2016 PubMed artikkeleita: ADAM17/ TACE
https://www.ncbi.nlm.nih.gov/gene/6868
- Preferred Names
- a disintegrin and metalloproteinase domain-containing protein 17
- Names
- ADAM metallopeptidase domain 18
- TNF-alpha convertase
- TNF-alpha converting enzyme
- snake venom-like protease
- tumor necrosis factor, alpha, converting enzyme
- Also known as
- CSVP; TACE; NISBD; ADAM18; CD156B; NISBD1
- Summary
- This gene encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biologic processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. The encoded preproprotein is proteolytically processed to generate the mature protease. The encoded protease functions in the ectodomain shedding of tumor necrosis factor-alpha, in which soluble tumor necrosis factor-alpha is released from the membrane-bound precursor. This protease also functions in the processing of numerous other substrates, including cell adhesion proteins, cytokine and growth factor receptors and epidermal growth factor (EGF) receptor ligands. The encoded protein also plays a prominent role in the activation of the Notch signaling pathway. Elevated expression of this gene has been observed in specific cell types derived from psoriasis, rheumatoid arthritis, multiple sclerosis and Crohn's disease patients, suggesting that the encoded protein may play a role in autoimmune disease. [provided by RefSeq, Feb 2016]
- Conserved Domains (4) summary
-
- smart00050
Location:484 → 560 - DISIN; Homologues of snake disintegrins
- cd04270
Location:223 → 477 - ZnMc_TACE_like; Zinc-dependent metalloprotease; TACE_like subfamily. TACE, the tumor-necrosis factor-alpha converting enzyme, releases soluble TNF-alpha from transmembrane pro-TNF-alpha.
- pfam01562
Location:56 → 152 - Pep_M12B_propep; Reprolysin family propeptide
- pfam16698
Location:581 → 641 - ADAM17_MPD; Membrane-proximal domain, switch, for ADAM17
- smart00050
Related articles in PubMed
- A novel inhibitor of ADAM17 sensitizes colorectal cancer cells to 5-Fluorouracil by reversing Notch and epithelial-mesenchymal transition in vitro and in vivo. Li DD, et al. Cell Prolif, 2018 Oct. PMID 30069943
- ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. Nishimi A, et al. Clin Rheumatol, 2018 Apr. PMID 29411180
- Short hairpin RNA-mediated gene silencing of ADAM17 inhibits the growth of breast cancer MCF‑7 cells in vitro and in vivo and its mechanism of action. Hu B, et al. Oncol Rep, 2018 Apr. PMID 29393483, Free PMC Article
- ADAM17, a New Player in the Pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder. Perna AF, et al. J Ren Nutr, 2017 Nov. PMID 29056164
- The shedding protease ADAM17: Physiology and pathophysiology. Zunke F, et al. Biochim Biophys Acta Mol Cell Res, 2017 Nov. PMID 28705384
GeneRIFs: Gene References Into FunctionsWhat's a GeneRIF?
- ADAM17 activation and secretion in the myeloid cells during HIV infection.
- A novel ADAM17 inhibitor ZLDI-8 may be a potential chemosensitizer which sensitized CRC cells to 5-fluorouracil or irinotecan by reversing Notch and EMT pathways.
- The isolated membrane proximal domain (MPD) of ADAM17 binds to phosphatidylserine (PS) but not to phosphatidylcholine liposomes. A cationic PS-binding motif is identified in this domain, replacement of which abrogates liposome-binding and renders the protease incapable of cleaving its substrates in cells.
- ADAM-17 in inflammatory myopathy was significantly higher than that in healthy control. ADAM-17 in post-treatment with corticosteroid and/or immunosuppressant serum was significantly decreased compared with that in pre-treatment serum.
- The present research suggests that ADAM17shRNA can inhibit MCF7 cell invasion and proliferation in vitro and inhibit MCF7 xenograft growth in vivo through the EGFR/PI3K/AKT and EGFR/MEK/ERK signaling pathways.
- Uev1A-Ubc13 complex catalyzes lysine63-linked ubiquitination of RHBDF2 to promote TACE maturation.
- ADAM17 plays a role in chronic kidney disease-mineral and bone disorder.
- Insulin-like growth factor-1 activates different catalytic subunits p110 of PI3K in a cell-type-dependent manner to induce lipogenesis-dependent epithelial-mesenchymal transition through the regulation of ADAM10 and ADAM17.
- ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157. Findings reveal a link between shedding of TREM2 and its regulation during inflammatory conditions or chronic neurodegenerative disease in which activity or expression of sheddases might be altered.
- Oxidative stress is correlated with hyperactivation of the ADAM17/Notch signaling pathway and a consequent increase in fibrosis in patients with endometriosis.
