EC Number   |
General Information |
Reference |
|---|
   3.4.24.B11 | malfunction |
silencing of Adamts1 blocks the adverse effects of ethanol on collagen and elastin levels |
734360 |
| 3.4.24.B11 | metabolism |
the enzyme is controlled by the FoxO1-sestrin 3-AMP-activated protein kinase signaling cascade and regulates ethanol-induced changes in collagen I and elastin levels |
734360 |
| 3.4.24.B11 | physiological function |
ADAMTS1 has an impact on bone mineral density and is a potent regulator of bone remodeling. Adamts1 induces parathyroid hormone levels in females and reduces osteocalcin levels in males |
720086 |
| 3.4.24.B11 | physiological function |
expression of ADAMTS1 increases in middle-aged and old wild-type mice compared with young, whereas in SPARC (i.e. secreted protein acidic and rich in cysteine) mice only old animals show increased ADAMTS1 expression. Levels of ADAMTS1 substrate versican decrease with age only in wild-type. SPARC treatment increases secretion of collagen I and ADAMTS1 (both the 110-kDa latent and 87-kDa active forms) into the conditioned media as well as the cellular expression of transforming growth factor-beta1-induced protein (Tgfbi) and phosphorylated Smad2 |
752441 |
| 3.4.24.B11 | physiological function |
HT-1080 cells overexpressing ADAMTS-1 exhibit a significant decrease in cell proliferation and migration velocity, both in presence of hepatocyte growth factor. ADAMTS-1 overexpression disturbs c-Met activation upon hepatocyte growth factor stimulation. Downstream ERK1/2 and FAK signaling pathways are also influenced. ADAMTS-1 decreases the size of the fibrosarcospheres, both under normal conditions and in the presence of hepatocyte growth factor. In presence of hepatocyte growth factor, ADAMTS-1 overexpression in HT-1080 disrupts microtumors formation in vivo |
753507 |
| 3.4.24.B11 | physiological function |
in Adamts1-deficient mice, alterations of organs like kidney, heart and aorta are found. In addition, the lack of ADAMTS1 differently affects lymphocyte and myeloid populations in the spleen and bone marrow. The substrate versican is altered the absence of the protease. the absence of ADAMTS1 creates a pro-inflammatory landscape, correlating with tumour blockade |
755491 |
| 3.4.24.B11 | physiological function |
macrophages at sites of muscle injury induce activation of satellite cells via expression of Adamts1. Overexpression of Adamts1 in macrophages in vivo is sufficient to increase satellite cell activation and improve muscle regeneration in young mice. NOTCH1 is a target of ADAMTS1 metalloproteinase activity, which reduces Notch signaling, leading to increased satellite cell activation |
754846 |
| 3.4.24.B11 | physiological function |
roles in angiogenesis and tumor biology, important regulatory factor of angiogenesis and tumor growth in prostate tumors |
711590 |
| 3.4.24.B11 | physiological function |
the enzyme inhibits cell proliferation, migration, and tube formation. The enzyme also inhibits vascular endothelial growth factor receptor 3 signaling under vascular endothelial growth factor-C stimulation |
733798 |
| 3.4.24.B11 | physiological function |
transgenic mice overexpressing ADAMTS-1 are similar to ADAMTS-1 wild-type mice pertaining collagen, elastin content and aortic diameter |
755146 |
