at the time
    • Functional significance of ArgBP1 interaction uncharacterized
    • Neurite outgrowth mechanism of meltrin β mini undefined
    • No in vivo validation of isoform-specific roles
  4. 2003 High

    Reconstitution of soluble ADAM19 with defined peptide substrates (TNF-α, TRANCE, KL-1 sites) and inhibitor profiling (sensitive to BB94, resistant to TIMPs 1–3) established its enzymatic specificity and showed it indirectly regulates KitL1 shedding rather than acting as its direct sheddase.

    Evidence In vitro protease assays with recombinant soluble ADAM19; peptide cleavage; COS-7 and ADAM-knockout MEF studies

    PMID:12682046

    Open questions at the time
    • Direct in vivo substrates versus indirect regulatory targets not fully delineated
    • Structural basis for TIMP resistance unknown
  5. 2004 High

    Mapping autolytic processing to a specific site in the cysteine-rich domain regulated by disulfide bonds and pH resolved how ADAM19 matures after furin-mediated prodomain removal.

    Evidence Site-directed mutagenesis of cysteines, DTT/pH manipulation, and Ilomastat inhibition in stable MDCK transfectants

    PMID:15242783

    Open questions at the time
    • Structural model of cysteine-rich domain lacking
    • Whether autolysis is required for all substrates untested
  6. 2004 High

    Localizing NRG-β1 shedding to lipid rafts and showing that ADAM19's membrane-anchoring region is required for raft targeting linked its subcellular positioning to substrate access.

    Evidence Lipid raft fractionation and deletion mutant analysis in neuronal cells

    PMID:15030395

    Open questions at the time
    • Raft-targeting determinants in the membrane anchor not mapped at residue level
  7. 2007 High

    Fluorescence correlation spectroscopy in living cells pinpointed the Golgi as the compartment where ADAM19 converts membrane-anchored NRG-β1 to soluble form, distinguishing its spatial activity from ADAM17 at the cell surface.

    Evidence Subcellular fractionation plus live-cell FCS with GFP-NRG-β1 in neurons

    PMID:17352738

    Open questions at the time
    • Mechanism of ADAM19 retention/recycling within the Golgi unresolved
  8. 2008 High

    Three concurrent studies expanded ADAM19's roles beyond proteolysis: it interacts with EphA4 to block ephrin endocytosis at the NMJ independently of its metalloprotease activity, it promotes Schwann cell remyelination via axon–Schwann cell Akt/Krox-20 signaling, and its knockdown in Xenopus disrupts neural crest migration and pAkt levels.

    Evidence KO mouse NMJ analysis with protease-dead mutants; sciatic nerve crush in KO mice with pAkt/Krox-20 readouts; Xenopus morpholino knockdown with marker analysis

    PMID:18830404 PMID:19027850 PMID:19049978

    Open questions at the time
    • Identity of the NRG/ErbB ligand processed by ADAM19 in Schwann cell signaling not confirmed
    • Whether EphA4 interaction and NRG shedding are coordinated at the NMJ unknown
  9. 2011 High

    Identifying the (pro)renin receptor as a Golgi-resident ADAM19 substrate, with secreted NTF activating prorenin, connected ADAM19 to renin-angiotensin signaling.

    Evidence Overexpression/dominant-negative in CHO cells; furin-deficient LoVo cell controls

    PMID:21270819

    Open questions at the time
    • In vivo confirmation of ADAM19 as the physiological (P)RR sheddase not yet shown
  10. 2017 Medium

    Neutralizing ADAM19 in diet-induced obese mice improved insulin sensitivity and reduced liver TNF-α, establishing a metabolic function and linking its TNF-α shedding capability to obesity phenotypes.

    Evidence In vivo neutralizing antibody in mouse obesity model; HOMA-IR and liver TNF-α measurement

    PMID:28265178

    Open questions at the time
    • Direct substrate(s) responsible for metabolic effects not identified
    • Antibody specificity for ADAM19 over other ADAMs not fully validated
  11. 2018 High

    Discovery that ADAM19 stabilizes ADAM13 by preventing its proteasomal degradation to sustain Wnt signaling during neural crest specification established a non-catalytic chaperone-like function for an ADAM protease.

    Evidence Xenopus morpholino knockdown; Co-IP of ADAM19–ADAM13; rescue with proteasome-resistant ADAM13 mutants; Wnt reporter

    PMID:29540504

    Open questions at the time
    • Whether this stabilization mechanism operates in mammals unknown
    • Structural basis of ADAM19–ADAM13 interaction undefined
  12. 2024 High

    Mass spectrometry mapping of the PTHR1 cleavage site and demonstration that a brachydactyly type E (BDE)-associated ADAM19 mutant cannot cleave PTHR1 linked ADAM19 loss-of-function to a Mendelian skeletal phenotype and showed cleavage biases PTHR1 signaling from Gs toward Gq/β-arrestin2.

    Evidence Linkage/WGS in BDE pedigree; in vitro cleavage with WT vs. mutant ADAM19; MS site mapping; Gq/Gs and β-arrestin2 assays

    PMID:38331475

    Open questions at the time
    • Whether ADAM19-PTHR1 axis explains the full BDE phenotype in vivo not demonstrated
    • Crystal structure of ADAM19–PTHR1 complex unavailable
  13. 2024 High

    Adam19 knockout mice showed altered pulmonary mechanics and attenuated LPS-induced neutrophil influx with negative enrichment for TNF signaling, causally establishing ADAM19 in lung function and inflammation.

    Evidence Knockout mouse flexiVent measurements; BAL analysis after LPS challenge; RNA-seq/GSEA

    PMID:39153120

    Open questions at the time
    • Specific pulmonary substrates of ADAM19 driving altered elastance not identified
  14. 2025 Medium

    ADAM19 knockdown or pharmacological inhibition reduced senescence-associated secretory phenotype (SASP) factors and senescence markers in human fibroblasts, suggesting a role in cellular senescence and age-related inflammation.

    Evidence siRNA in human primary fibroblasts; batimastat-94 in mice; secretome proteomics; SA-β-gal assay

    PMID:40117561

    Open questions at the time
    • Batimastat-94 is not ADAM19-specific; contribution of other metalloproteases not excluded
    • Mechanism linking ADAM19 cleavage to SASP factor regulation unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions include the structural basis for ADAM19's TIMP resistance, the full in vivo substrate repertoire in specific tissues, whether its non-proteolytic functions (ADAM13 stabilization, EphA4 interaction) are conserved in mammals, and the identity of the specific substrates mediating its pulmonary and metabolic phenotypes.
  • No crystal structure of ADAM19 catalytic or cysteine-rich domains
  • Comprehensive in vivo substrate identification by unbiased proteomics lacking
  • Mammalian validation of ADAM13-stabilization mechanism absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 7 GO:0016787 hydrolase activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005794 Golgi apparatus 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-112316 Neuronal System 2 R-HSA-168256 Immune System 1 R-HSA-392499 Metabolism of proteins 1
Partners
ADAM13APPATP6AP2CRIP2EPHA4NRG1PTH1RSORBS2

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 ADAM19 (meltrin beta) participates in the proteolytic processing of membrane-anchored neuregulin-1 beta (NRG-beta1), with preference for beta-type NRGs over alpha-type; overexpression potentiates NRG-beta1 processing while protease-deficient mutants exert dominant negative effects; processing occurs intracellularly rather than at the cell surface. Overexpression of wild-type and protease-deficient dominant-negative mutants in L929 cells; secretory pathway inhibitor treatment; western blot for extracellular domain release The Journal of biological chemistry High 11116142
2003 Recombinant soluble ADAM19 exhibits metalloprotease activity (autocatalytic tag removal, cleavage of myelin basic protein and insulin B chain), is inhibited by hydroxamic acid metalloprotease inhibitor BB94 but not by TIMPs 1-3, cleaves peptides corresponding to TNF-alpha, TRANCE, and KL-1 cleavage sites in vitro, and negatively regulates KL-1 shedding in cells rather than acting directly as its sheddase. In vitro protease assay with recombinant soluble ADAM19; peptide cleavage assays; BB94 and TIMP inhibition assays; COS-7 and MEF overexpression/knockout studies The Journal of biological chemistry High 12682046
2001 Human ADAM19 forms a complex with and cleaves alpha-2 macroglobulin; its proteolytic activity is blocked by 1,10-phenanthroline, EDTA, EGTA, and a synthetic MMP inhibitor but not by TIMP-1 or TIMP-2. Recombinant protein expression in human cells; co-immunoprecipitation/complex detection; metalloprotease inhibitor assays Biochemical and biophysical research communications Medium 11162584
2004 ADAM19-mediated ectodomain shedding of NRG-beta1 occurs specifically in lipid rafts of neurons; the membrane-anchoring region of ADAM19 is required for its lipid raft localization, and NRG-beta1 shedding is not enhanced if ADAM19 cannot reach the lipid rafts. Lipid raft fractionation; deletion mutant analysis of membrane-anchoring region; NRG-beta1 shedding assay in neuronal cells Journal of neurochemistry High 15030395
2007 ADAM19 (meltrin beta) mediates ectodomain shedding of NRG-beta1 in the Golgi apparatus (not at the cell surface); subcellular fractionation showed soluble NRG-beta1 generated by ADAM19 is recovered in Golgi-enriched fractions, whereas TACE/ADAM17-cleaved NRG-beta1 is in lighter fractions; fluorescence correlation spectroscopy in living cells confirmed conversion of GFP-tagged NRG-beta1 from membrane-anchored to soluble form within the Golgi. Subcellular fractionation; fluorescence correlation spectroscopy (FCS) in living cells; localization by immunofluorescence in developing sensory neurons Genes to cells : devoted to molecular & cellular mechanisms High 17352738
2007 ADAM19 overexpression reduces the amount of Endo-H-resistant mature KitL1 available for phorbol ester-stimulated ectodomain shedding, thereby indirectly decreasing ADAM17-mediated KitL1 shedding; ADAM17, not ADAM19, is the major phorbol-ester-stimulated sheddase of KitL1 and KitL2. Overexpression of ADAM family members in COS-7 cells; Endo-H glycosylation assay; phorbol ester stimulation; KitL shedding assay in MEFs from ADAM-knockout mice Journal of cell science High 17344430
2006 ADAM19 has constitutive alpha-secretase activity for amyloid precursor protein (APP): overexpression in HEK293 cells increases sAPP-alpha release; RNAi knockdown in A172 cells reduces constitutive sAPP-alpha by ~21%; no regulated (PMA-stimulated) activity was detected. Overexpression in HEK293 cells with sAPP-alpha ELISA/western blot; RNAi knockdown in A172 cells; phorbol ester (PMA) stimulation assay Biochemical and biophysical research communications Medium 17112471
2004 Human ADAM19 autolytic processing within its cysteine-rich domain (at Glu586-Ser587) is regulated by disulfide bonds; DTT treatment and acidic pH (6.5) block autolytic processing, while pH 8.5 promotes it; specific cysteine residues (Cys605, Cys633, Cys639, Cys643) in the C-fragment are partially responsible for covalent association between N- and C-fragments; ADAM19 is activated by furin-mediated prodomain cleavage followed by intramolecular autolysis. Stable MDCK transfectants expressing soluble ADAM19; DTT and pH manipulation; site-directed mutagenesis of cysteine residues; Ilomastat/GM6001 inhibition; identification of new autolytic cleavage site Experimental cell research High 15242783
2011 ADAM19 is the protease responsible for cleaving the (pro)renin receptor ((P)RR) in the Golgi, generating an amino-terminal fragment (NTF-(P)RR) that is secreted into the extracellular space; transfected ADAM19 evokes (P)RR shedding and dominant-negative ADAM19 suppresses it; furin is not responsible for this cleavage; secreted NTF-(P)RR induces prorenin activity. Overexpression and dominant-negative ADAM19 in CHO cells; western blot for (P)RR fragments; immunofluorescence localization; furin-deficient LoVo cells and furin inhibitor controls Hypertension research : official journal of the Japanese Society of Hypertension High 21270819
2008 In Xenopus, ADAM19 knockdown decreases phospho-AKT (a downstream target of EGF signaling), reduces neural markers (N-tubulin, NRP1), neural crest markers, and disrupts cranial neural crest migration in a cell-autonomous manner; somite organization and fibronectin localization at intersomitic boundaries are also perturbed. Morpholino knockdown in Xenopus embryos; targeted (cell-autonomous) knockdown; phospho-AKT western blot; in situ hybridization for marker genes; EGF receptor inhibitor treatment Mechanisms of development Medium 19027850
2008 ADAM19 (meltrin beta) interacts with EphA4 in developing motor neurons; coexpression of ADAM19 and EphA4 blocks vesicular internalization of ephrin-A5-EphA4 complexes independently of ADAM19's protease activity, stabilizing ephrin-A5-EphA4 interaction and contributing to neuromuscular junction (NMJ) formation; meltrin-beta-deficient mice show broader AChR alpha mRNA distribution and excess motor nerve terminal sprouting. Co-immunoprecipitation of ADAM19 and EphA4; knockout mouse analysis (AChR distribution, nerve sprouting); microarray; protease-dead mutant analysis of ephrin endocytosis PloS one High 18830404
2008 ADAM19 (meltrin beta) promotes Schwann cell differentiation and remyelination after sciatic nerve crush injury; ADAM19-deficient mice show delayed Krox-20 activation and myelin protein expression; ADAM19 modulates juxtacrine axon-Schwann cell signaling that activates Akt (but not Erk) phosphorylation, which is required for Krox-20 expression and myelination. Sciatic nerve crush in ADAM19 knockout mice; morphometric analysis of remyelination; western blot for pAkt, pErk, Krox-20, myelin proteins; membrane-loaded Schwann cell Akt activation assay The Journal of biological chemistry High 19049978
2002 The cytoplasmic tail of ADAM19 interacts with ArgBP1 through ADAM19's SH3 ligand-binding sites and the P4 region of ArgBP1; this interaction is specific (ArgBP1 does not bind ADAM22, ADAM29, or ADAM9); beta-COP, ubiquitin, and a novel protein also interact with the ADAM19 cytoplasmic tail. Yeast two-hybrid screen of human fetal brain cDNA library; GST-pulldown confirmation; deletion mutant mapping of interaction domains Molecular biology reports Medium 12463424
2010 ADAM19 undergoes autolytic processing activated by LPS stimulation, and through its disintegrin and cysteine-rich domains interacts with and promotes non-classical secretion of cysteine-rich protein 2 (CRIP2); CRIP2 secretion increases with ADAM19 autolytic processing and decreases upon ADAM19 knockdown. Yeast two-hybrid screen using ADAM19 extracellular domain; LPS stimulation of cells; western blot for ADAM19 processing and CRIP2 secretion; ADAM19 siRNA knockdown Biochemical and biophysical research communications Medium 20460109
2018 In Xenopus, ADAM19 functions non-proteolytically in neural crest specification by physically interacting with its close paralog ADAM13 and inhibiting its proteasomal degradation, thereby sustaining Wnt signaling at the neural plate border; canonical Wnt signaling activity is severely downregulated upon ADAM19 knockdown, and ectopic expression of proteasome-resistant ADAM13 mutants rescues neural crest induction via Wnt signaling. Morpholino knockdown in Xenopus; Co-immunoprecipitation of ADAM19 with ADAM13; proteasome inhibitor rescue; epistasis with stabilized ADAM13 mutants; Wnt reporter assay Development (Cambridge, England) High 29540504
2002 A novel ADAM19 splice isoform (meltrin beta mini) lacking the prodomain, metalloprotease, and disintegrin domains induces neurite outgrowth in neuronal cells, a function not shared by full-length ADAM19, suggesting a distinct non-proteolytic role mediated by the remaining domains. RT-PCR identification of isoform; cDNA/genomic sequence comparison; overexpression of meltrin beta mini vs. full-length ADAM19 in neuronal cell lines FEBS letters Medium 12482604
2009 ADAM19 overexpression in JEG-3 trophoblast cells reduces cell invasion and increases cell adhesiveness and E-cadherin expression without changing beta-catenin expression. ADAM19 overexpression in JEG-3 choriocarcinoma cells; invasion assay; adhesion assay; western blot for E-cadherin and beta-catenin Science in China. Series C, Life sciences Low 19727588
2013 ADAM19 and phospho-ErbB3 co-localize in co-cultured neural NG108-15 cells; electrical stimulation increases ADAM19 precursor and activated form, phospho-ErbB3, and ERK1 levels in a stimulation duration-dependent manner, implicating ADAM19/neuregulin/ErbB signaling in NMJ formation. Immunofluorescence localization; immunoblotting for ADAM19, pErbB3, ERK1, synapsin 1 in electrically stimulated co-cultures Neuroscience letters Low 23603262
2024 ADAM19 cleaves the parathyroid hormone receptor (PTHR1) at a site mapped between amino acids 64-65 (verified by mass spectrometry); WT ADAM19 cleaves PTHR1 while a truncated/mutated ADAM19 allele found in brachydactyly type E patients does not; ADAM19-mediated PTHR1 cleavage increases Gq and decreases Gs activation, and increases beta-arrestin2 recruitment without altering cAMP accumulation. Linkage and whole genome sequencing in BDE pedigree; ADAM19 cleavage assay with WT vs. mutant ADAM19; mass spectrometry cleavage site mapping; Gq/Gs activation assays; beta-arrestin2 recruitment assay; cAMP accumulation assay Life science alliance High 38331475
2025 ADAM19 inhibition (siRNA knockdown or pharmacological inhibition with batimastat-94) in human primary fibroblasts decreases specific SASP factor expression and SA-beta-gal levels in senescent cells; proteomics of senescent cell secretome reveals decreased SASP factors associated with ADAM19 cleavage sites; in mice, batimastat-94 treatment reduces gut permeability and gut inflammation. siRNA knockdown in human primary fibroblasts; pharmacological inhibition (batimastat-94) in mice; secretome proteomics; SA-beta-gal assay; Drosophila meltrin GWAS/knockdown for initial identification Aging Medium 40117561
2008 TGF-beta1 signaling induces SMAD4 nuclear translocation and upregulates ADAM19 transcription in normal ovarian surface epithelial cells; in TGF-beta1-refractory ovarian cancer cells, impaired SMAD4 nuclear translocation correlates with repressive histone modifications (trimethyl-H3K27, dimethyl-H3K9) and HDAC association at the ADAM19 promoter, leading to ADAM19 silencing. TGF-beta1 stimulation; nuclear fractionation for SMAD4; ChIP for histone modifications (H3K27me3, H3K9me2) and HDAC at ADAM19 promoter; RT-PCR; promoter CpG methylation analysis Neoplasia (New York, N.Y.) Medium 18714391
2005 ADAM19 (MADDAM) expression in dendritic cells (but not macrophages) is regulated by histone acetylation: TSA (HDAC inhibitor) induces ADAM19 mRNA in THP-1 monocytic cells; ChIP assays show high acetylated histone H3 at the ADAM19 proximal promoter in TSA-treated THP-1 and dendritic cells compared to macrophages. TSA treatment; RT-PCR; ChIP with anti-acetylated H3 antibody; reporter assay with minimal promoter construct Biochemical and biophysical research communications Medium 15896713
2017 Neutralizing ADAM19 in a diet-induced obesity mouse model results in weight loss, improved insulin sensitivity, and reduced liver TNF-alpha levels, implicating ADAM19 as a pro-obesogenic factor that enhances insulin resistance. In vivo neutralizing antibody treatment in diet-induced obesity mouse model; body weight measurement; insulin sensitivity testing (HOMA-IR); liver TNF-alpha quantification Mediators of inflammation Medium 28265178
2024 Adam19 knockout mice show altered pulmonary function (decreased respiratory system elastance, tissue damping, tissue elastance, FEF50 but higher FEV0.1 and FVC at baseline), attenuated inflammatory responses to LPS (reduced neutrophil extravasation), and negative enrichment for TNF signaling pathways by RNA-seq, establishing a causal role for ADAM19 in lung function regulation. Adam19 knockout mouse generation; flexiVent lung function measurement; LPS challenge; BAL neutrophil counting; RNA-seq with gene set enrichment analysis Lung High 39153120

Source papers

Stage 0 corpus · 58 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Roles of Meltrin beta /ADAM19 in the processing of neuregulin. The Journal of biological chemistry 161 11116142
2011 The (pro)renin receptor is cleaved by ADAM19 in the Golgi leading to its secretion into extracellular space. Hypertension research : official journal of the Japanese Society of Hypertension 110 21270819
2003 Catalytic properties of ADAM19. The Journal of biological chemistry 103 12682046
1998 Spatially- and temporally-restricted expression of meltrin alpha (ADAM12) and beta (ADAM19) in mouse embryo. Mechanisms of development 90 9622634
2014 MiR-153 inhibits migration and invasion of human non-small-cell lung cancer by targeting ADAM19. Biochemical and biophysical research communications 75 25475731
2008 Aberrant transforming growth factor beta1 signaling and SMAD4 nuclear translocation confer epigenetic repression of ADAM19 in ovarian cancer. Neoplasia (New York, N.Y.) 60 18714391
2007 Different ADAMs have distinct influences on Kit ligand processing: phorbol-ester-stimulated ectodomain shedding of Kitl1 by ADAM17 is reduced by ADAM19. Journal of cell science 54 17344430
2007 Meltrin beta (ADAM19) mediates ectodomain shedding of Neuregulin beta1 in the Golgi apparatus: fluorescence correlation spectroscopic observation of the dynamics of ectodomain shedding in living cells. Genes to cells : devoted to molecular & cellular mechanisms 53 17352738
2009 ADAM19/adamalysin 19 structure, function, and role as a putative target in tumors and inflammatory diseases. Current pharmaceutical design 52 19601835
2015 Role of microRNA-30c targeting ADAM19 in colorectal cancer. PloS one 49 25799050
2006 ADAM19 is tightly associated with constitutive Alzheimer's disease APP alpha-secretase in A172 cells. Biochemical and biophysical research communications 48 17112471
2001 Expression and enzymatic activity of human disintegrin and metalloproteinase ADAM19/meltrin beta. Biochemical and biophysical research communications 48 11162584
2004 Lipid rafts identified as locations of ectodomain shedding mediated by Meltrin beta/ADAM19. Journal of neurochemistry 38 15030395
2008 Xenopus ADAM19 is involved in neural, neural crest and muscle development. Mechanisms of development 37 19027850
2008 Meltrin beta/ADAM19 interacting with EphA4 in developing neural cells participates in formation of the neuromuscular junction. PloS one 36 18830404
2022 Human umbilical cord mesenchymal stem cell-derived exosomal miR-335-5p attenuates the inflammation and tubular epithelial-myofibroblast transdifferentiation of renal tubular epithelial cells by reducing ADAM19 protein levels. Stem cell research & therapy 33 35902972
2022 Exosomal circPABPC1 promotes colorectal cancer liver metastases by regulating HMGA2 in the nucleus and BMP4/ADAM19 in the cytoplasm. Cell death discovery 32 35871166
2006 ADAM19 expression in human nephrogenesis and renal disease: associations with clinical and structural deterioration. Kidney international 32 16900093
2008 Roles of meltrin-beta/ADAM19 in progression of Schwann cell differentiation and myelination during sciatic nerve regeneration. The Journal of biological chemistry 30 19049978
2003 Inverse regulation of the ADAM-family members, decysin and MADDAM/ADAM19 during monocyte differentiation. Immunology 29 14632642
2023 Synovial mesenchymal stem cell-derived exosomal microRNA-320c facilitates cartilage damage repair by targeting ADAM19-dependent Wnt signalling in osteoarthritis rats. Inflammopharmacology 27 36862227
2020 Long noncoding RNA NORAD regulates lung cancer cell proliferation, apoptosis, migration, and invasion by the miR-30a-5p/ADAM19 axis. International journal of clinical and experimental pathology 27 32055266
2015 MiR-145 suppressed human retinoblastoma cell proliferation and invasion by targeting ADAM19. International journal of clinical and experimental pathology 27 26823772
2016 Genetic Variants in IL6R and ADAM19 are Associated with COPD Severity in a Mexican Mestizo Population. COPD 26 27078193
2005 Expression of adamalysin 19/ADAM19 in the endometrium and placenta of rhesus monkey (Macaca mulatta) during early pregnancy. Molecular human reproduction 26 15901844
2021 The elevated transcription of ADAM19 by the oncohistone H2BE76K contributes to oncogenic properties in breast cancer. The Journal of biological chemistry 23 33548228
2013 High expression of the "A Disintegrin And Metalloprotease" 19 (ADAM19), a sheddase for TNF-α in the mucosa of patients with inflammatory bowel diseases. Inflammatory bowel diseases 22 23429442
2020 Circular RNA has_circ_0000034 accelerates retinoblastoma advancement through the miR-361-3p/ADAM19 axis. Molecular and cellular biochemistry 21 32844346
2019 MiR-145 changes sensitivity of non-small cell lung cancer to gefitinib through targeting ADAM19. European review for medical and pharmacological sciences 20 31298334
2021 Synovial mesenchymal stem cell-derived exosomal miR-320c enhances chondrogenesis by targeting ADAM19. Future medicinal chemistry 19 34927445
2018 Xenopus ADAM19 regulates Wnt signaling and neural crest specification by stabilizing ADAM13. Development (Cambridge, England) 18 29540504
2013 Electrical stimulation accelerates neuromuscular junction formation through ADAM19/neuregulin/ErbB signaling in vitro. Neuroscience letters 17 23603262
2023 Promotion of colorectal cancer by transcription factor BHLHE40 involves upregulation of ADAM19 and KLF7. Frontiers in oncology 16 36890812
2006 Upregulation of ADAM19 in chronic allograft nephropathy. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 16 16827870
2002 Meltrin beta mini, a new ADAM19 isoform lacking metalloprotease and disintegrin domains, induces morphological changes in neuronal cells. FEBS letters 15 12482604
2017 ADAM19: A Novel Target for Metabolic Syndrome in Humans and Mice. Mediators of inflammation 14 28265178
2002 Screen and identification of proteins interacting with ADAM19 cytoplasmic tail. Molecular biology reports 13 12463424
2000 Meltrin beta (ADAM19) gene: cloning, mapping, and analysis of the regulatory region. Biochemical and biophysical research communications 13 10753657
2017 MiR-145 inhibits the epithelial-to-mesenchymal transition via targeting ADAM19 in human glioblastoma. Oncotarget 11 29190936
2014 ADAM19 and HTR4 variants and pulmonary function: Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium Targeted Sequencing Study. Circulation. Cardiovascular genetics 11 24951661
2011 Regional expression of ADAM19 during chicken embryonic development. Development, growth & differentiation 11 21492148
2009 Dynamic change of Adamalysin 19 (ADAM19) in human placentas and its effects on cell invasion and adhesion in human trophoblastic cells. Science in China. Series C, Life sciences 11 19727588
2005 Epigenetic regulation of the dendritic cell-marker gene ADAM19. Biochemical and biophysical research communications 11 15896713
2015 Variants in SELL, MRPS36P2, TP63, DDB2, CACNA1H, ADAM19, GNAI1, CDH13 and GABRG2 interact to confer risk of acne in Chinese population. The Journal of dermatology 10 25573302
2025 Rejuvenating Hyaline Cartilage with Senescence-Targeting Si-ADAM19 Delivery for Osteoarthritis Therapy. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 7 39927476
2023 miR-146b-5p downregulates IRAK1 and ADAM19 to suppress trophoblast proliferation, invasion, and migration in miscarriage†. Biology of reproduction 6 37676254
2010 ADAM19 autolysis is activated by LPS and promotes non-classical secretion of cysteine-rich protein 2. Biochemical and biophysical research communications 6 20460109
2006 Developmental and hormonal regulation of meltrin beta (ADAM19) expression in mouse testes during embryonic and postnatal life. Life sciences 6 16884740
2024 YY1-induced lncRNA00511 promotes melanoma progression via the miR-150-5p/ADAM19 axis. American journal of cancer research 5 38455406
2004 Evidence for disulfide involvement in the regulation of intramolecular autolytic processing by human adamalysin19/ADAM19. Experimental cell research 5 15242783
2025 Inhibition of the metalloprotease ADAM19 as a novel senomorphic strategy to ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP). Aging 2 40117561
2008 [Expression and clinical significance of ADAM19 in endometrial carcinoma]. Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 2 18458692
2025 Cell-free miRNA-150-5p serves as a biomarker and regulator of PROM-related preterm labor by targeting chorionic ADAM19. American journal of physiology. Endocrinology and metabolism 1 40658522
2024 ADAM19 cleaves the PTH receptor and associates with brachydactyly type E. Life science alliance 1 38331475
2024 Adam19 Deficiency Impacts Pulmonary Function: Human GWAS Follow-up in a Mouse Knockout Model. Lung 1 39153120
2024 Adam19 Deficiency Impacts Pulmonary Function: Human GWAS Follow-up in Mouse. Research square 0 38659817
2023 Long non-coding RNA LINC00565 regulates ADAM19 expression through sponging microRNA-532-3p, thereby facilitating clear cell renal cell carcinoma progression. The Chinese journal of physiology 0 38149560
2020 Comparison of ADAM19 and CUEDC2 expression in EHCC and their clinicopathological significance. Biomarkers in medicine 0 32960074