ADAM Proteins

• 

  Subject Areas on Research

  • ADAM metallopeptidase domain 17 (ADAM17) is naturally processed through major histocompatibility complex (MHC) class I molecules and is a potential immunotherapeutic target in breast, ovarian and prostate cancers. 
  • ADAM10 controls collagen signaling and cell migration on collagen by shedding the ectodomain of discoidin domain receptor 1 (DDR1). 
  • ADAM10 is essential for proteolytic activation of Notch during thymocyte development. 
  • ADAM12: a genetic modifier of preclinical peripheral arterial disease. 
  • ADAM9 inhibition increases membrane activity of ADAM10 and controls α-secretase processing of amyloid precursor protein. 
  • ADAMTS metalloproteases generate active versican fragments that regulate interdigital web regression. 
  • Adam10 is essential for early embryonic cardiovascular development. 
  • Altered proteolytic activities of ADAMTS-4 expressed by C-terminal processing. 
  • Cartilage viability and catabolism in the intact porcine knee following transarticular impact loading with and without articular fracture. 
  • Catalytic properties of ADAM12 and its domain deletion mutants. 
  • Characterization of and osteoarthritis susceptibility in ADAMTS-4-knockout mice. 
  • Characterization of angiotensin-converting enzyme 2 ectodomain shedding from mouse proximal tubular cells. 
  • Collagen and aggrecan degradation is blocked in interleukin-1-treated cartilage explants by an inhibitor of IkappaB kinase through suppression of metalloproteinase expression. 
  • Diacetyl induces amphiregulin shedding in pulmonary epithelial cells and in experimental bronchiolitis obliterans. 
  • IL-1 beta induces COX2, MMP-1, -3 and -13, ADAMTS-4, IL-1 beta and IL-6 in human tendon cells. 
  • Identification of an ADAMTS-4 cleavage motif using phage display leads to the development of fluorogenic peptide substrates and reveals matrilin-3 as a novel substrate. 
  • Identification of candidate substrates for ectodomain shedding by the metalloprotease-disintegrin ADAM8. 
  • Is it quinine TTP/HUS or quinine TMA? ADAMTS13 levels and implications for therapy. 
  • Maladaptive matrix remodeling and regional biomechanical dysfunction in a mouse model of aortic valve disease. 
  • Modulating hedgehog signaling can attenuate the severity of osteoarthritis. 
  • Monitoring changes in gene expression in renal ischemia-reperfusion in the rat. 
  • Mutations near amino end of alpha1(I) collagen cause combined osteogenesis imperfecta/Ehlers-Danlos syndrome by interference with N-propeptide processing. 
  • Proteolytic activities of human ADAMTS-5: comparative studies with ADAMTS-4. 
  • Reactive-site mutants of N-TIMP-3 that selectively inhibit ADAMTS-4 and ADAMTS-5: biological and structural implications. 
  • Regulation of Cholesterol Homeostasis by Hedgehog Signaling in Osteoarthritic Cartilage. 
  • Relapse of thrombotic thrombocytopenic purpura: is it a continuum of disease? 
  • Role of miR-29b on the regulation of the extracellular matrix in human trabecular meshwork cells under chronic oxidative stress. 
  • Screen and identification of proteins interacting with ADAM19 cytoplasmic tail. 
  • Stall encodes an ADAMTS metalloprotease and interacts genetically with Delta in Drosophila ovarian follicle formation. 
  • The ADAM10 prodomain is a specific inhibitor of ADAM10 proteolytic activity and inhibits cellular shedding events. 
  • The C-terminal domains of ADAMTS-4 and ADAMTS-5 promote association with N-TIMP-3. 
  • The low affinity IgE receptor (CD23) is cleaved by the metalloproteinase ADAM10. 
  • The secreted metalloprotease ADAMTS20 is required for melanoblast survival. 
  • Thrombotic thrombocytopenic purpura: 2012 American Society for Apheresis (ASFA) consensus conference on classification, diagnosis, management, and future research. 
  • Ticlopidine- and clopidogrel-associated thrombotic thrombocytopenic purpura (TTP): review of clinical, laboratory, epidemiological, and pharmacovigilance findings (1989-2008). 
  • Ticlopidine-associated ADAMTS13 activity deficient thrombotic thrombocytopenic purpura in 22 persons in Japan: a report from the Southern Network on Adverse Reactions (SONAR).