EC Number   |
General Information |
Reference |
|---|
   2.4.1.212 | evolution |
the three HAS isoenzymes, HAS1, HAS2, and HAS3, expressed in mammalian cells differ in their enzymatic properties and regulation by external stimuli |
736219 |
| 2.4.1.212 | malfunction |
catalytically inactive mutant K190R HAS2 forms dimers with wild-type HAS2 and quenches the activity of wild-type HAS2 |
722678 |
| 2.4.1.212 | malfunction |
downregulation of HAS2 initiates and regulates fibroblast senescence through a p27-CDK2-SKP2 pathway. Deletion of HAS2 in mouse mesenchymal cells increases the cellular senescence of fibroblasts in bleomycin-induced mouse lung fibrosis in vivo. Overexpression of HAS2 in mesenchymal cells promotes an invasive phenotype resulting in severe fibrosis and downregulation of HAS2 promotes resolution. HAS2 deficiency leads to embryonic lethality. Downregulation of HAS2 increases p27 protein stability. p27 inhibits cell proliferation by regulating CDK2 activity. HAS2 deletion enhances cell stress responses. Phenotypes, detailed overview |
736725 |
| 2.4.1.212 | malfunction |
embryonic lethality of genetic deletion of HAS2, some HAS2-specific functions are not compensated for by isozyme HAS1 or HAS3 |
735574 |
| 2.4.1.212 | malfunction |
HAS-1 overexpression in dermal wounds decreases elements of scar formation |
-, 721994 |
| 2.4.1.212 | malfunction |
Has2-/- mice are embryonic lethal. Has2-/- embryos die between embryonic day 9.5 and 10.5 and exhibit severe cardiac and vascular abnormalities, in addition to yolk sac and somite deformities |
759182 |
| 2.4.1.212 | malfunction |
Has3/Apoe double deficient mice develop less atherosclerosis characterized by decreased Th1-cell responses, decreased IL-12 release, and decreased macrophage-driven inflammation |
759705 |
| 2.4.1.212 | malfunction |
in a ligation-induced carotid artery injury model, attenuated neointimal hyperplasia occurs in HAS3-null animals compared with wild-type control C57BL/6J mice. No changes are observed in medial and neointimal cell density, proliferation, or apoptosis. A lack of compensatory upregulation of isozymes HAS1 or HAS2, HAS3 deletion is associated with a reduction in vascular hyaluronan content, most dramatically in the media rather than the neointima. Transcriptome analysis of injured vessels from wild-type and HAS3-null mice reveals differential activation of pathways associated with a migratory VSMC phenotype. Isozyme HAS3 overexpression in VSMCs supports a migratory phenotype in response to platelet-derived growth factor BB (PDGF-BB), whereas knockdown of HAS3 results in reduced PDGF-BB-induced migration. Isozyme HAS3 knockdown also leads to a decrease in PDGF-B mRNA levels |
-, 735574 |
| 2.4.1.212 | malfunction |
isozyme HAS3 overexpression downregulates MV3 melanoma cell proliferation, migration and adhesion. Overexpression of isozyme HAS3 decreases cell proliferation, directional and random cell migration, and promotes cell cycle arrest at G1/G0 and decreases ERK1/2 phosphorylation suggesting that inhibition of MAP-kinase signaling is responsible for the suppressive effects on the malignant phenotype of MV3 melanoma cells. EGFP-HAS3 overexpression downregulates several signaling pathways in MV3 melanoma cells |
736067 |
| 2.4.1.212 | malfunction |
reduction of HA due to decreased HAS activity, caused by phosphorylation at Thr110 through AMP-activated protein kinase, decreases the ability of aortic smooth muscle cells to proliferate, migrate, and recruit immune cells, thereby reducing the pro-atherosclerotic AoSMC phenotype. AMP-activated protein kinase can block the pro-atherosclerotic signals driven by HA by interaction with its receptors |
722741 |
