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Literature summary for 3.4.24.86 extracted from

  • Shen, M.; Hu, M.; Fedak, P.; Oudit, G.; Kassiri, Z.
    Cell-specific functions of ADAM17 regulate the progression of thoracic aortic aneurysm (2018), Circ. Res., 123, 372-388 .
    View publication on PubMed
Search for more literature for 3.4.24.86

Inhibitors

Inhibitors Comment Organism Structure
PF-548 selective inhibitor Homo sapiens
PF-548 selective inhibitor Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
membrane
-
 Mus musculus 16020
-
membrane
-
 Homo sapiens 16020
-

Organism

Organism UniProt Comment Textmining
Homo sapiens P78536
-
-
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
aorta
-
 Mus musculus
-
aorta
-
 Homo sapiens
-
endothelial cell
-
 Mus musculus
-
endothelial cell
-
 Homo sapiens
-
smooth muscle cell
-
 Mus musculus
-
smooth muscle cell
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
a disintegrin and metalloproteinase-17
-
 Mus musculus
a disintegrin and metalloproteinase-17
-
 Homo sapiens
ADAM17
-
 Mus musculus
ADAM17
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens in aneurysmal thoracic aorta from patients, the enzyme Is increased in tunica media and intima up

General Information

General Information Comment Organism
malfunction enzyme inhibition prevents progression of aneurysmal growth. Enzyme deficiency in smooth muscle and endothelial cells is sufficient to suppress thoracic aortic aneurysm dilation markedly. Enzyme deficiency in smooth muscle cells prevented the contractile-to-synthetic phenotypic switching in these cells after TAA induction, preventing perivascular fibrosis, inflammation, and adverse aortic remodeling. Loss of enzyme in endothelial cells protects the integrity of the intimal barrier by preserving the adherens junction (vascular endothelial-cadherin) and tight junctions (junctional adhesion molecule-A and claudin) Mus musculus
malfunction enzyme inhibition prevents progression of aneurysmal growth. Enzyme deficiency in smooth muscle and endothelial cells is sufficient to suppress thoracic aortic aneurysm dilation markedly. Enzyme deficiency in smooth muscle cells prevented the contractile-to-synthetic phenotypic switching in these cells after TAA induction, preventing perivascular fibrosis, inflammation, and adverse aortic remodeling. Loss of enzyme in endothelial cells protects the integrity of the intimal barrier by preserving the adherens junction (vascular endothelial-cadherin) and tight junctions (junctional adhesion molecule-A and claudin) Homo sapiens