Affinage

ADAM28

Disintegrin and metalloproteinase domain-containing protein 28 · UniProt Q9UKQ2

Length
775 aa
Mass
87.1 kDa
Annotated
2026-06-09
57 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ADAM28 is a zinc-dependent ADAM-family metalloprotease that operates principally at the cell surface and as a secreted isoform to regulate growth-factor bioavailability, cell adhesion, and apoptosis (PMID:10794709, PMID:17047053, PMID:22636800). It matures through at least partly autocatalytic pro-domain removal in a late Golgi compartment, with a catalytic-site glutamate required for processing, and functions chiefly on the cell surface (PMID:10794709); the secreted pro-form is further processed extracellularly by active MMP-7 (PMID:15013428). Its catalytic activity is intrinsic and insensitive to TIMP-1/-2 but blocked by TIMP-3/-4 and broad metalloprotease inhibitors (PMID:11389903, PMID:15013428). ADAM28 cleaves a defined set of substrates: it degrades IGFBP-3 to release bioavailable IGF-I and drive tumor cell proliferation (PMID:17047053, PMID:30429106), cleaves von Willebrand factor to protect carcinoma cells from VWF-induced apoptosis and enable metastatic survival (PMID:22636800, PMID:33675784), and sheds the ectodomains of CD23, CD200, and TNF-α (PMID:12777399, PMID:23010875, PMID:23643150) as well as cleaving CTGF to liberate active VEGF165 (PMID:20971063) and Notch2 to drive marginal-zone B cell differentiation (PMID:28707394). Independent of catalysis, its disintegrin-like domain binds integrin α4β1 and PSGL-1 to promote leukocyte adhesion, transendothelial migration, and trafficking (PMID:17597069, PMID:21332445). In carcinoma cells ADAM28 expression is induced by Src kinase signaling through MEK/ERK and PI3K/mTOR pathways (PMID:24007880), and a neutralizing antibody targeting ADAM28 blocks IGFBP-3 cleavage and tumor growth in vivo (PMID:30190423). Beyond its tumor-promoting cell-intrinsic roles, ADAM28 contributes to inflammatory and remodeling phenotypes including airway remodeling, metabolic dysfunction, and trophoblast survival (PMID:28430139, PMID:28623976, PMID:36685493), while host-derived ADAM28 plays a counter-protective anti-metastatic role linked to CD8+ T cell mobilization (PMID:30647853).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 2000 High

    Established how ADAM28 matures and where it acts, showing that pro-domain removal is at least partly autocatalytic and that the mature enzyme functions at the cell surface.

    Evidence Catalytic-glutamate mutagenesis, cell surface trypsinization, and subcellular fractionation in COS-7 cells

    PMID:10794709

    Open questions at the time
    • Does not establish whether trans-cleavage by other proteases contributes to maturation in vivo
    • No structural detail of the active site
  2. 2001 High

    Demonstrated intrinsic proteolytic activity of ADAM28 with defined cleavage and a TIMP-insensitivity profile distinguishing it from other metalloproteases.

    Evidence In vitro protease assay on myelin basic protein with catalytic mutant and TIMP-1/-2 controls

    PMID:11389903

    Open questions at the time
    • MBP is a model substrate, not necessarily physiological
    • Did not test full TIMP panel
  3. 2003 High

    Identified the first ectodomain shedding substrate (CD23) and defined ADAM28 peptide specificity relative to other ADAMs.

    Evidence Synthetic peptide library screening and shedding assay with recombinant soluble enzyme

    PMID:12777399

    Open questions at the time
    • Cellular context of CD23 shedding by endogenous ADAM28 not established
  4. 2004 High

    Showed that the secreted pro-isoform is activated extracellularly by MMP-7 and that active ADAM28 cleaves IGFBP-3 free and in IGF complexes, linking ADAM28 to growth-factor bioavailability.

    Evidence In vitro MMP-7 activation, immunoblotting, and a metalloprotease/TIMP inhibitor panel

    PMID:15013428

    Open questions at the time
    • Whether MMP-7 is the physiological activator in tissues not shown
    • Membrane isoform activation route not addressed
  5. 2006 High

    Connected IGFBP-3 cleavage to a cancer phenotype, establishing ADAM28 as a driver of tumor cell proliferation via IGF-I liberation.

    Evidence siRNA, inhibitor, and neutralizing antibody loss-of-function with proliferation, cleavage assays, and breast cancer xenografts

    PMID:17047053

    Open questions at the time
    • Does not address ADAM28 contributions independent of IGF-I axis
  6. 2007 High

    Revealed a non-catalytic adhesive function: the disintegrin domain binds PSGL-1 to promote leukocyte adhesion and trafficking in inflammation.

    Evidence Yeast two-hybrid, reciprocal co-IP, P-selectin adhesion assay, and mouse endotoxin model

    PMID:17597069

    Open questions at the time
    • Did not resolve whether catalytic activity modulates this adhesive role
  7. 2010 High

    Expanded the substrate repertoire to CTGF, mapping cleavage sites and showing release of active VEGF165 from the CTGF/VEGF complex.

    Evidence Yeast two-hybrid, binding assay, and in vitro cleavage with site mapping

    PMID:20971063

    Open questions at the time
    • In vivo angiogenic consequence not demonstrated
  8. 2011 Medium

    Defined a second integrin partner (α4β1) bound through the disintegrin domain, mechanistically linking ADAM28 to lymphocyte adhesion and transendothelial migration.

    Evidence Cell adhesion assays with recombinant ADAM28, integrin-blocking antibodies, and Mn2+/9EG7 activation

    PMID:21332445

    Open questions at the time
    • Single lab; direct affinity not quantified
    • Physiological in vivo relevance to lymphocyte trafficking not tested
  9. 2012 High

    Established that ADAM28 cleavage of VWF confers resistance to VWF-induced apoptosis, explaining a pro-metastatic survival mechanism distinct from proliferation.

    Evidence Yeast two-hybrid, binding assay, shRNA/siRNA, neutralizing antibody, and xenograft lung metastasis imaging

    PMID:22636800

    Open questions at the time
    • VWF cleavage site not mapped here
    • Mechanism by which VWF triggers apoptosis not fully defined
  10. 2012 Medium

    Added TNF-α as a shedding substrate, implicating ADAM28 in inflammatory cytokine release by macrophages.

    Evidence Co-IP, co-localization, overexpression in HEK293, siRNA, inhibitor, and TNF-α ELISA in THP-1 cells

    PMID:23010875

    Open questions at the time
    • Overlap/redundancy with ADAM17-mediated TNF-α shedding not delineated
    • Single lab
  11. 2013 Medium

    Identified CD200 as a shedding substrate in B-CLL cells, broadening immune-modulatory roles.

    Evidence siRNA knockdown and ADAM28 transfection with soluble CD200 ELISA

    PMID:23643150

    Open questions at the time
    • Cleavage site not mapped
    • In vivo immune consequence not tested
  12. 2013 Medium

    Defined the upstream signaling that drives ADAM28 expression in cancer: Src acting through MEK/ERK and PI3K/mTOR.

    Evidence Oncogene transformation panel, kinase inhibitors, immunoblotting, and human tissue co-expression

    PMID:24007880

    Open questions at the time
    • Transcription factors directly binding the ADAM28 promoter not identified
    • Single lab
  13. 2016 High

    Showed a cytoprotective function in epithelial cells via C1q binding, where ADAM28 reduces C1q-induced apoptosis and autophagy.

    Evidence Yeast two-hybrid, SPR, IP, siRNA, and cell death/autophagy markers in bronchial epithelial cells

    PMID:26918856

    Open questions at the time
    • Whether C1q is a cleavage substrate or only a binding partner not resolved
  14. 2017 Medium

    Placed ADAM28 in a developmental B cell pathway, cleaving Notch2 downstream of CD19 to drive marginal-zone B cell differentiation.

    Evidence CD19 knockout/rescue mice, Notch2 cleavage assay, and Foxo1 analysis

    PMID:28707394

    Open questions at the time
    • Direct demonstration of ADAM28 acting on Notch2 in vivo limited
    • Single lab
  15. 2017 Medium

    Demonstrated a role in trophoblast biology, where ADAM28 supports column outgrowth and protects invading trophoblasts from apoptosis.

    Evidence Immunofluorescence localization and siRNA knockdown in placental explant cultures

    PMID:28623976

    Open questions at the time
    • Substrate responsible for trophoblast survival not identified
    • Single lab
  16. 2017 Medium

    Implicated ADAM28 in metabolic dysfunction, with loss reducing weight gain and improving glucose handling.

    Evidence siRNA in diet-induced obese mice and ADAM28 knockout mice with metabolic phenotyping

    PMID:28430139

    Open questions at the time
    • Mechanistic substrate linking ADAM28 to metabolism not defined
    • Single lab
  17. 2018 Medium

    Extended the IGFBP-3/IGF-I proliferation mechanism to leukemia, showing ADAM28 promotes AML growth and dissemination.

    Evidence CRISPR knockout in HL-60 cells, invasion assays, IGFBP-3 cleavage, and xenotransplantation

    PMID:30429106

    Open questions at the time
    • Single lab; relative contribution of non-IGF mechanisms not assessed
  18. 2018 Medium

    Provided therapeutic proof-of-concept that targeting a defined ADAM28 epitope blocks both IGFBP-3 cleavage and VWF protection, reducing tumor growth and metastasis.

    Evidence Neutralizing antibody 211-14 with IC50/KD measurement, dual substrate assays, and lung metastasis/survival models

    PMID:30190423

    Open questions at the time
    • Single lab; human clinical validation absent
  19. 2018 Medium

    Distinguished a counter-protective host role, where microenvironment-derived ADAM28 limits metastasis via CD8+ T cell mobilization, contrasting with the tumor-cell-intrinsic pro-metastatic function.

    Evidence ADAM28 knockout mice in experimental metastasis models with CD8+ T cell flow cytometry

    PMID:30647853

    Open questions at the time
    • Molecular substrate mediating T cell mobilization not identified
    • Single lab
  20. 2018 Medium

    Defined transcriptional repression of the ADAM28 locus by EBV EBNA3C through two epigenetic mechanisms, providing regulatory context for ADAM28 silencing.

    Evidence Recombinant EBV mutants, ChIP for H3K4me3/H3K27me3/BMI1/SUZ12, and EBNA3C-KDM2B interaction in LCLs

    PMID:30135119

    Open questions at the time
    • Endogenous (non-viral) regulators of this chromatin state not addressed
  21. 2021 Medium

    Generalized the VWF-cleavage survival mechanism to gastric cancer with stromal endothelial ADAM28 contributing, linking VWF removal to integrin β3/p53/caspase-3 signaling.

    Evidence Overexpression/knockdown in gastric cancer cells and HUVECs in co-culture with VWF rescue

    PMID:33675784

    Open questions at the time
    • Single lab; direct cleavage of VWF in this system inferred from supernatant levels
  22. 2023 Medium

    Implicated ADAM28 in airway remodeling, with knockout reducing Th2 responses, fibrosis, and fibroblast proliferation in an asthma model.

    Evidence ADAM28 knockout mice in ovalbumin model with flexiVent, BAL, histology, and ex vivo fibroblast assays

    PMID:36685493

    Open questions at the time
    • Substrate driving remodeling not identified
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular substrates and effectors connecting ADAM28 to its metabolic, trophoblast, airway-remodeling, and host anti-metastatic immune phenotypes remain undefined, as does a structural basis for distinguishing its catalytic from disintegrin-dependent functions.
  • No structural model of the catalytic or disintegrin domain in the corpus
  • Substrates mediating the in vivo metabolic and immune phenotypes unidentified
  • Relative contributions of membrane vs secreted isoforms in vivo unresolved

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 4 GO:0098772 molecular function regulator activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005576 extracellular region 2 GO:0005794 Golgi apparatus 1 GO:0005886 plasma membrane 1
Pathway
GO:0140096 catalytic activity, acting on a protein 5
Partners
C1QACTGFIGFBP3ITGA4MMP7NOTCH2PSGL-1VWF

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 ADAM28 undergoes autocatalytic pro-domain removal: a glutamate-to-alanine mutation in the catalytic site abolishes pro-domain removal even though the mutant is transported to the cell surface normally, indicating maturation is at least partly autocatalytic. Mature ADAM28 is accessible to cell surface trypsinization in COS-7 cells, indicating it functions mainly on the cell surface. Processing occurs in a late Golgi compartment. Site-directed mutagenesis of catalytic glutamate, cell surface trypsinization, subcellular fractionation, expression in COS-7 cells The Biochemical journal High 10794709
2001 Recombinant ADAM28 cleaves myelin basic protein at two sites; catalytic activity is abolished by a catalytic-site mutation and is insensitive to TIMP-1 and TIMP-2. In vitro protease assay with recombinant ADAM28, site-directed mutagenesis, TIMP inhibition assay FEBS letters High 11389903
2003 Soluble recombinant ADAM28 (MDC-L) catalyzes ectodomain shedding of CD23 (low-affinity IgE receptor); its substrate specificity on synthetic peptide libraries is similar to ADAM8 and ADAM15 but distinct from ADAM17. Synthetic peptide substrate library screening, ectodomain shedding assay with recombinant enzyme, metalloprotease inhibitor treatment The Journal of biological chemistry High 12777399
2004 ProADAM28s (65 kDa secreted isoform) is processed and activated by active MMP-7 (matrilysin-1), generating 42- and 40-kDa active forms lacking the propeptide. Active ADAM28s cleaves IGFBP-3 in both free form and in complex with IGF-I or IGF-II; cleavage is blocked by EDTA, 1,10-phenanthroline, KB-R7785, TIMP-3, and TIMP-4. In vitro MMP-7 activation assay, immunoblotting, metalloprotease inhibitor panel, TIMP inhibition assay Biochemical and biophysical research communications High 15013428
2005 Mouse ADAM28 gene expression in the epididymis is regulated by testicular factors (but not androgen), whereas ADAM7 is regulated by both androgen and testicular factors. Unlike ADAM7, ADAM28 protein is not transferred to the sperm surface during epididymal transit. RT-PCR, protein analysis, castration/androgen supplementation experiments, epididymis-sperm transfer assay Biochemical and biophysical research communications Medium 15883027
2006 ADAM28 promotes breast carcinoma cell proliferation by cleaving IGFBP-3, thereby releasing bioavailable IGF-I. ADAM28 siRNA knockdown reduces IGFBP-3 cleavage, IGF-I signaling, cell proliferation in vitro, and xenograft tumor growth in vivo. siRNA knockdown, ADAM28 inhibitor and neutralizing antibody treatment, proliferation assay, IGFBP-3 cleavage assay by immunoblot, xenograft mouse model Cancer research High 17047053
2007 The disintegrin-like domain of secreted ADAM28 binds to PSGL-1 (P-selectin glycoprotein ligand-1) on leukocytes. This binding enhances PSGL-1/P-selectin-mediated leukocyte adhesion to endothelial cells and increases leukocyte accumulation in pulmonary microcirculation in a mouse model of endotoxin-induced inflammation. Yeast two-hybrid screen, domain-specific binding assay, PSGL-1 stable transfectants, co-immunoprecipitation, co-immunolocalization, P-selectin adhesion assay, in vivo mouse endotoxin model The Journal of biological chemistry High 17597069
2009 ATRA stimulation induces ADAM28 expression in human chondrocytes (HCS-2/8 cells and primary chondrocytes). Transfection of ADAM28 or its soluble alternatively spliced form augments proteoglycan release from cartilage; a mutant lacking part of the disintegrin domain does not, indicating the disintegrin domain is required for localization/substrate recognition in cartilage degradation. RT-PCR, transfection overexpression and domain-deletion mutant, proteoglycan release assay from bovine nasal cartilage Biochemical and biophysical research communications Medium 19527685
2010 ADAM28 cleaves CTGF at the Ala181-Tyr182 and Asp191-Pro192 bonds in the hinge region. ADAM28 selectively digests CTGF in the CTGF/VEGF165 complex, releasing biologically active VEGF165. CTGF binds to proADAM28. Yeast two-hybrid screen, protein binding assay, in vitro cleavage assay with site mapping by immunoblot, VEGF165 release assay Biochemical and biophysical research communications High 20971063
2011 ADAM28 binds to integrin α4β1 via its disintegrin domain. Soluble ADAM28 enhances α4β1-dependent cell adhesion to VCAM-1 and promotes lymphocyte adhesion to and transendothelial migration through endothelial monolayers. Binding is attenuated by anti-functional integrin antibodies and enhanced by Mn2+ and activating antibody 9EG7. Affymetrix microarray, RT-PCR, immunohistochemistry, cell adhesion assay with recombinant murine ADAM28, integrin-blocking antibodies, Mn2+ activation, transendothelial migration assay Cell biology international Medium 21332445
2012 ADAM28 binds to and cleaves von Willebrand factor (VWF). High ADAM28 expression in carcinoma cells confers resistance to VWF-induced apoptosis. Knockdown of ADAM28 by shRNA increases carcinoma cell apoptosis in lung blood vessels and significantly decreases lung metastasis in xenograft models. Yeast two-hybrid screen, protein binding assay, immunoblotting of VWF cleavage, shRNA and siRNA knockdown, neutralizing antibody, mouse xenograft in vivo imaging model Journal of the National Cancer Institute High 22636800
2012 ADAM28 co-localizes and co-immunoprecipitates with TNF-α; overexpression of ADAM28 with TNF-α in HEK293 cells promotes TNF-α shedding, which is significantly reduced by ADAM28 siRNA knockdown or pharmacological inhibition. Endogenous ADAM28 in THP-1 macrophages similarly mediates TNF-α shedding. Co-immunoprecipitation, co-localization imaging, overexpression in HEK293 cells, siRNA knockdown, pharmacological inhibition, ELISA for TNF-α Immunology and cell biology Medium 23010875
2013 ADAM28 mediates ectodomain shedding of CD200 from B-CLL cells: siRNA knockdown of ADAM28 decreases soluble CD200 release, and transfection of cloned ADAM28 into CD200+ cells enhances sCD200 release. siRNA knockdown, ADAM28 gene transfection, ELISA for soluble CD200 Leukemia research Medium 23643150
2013 Src kinase induces ADAM28 gene expression in v-src-transformed epithelial cells through the MEK/ERK and PI3K/mTOR pathways. ADAM28 expression in human carcinoma cell lines correlates with phosphorylated c-Src and is suppressed by Src, MEK, and PI3K inhibitors. Oncogene transformation panel, Src/MEK/PI3K kinase inhibitors, immunoblotting for ADAM28, co-expression immunohistochemistry in human tissues The American journal of pathology Medium 24007880
2016 ADAM28 binds C1q (identified by yeast two-hybrid); recombinant ADAM28 pre-treatment of C1q reduces C1q-induced apoptosis and autophagy in bronchial epithelial cells. ADAM28 siRNA knockdown increases C1q-induced cell death, establishing a cytoprotective function for ADAM28 in epithelial cells against C1q cytotoxicity. Binding confirmed by binding assays, immunoprecipitation, and surface plasmon resonance. Yeast two-hybrid, protein binding assay, immunoprecipitation, surface plasmon resonance, siRNA knockdown, cell death assay, autophagy (LC3-II) and apoptosis (caspase-3, p38) markers The FEBS journal High 26918856
2017 CD19 promotes ADAM28-mediated cleavage of Notch2 in marginal zone precursors (MZP) to drive their differentiation into MZ B cells. CD19 upregulates ADAM28 expression by suppressing Foxo1. CD19-deficient MZP fail to differentiate into MZ B cells, and re-expression of CD19 rescues this. CD19 knockout mice, CD19 rescue experiments, ADAM28 expression analysis, Notch2 cleavage assay, Foxo1 expression analysis Journal of cellular and molecular medicine Medium 28707394
2017 ADAM28 siRNA knockdown in diet-induced obese mice prevents weight gain, promotes insulin sensitivity/glucose tolerance, and decreases liver TNF-α levels. ADAM28 knockout mice show reduced body weight and elevated HDL cholesterol, confirming a functional role for ADAM28 in metabolic dysfunction. siRNA knockdown in diet-induced obesity model, ADAM28 knockout mice, metabolic phenotyping (weight, glucose tolerance, insulin sensitivity, serum lipids, liver enzymes) International journal of molecular sciences Medium 28430139
2018 ADAM28 promotes AML leukemic cell proliferation, migration, and invasion through IGFBP-3 degradation and consequent IGF-I-induced cell proliferation. Knockout of ADAM28 in HL-60 cells reduces growth and dissemination in a xenotransplantation mouse model. ADAM28 CRISPR/Cas9 knockout, proliferation/migration/invasion assays, IGFBP-3 cleavage assay, IGF-I stimulation, xenotransplantation mouse model Cancer letters Medium 30429106
2018 A neutralizing antibody (211-14) against the junctional region between the cysteine-rich domain and secreted-specific domain of ADAM28 inhibits IGFBP-3 cleavage, blocks IGF-1-stimulated proliferation, and promotes VWF-induced cell death in lung adenocarcinoma cells. In vivo, it reduces tumor growth and metastasis and prolongs survival in lung metastasis models. Human neutralizing antibody generation, IC50 determination, KD measurement by binding assay, proliferation assay, VWF-induced apoptosis assay, lung metastasis mouse model, survival analysis Molecular cancer therapeutics Medium 30190423
2018 Host (microenvironment)-derived ADAM28 in ADAM28 knockout mice is associated with decreased CD8+ T cell numbers in spleen and lungs and increased lung colonization by tumor cells, indicating a protective role for host ADAM28 against metastasis through T cell mobilization (not proliferation, migration, or activation of CD8+ T cells per se). ADAM28 full knockout mouse model, experimental tumor metastasis models, flow cytometry for CD8+ T cells, ex vivo CD8+ T cell characterization Oncotarget Medium 30647853
2021 ADAM28 from both gastric cancer cells and endothelial cells (HUVECs) cleaves VWF to eliminate VWF-induced apoptosis of gastric cancer cells. ADAM28 knockdown in HUVECs increases VWF in supernatant and elevates integrin β3, p-TP53, and cleaved caspase-3 in co-cultured gastric cancer cells; these effects are reversed by VWF knockdown. ADAM28 overexpression/knockdown in gastric cancer cells and HUVECs, co-culture system, ELISA for VWF, Western blot for apoptosis markers, MTT, wound healing, flow cytometry European journal of pharmacology Medium 33675784
2017 ADAM28 localizes to HLA-G+ trophoblasts in distal anchoring columns and decidua. siRNA-mediated ADAM28 knockdown in placental explant cultures impairs trophoblast column outgrowth and increases apoptosis in matrix-invading trophoblasts. qPCR, immunofluorescence microscopy on purified placental cell populations, siRNA knockdown in Matrigel-embedded placental explant cultures, apoptosis assay Placenta Medium 28623976
2023 In ADAM28 knockout mice exposed to ovalbumin, airway responsiveness, Th2 cell proportion, B cell numbers, collagen deposition, smooth muscle hyperplasia, and mucous hyperplasia are all significantly reduced compared to wild-type. Lung fibroblasts from ADAM28 KO OVA-exposed mice show decreased proliferative capacity, suggesting ADAM28 directly contributes to airway remodelling. ADAM28 knockout mice, ovalbumin sensitization/challenge model, flexiVent airway responsiveness measurement, BAL analysis, lung histology, fibroblast proliferation assay ex vivo Frontiers in immunology Medium 36685493
2018 EBV nuclear antigen EBNA3C represses the ADAM28-ADAMDEC1 locus through interaction with KDM2B (histone lysine demethylase), which removes the activating mark H3K4me3. Concurrently, EBNA3C recruits Polycomb proteins BMI1 and SUZ12 to deposit H3K27me3 at the locus. These are two distinct repressive mechanisms. Recombinant EBV mutant viruses (RBPJ interaction motifs), ChIP for BMI1, SUZ12, H3K27me3, H3K4me3, gene expression analysis in LCLs, EBNA3C-KDM2B interaction assay Journal of virology Medium 30135119

Source papers

Stage 0 corpus · 57 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
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 149 12777399
2006 ADAM28 is overexpressed in human breast carcinomas: implications for carcinoma cell proliferation through cleavage of insulin-like growth factor binding protein-3. Cancer research 107 17047053
2000 Cloning and characterization of ADAM28: evidence for autocatalytic pro-domain removal and for cell surface localization of mature ADAM28. The Biochemical journal 99 10794709
2004 ADAM28 is activated by MMP-7 (matrilysin-1) and cleaves insulin-like growth factor binding protein-3. Biochemical and biophysical research communications 95 15013428
2012 Effect of ADAM28 on carcinoma cell metastasis by cleavage of von Willebrand factor. Journal of the National Cancer Institute 79 22636800
2006 ADAM28 is overexpressed in human non-small cell lung carcinomas and correlates with cell proliferation and lymph node metastasis. International journal of cancer 76 16052521
2001 Catalytic activity of ADAM28. FEBS letters 57 11389903
2022 CD20+CD22+ADAM28+ B Cells in Tertiary Lymphoid Structures Promote Immunotherapy Response. Frontiers in immunology 54 35634306
2021 CircRNA_100565 contributes to cisplatin resistance of NSCLC cells by regulating proliferation, apoptosis and autophagy via miR-337-3p/ADAM28 axis. Cancer biomarkers : section A of Disease markers 54 33682697
2005 Molecular, biochemical, and cellular characterization of epididymal ADAMs, ADAM7 and ADAM28. Biochemical and biophysical research communications 43 15883027
2007 Binding of ADAM28 to P-selectin glycoprotein ligand-1 enhances P-selectin-mediated leukocyte adhesion to endothelial cells. The Journal of biological chemistry 35 17597069
2010 Connective tissue growth factor is a substrate of ADAM28. Biochemical and biophysical research communications 32 20971063
2013 Ectodomain shedding of CD200 from the B-CLL cell surface is regulated by ADAM28 expression. Leukemia research 30 23643150
2011 Characterization of ADAM28 as a biomarker of bladder transitional cell carcinomas by urinary proteome analysis. Biochemical and biophysical research communications 28 21782798
2010 ADAM28 is a serological and histochemical marker for non-small-cell lung cancers. International journal of cancer 28 20112342
2019 MiR-198 affects the proliferation and apoptosis of colorectal cancer through regulation of ADAM28/JAK-STAT signaling pathway. European review for medical and pharmacological sciences 25 30840270
2011 Modulation of integrin α4β1 by ADAM28 promotes lymphocyte adhesion and transendothelial migration. Cell biology international 25 21332445
2022 LncRNA NEAT1 induces autophagy through the miR-128-3p/ADAM28 axis to suppress apoptosis of nonsmall-cell lung cancer. The Kaohsiung journal of medical sciences 24 36054559
2012 ADAM28 is elevated in humans with the metabolic syndrome and is a novel sheddase of human tumour necrosis factor-α. Immunology and cell biology 23 23010875
2009 ADAM28 as a target for human cancers. Current pharmaceutical design 23 19601836
2011 Urinary protein profiling by liquid chromatography/tandem mass spectrometry: ADAM28 is overexpressed in bladder transitional cell carcinoma. Rapid communications in mass spectrometry : RCM 19 21913264
2010 ADAM28: a potential oncogene involved in asbestos-related lung adenocarcinomas. Genes, chromosomes & cancer 19 20544843
2015 ADAM28 overexpression regulated via the PI3K/Akt pathway is associated with relapse in de novo adult B-cell acute lymphoblastic leukemia. Leukemia research 18 26340916
2018 ADAM28 promotes tumor growth and dissemination of acute myeloid leukemia through IGFBP-3 degradation and IGF-I-induced cell proliferation. Cancer letters 17 30429106
2016 ADAM28 is expressed by epithelial cells in human normal tissues and protects from C1q-induced cell death. The FEBS journal 17 26918856
2011 ADAM28 manipulates proliferation, differentiation, and apoptosis of human dental pulp stem cells. Journal of endodontics 15 21329817
2021 ADAM28 from both endothelium and gastric cancer cleaves von Willebrand Factor to eliminate von Willebrand Factor-induced apoptosis of gastric cancer cells. European journal of pharmacology 14 33675784
2020 ADAM28: Another ambivalent protease in cancer. Cancer letters 14 32861707
2017 CD19 regulates ADAM28-mediated Notch2 cleavage to control the differentiation of marginal zone precursors to MZ B cells. Journal of cellular and molecular medicine 13 28707394
2017 Serum levels of ADAM10, ADAM12, ADAM17 AND ADAM28 in colorectal cancer patients. Journal of biological regulators and homeostatic agents 13 29254295
2006 ADAM28 participates in the regulation of tooth development. Archives of oral biology 13 16836973
2018 Selective Inhibition of ADAM28 Suppresses Lung Carcinoma Cell Growth and Metastasis. Molecular cancer therapeutics 12 30190423
2017 The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice. International journal of molecular sciences 12 28430139
2008 Essential role of ADAM28 in regulating the proliferation and differentiation of human dental papilla mesenchymal cells (hDPMCs). Histochemistry and cell biology 11 18690470
2018 Microenvironment-derived ADAM28 prevents cancer dissemination. Oncotarget 10 30647853
2013 Expression of ADAM28 and IGFBP-3 genes in patients with colorectal cancer - a preliminary report. International journal of immunopathology and pharmacology 10 23527725
2009 All-trans retinoic acid-induced ADAM28 degrades proteoglycans in human chondrocytes. Biochemical and biophysical research communications 10 19527685
2018 Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression of COBLL1 and the ADAM28-ADAMDEC1 Locus via Interaction with the Histone Lysine Demethylase KDM2B. Journal of virology 9 30135119
2013 Src plays a key role in ADAM28 expression in v-src-transformed epithelial cells and human carcinoma cells. The American journal of pathology 9 24007880
2020 MicroRNA-574-3p inhibits the malignant behavior of liver cancer cells by targeting ADAM28. Oncology letters 7 32782619
2023 Role for the metalloproteinase ADAM28 in the control of airway inflammation, remodelling and responsiveness in asthma. Frontiers in immunology 4 36685493
2017 ADAM28 localizes to HLA-G+ trophoblasts and promotes column cell outgrowth. Placenta 4 28623976
2009 Influence of ADAM28 on biological characteristics of human dental follicle cells. Archives of oral biology 4 19580958
2025 Research progress on ADAM28 in malignant tumors. Discover oncology 1 40252142
2018 ADAM28 dramatically regulates the biological features of human gingival fibroblasts. Odontology 1 30552542
2014 [Research advances on ADAM28 expression and ADAM28-mediated tumor metastasis]. Zhongguo shi yan xue ye xue za zhi 1 25130845
2009 [Effects of ADAM28 AS-ODN on proliferation, differentiation and apoptosis of HPDLSC]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 1 19907862
2007 Genomic organization of the region spanning D14Mit262 and D14Mit86 on mouse chromosome 14 and exclusion of Adam28 and Adamdec1 as the cataract-causing gene, lr2. Cytogenetic and genome research 1 17268172
2025 ADAM28 promotes epithelial mesenchymal transition and impairs tight junctions in non-eosinophilic chronic rhinosinusitis with nasal polyps by inducing M1 polarization of macrophages. International immunopharmacology 0 39954661
2025 Histone-, Receptor-, and Integrin-Related Gene Products and ADAM28 as Relevant to B-Cell Acute Lymphoblastic Leukemia (B-ALL). Current issues in molecular biology 0 41020821
2023 Differential Expressions of ADAM28 and ADAMTSL3 in Gingival Tissue of Patients with Periodontitis. The Tohoku journal of experimental medicine 0 36927684
2020 [Construction of ADAM28 shRNA interference vector and its inhibitory effect on human periodontal ligament stem cells]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 33543212
2014 [The effects of ADAM28 AS-ODN on biological function of human gingival fibroblasts]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 25543593
2010 [Effects of ADAM28 on biological functions of human dental pulp stem cells]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 20635038
2008 [The effects of ADAM28 on HDPC biological characteristics]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 18661070
2007 [The construction of ADAM28 eukaryotic expression plasmid and expression after transfected into HDFC]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 17924028
2006 [Effects of ADAM28 AS-ODN on proliferation and AKPase of HDFCs]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 16685358

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