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Details for receptor: ADAM17

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EndoNet ID: ENR01190

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Synonyms

  • ADAM17
  • TACE
  • ADAM 17
  • TACE/ADAM17
  • ADAM metallopeptidase domain 17
  • A Disintegrin And Metalloprotease 17
  • TNF-alpha-converting enzyme
  • TNF-alpha convertase
  • snake venom-like protease
  • CD156b antigen
  • cSVP
  • ADAM-17
  • CD156q

General information

  • ADAM17 mediates regulated ectodomain shedding of the SARS-CoV receptor, ACE2. [1]
  • Cannabinoids induce cancer cell proliferation via TACE/ADAM17-mediated transactivation of the EGF receptor. [2]
  • Multi-domain, type I transmembrane protein that includes an extracellular zinc-dependent protease domain. [3]
  • Cleavage by TACE generates the soluble forms of tumor necrosis factor, transforming growth factor-alpha, and other proteins from their membrane-bound precursors (a phenomenon termed 'shedding'). [3]
  • Acts as an alpha-secretase.
  • Tumor necrosis factor-alpha-converting enzyme mediates the cleavage and shedding of fractalkine (CX3CL1). [4]
  • Interleukin-1alpha stimulates ADAM-17 synthesis, consistent with activation of the soluble fragment of Amyloid Precursor Protein (sAPPalpha) in human astrocytes. [5]
  • The proteolytic activity of ADAM17 is required to release ligands that activate the epidermal growth factor receptor, a tyrosine kinase receptor which contributes to tumor development by regulating cell proliferation, apoptosis, and migration. [6]
  • Up-regulated in colon carcinoma.
  • In the absence of ectodomain shedding, a membrane-anchored ligand (such as TNFalpha or an EGFR ligand) could theoretically only engage a receptor on the same cell (autocrine signalling) or on an immediately adjacent cell (juxtaccrine signalling). [7]
  • Cellular cholesterol depletion triggers shedding of the human interleukin-6 receptor by ADAM10 and ADAM17. [8]
  • The shedding of ADAM17 substrates can be stimulated by phorbol esters such as TPA or PMA, and by the phosphatase inhibitor pervanadate. [7]
  • TIMP-3, a small protein that inhibits most matrix metalloproteases, also inhibits TACE. [3]
  • During its transport through the Golgi apparatus, ADAM17 is included in cholesterol-rich membrane microdomains (lipid rafts) where its prodomain is cleaved by furin. [9]

Links to other resources

UniProt P78536
Ensembl ENST00000310823

Binding hormones

  • mucin-1 isoform 1
  • TNF-alpha
  • sACE2
  • fractalkine
  • soluble ectodomain of transferrin receptor
  • soluble ectodomain of desmoglein-2
  • EPR
  • amphiregulin
  • TGF-alpha
  • HB-EGF

Anatomical structures with this receptor

  • astrocyte

  • brain

  • continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

    Induced phenotypes

    • regulation of angiogenesis
      • ADAM-17 regulates angiogenesis via its effects on the proliferation of endothelial cells, network formation, invasion and activation of MMP-2. [10]

  • neuron

  • cerebellar_cortex

  • cerebral_cortex

  • hippocampus

  • keratinocyte

  • macrophage

  • monocyte

    Induced phenotypes

    • ectodomain shedding
      • ADAM17 deficient monocytes failed to shed L-selectin in response to PMA. [11]

  • T-lymphocyte

    Induced phenotypes

    • ectodomain shedding
      • ADAM17 deficient lymphocytes failed to shed L-selectin in response to PMA. [11]

  • uterus

  • neutrophil_granulocyte

    Induced phenotypes

    • ectodomain shedding
      • ADAM17 deficient neutrophils failed to shed L-selectin in response to PMA. [11]

  • lung

Reference