Any feedback?
Please rate this page
(all_enzymes.php)
(0/150)

BRENDA support

2.4.1.212: hyaluronan synthase

This is an abbreviated version!
For detailed information about hyaluronan synthase, go to the full flat file.

Word Map on EC 2.4.1.212

Reaction

UDP-alpha-D-glucuronate
+
N-acetyl-beta-D-glucosaminyl-(1->4)-beta-D-glucuronosyl-(1->3)-[nascent hyaluronan]
=
UDP
+
beta-D-glucuronosyl-(1->3)-N-acetyl-beta-D-glucosaminyl-(1->4)-beta-D-glucuronosyl-(1->3)-[nascent hyaluronan]

Synonyms

CHAS2, CHAS3, class I hyaluronan synthase, CPS1, DG42 protein, HA synthase, HA synthase 3, HA1, HA2, HA3, HAS, HAS-1, HAS-2, HAS-3, HAS1, Has2, Has3, hasA, HASs, HsHAS1, HuHAS1, HyaD, hyaluronan synthase, hyaluronan synthase 1, hyaluronan synthase 2, hyaluronan synthase 3, hyaluronan synthase-1, hyaluronan synthase-2, hyaluronan synthases 2, hyaluronan synthethase, hyaluronate synthase, hyaluronate synthetase, hyaluronic acid synthase, hyaluronic acid synthetase, More, PmHAS, seHAS, XHAS1, XHAS2, XHAS3

ECTree

     2 Transferases
         2.4 Glycosyltransferases
             2.4.1 Hexosyltransferases
                2.4.1.212 hyaluronan synthase

Expression

Expression on EC 2.4.1.212 - hyaluronan synthase

Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
17beta-estradiol and different combinations of estradiol, gonadotropins, insulin-like growth factor 1 and insulin iduce the enzyme expression of HAS1-3
17beta-estradiol and different combinations of estradiol, gonadotropins, insulin-like growth factor 1 and insulin iduce the expression of HAS1-3
a cytokine-and glucose-inducible enzyme
-
basic fibroblast growth factor bFGF increases HA-synthase-1 and -2 expression and enhances high molecular weight hyaluronan deposition in the pericellular matrix
both tumor necrosis factor TNFalpha and interferon INFgamma significantly induce HAS3 expression
both tumor necrosis factor TNFalpha and transforming growth factor 1beta significantly increase HAS1 expression and protein synthesis. Exposure to reactive oxygen species results in increased gene expression and protein formation of HAS1
both tumor necrosis factor TNFalpha and transforming growth factor 1beta significantly increase HAS2 expression and protein synthesis. Exposure to reactive oxygen species results in increased gene expression and protein formation of HAS2
chondroitin sulfate increases hyaluronan production by osteoarthritic fibroblast-like synoviocytes through up-regulation of the expression of HAS1 and HAS2 associated with activation of ERK-1/2, p38, and Akt, although to a lesser extent. Both p38 and Akt are involved in chondroitin sulfate-induced hyaluronan accumulation. IL-1 increases hyaluronan production and levels of mRNA for HAS1, HAS2, and HAS3. Chondroitin sulfate enhances the IL-1induced level of HAS2 mRNA and reduces the level of HAS3 mRNA. IL-1induced activation of p38 and JNK is slightly decreased by chondroitin sulfate, whereas that of ERK-1/2 and Akt is enhanced. More high molecular weight hyaluronan is found in chondroitin sulfate plus IL-1treated fibroblast-like synoviocytes than in fibroblast-like synoviocytes treated with IL-1 alone
comparison of full-length HAS1 isoform and its splice variants Va, Vb, and Vc. When co-expressed, the properties of HAS1 variants are dominant over those of full length HAS1. Full length HAS1 appears to be diffusely expressed in the cell, but HAS1 variants are concentrated in the cytoplasm and/or Golgi apparatus. HAS1 variants synthesize detectable de novo hyaluronan intracellularly. Each of the HAS1 variants is able to relocalize full length HAS1 protein from diffuse cytoskeleton-anchored locations to deeper cytoplasmic spaces. The HAS1-variants-mediated relocalization occurs through strong molecular interactions, which also serve to protect full length HAS1 from its otherwise high turnover kinetics
doxycycline treatment causes a strong upregulation of HAS3 expression. A distinct EGFP-HAS3 signal is observed already 2 h after starting the doxycycline induction, localized mainly at the plasma membrane and in the Golgi area. After 24 h induction EGFP-HAS3 signal has become more intense, localizing strongly at the Golgi area and at the plasma membrane
-
during atresia, HAS1 mRNA and protein expression is markedly up-regulated inovary. HAS2 and HAS3 mRNA expression levels are low and very low to undetectable, respectively
-
Has1 is upregulated in states associated with inflammation, like atherosclerosis, osteoarthritis, and infectious lung disease. The enzyme expression is increased in transcriptional regulation by factors EGF, FGF2, FGF, forskolin, IGF, IL-1beta, PDGF, progesterone, prostaglandin D2, prostaglandin E2, and TGF-beta
HAS2 is the major isoenzyme in MCF-7 cells. The mRNA expression is lowered by 4-methylumbelliferone by 81% in MCF-7 cells, and by 88% in A2058 cells. Both HAS substrate and HAS2 and/or HAS3 mRNA are targeted by 4-methylumbelliferone. The reduction of hyaluronan caused by 4-methylumbelliferone is associated with a significant inhibition of cell migration, proliferation and invasion
Has3 expression is increased early during lesion formation when macrophages enter atherosclerotic plaques
histamine increases hyaluronan degradation by up-regulating HYBID (hyaluronan-binding protein) and down-regulating hyaluronan synthase 2 in human skin fibroblasts in a dose- and time-dependent manner and thereby decreases the total amounts and sizes of newly produced hyaluronan
hyaluronan synthase 2 expression is elevated in both human and murine liver fibrosis. The enzyme is transcriptionally up-regulated by transforming growth factor-beta through Wilms tumor 1 to promote fibrogenic, proliferative, and invasive properties of HSCs via CD44, Toll-like receptor 4, and newly identified downstream effector Notch1
in MDA-MB-361, A2058 and SKOV-3 cells, treatment with 4-methylumbelliferone decreases HAS3 mRNA by 84-60%. The reduction of hyaluronan caused by 4-methylumbelliferone is associated with a significant inhibition of cell migration, proliferation and invasion
isoform HAS2 is a primary target of the cAMP activator forskolin and the nuclear hormone alltrans-retinoic acid. Forskolin and all-trans-retinoic acid modulate the formation of complexes between transcription factor CREB1 and retinoic acid receptor with various co-regulators at the predicted sites.Mediator MED1 and co-repressor nuclear receptor co-repressor NCoR1 are central for the all-trans-retinoic acid induction of the HAS2 gene and CREB-binding protein CBP dominates its forskolin response
isozyme HAS2 is suppressed in senescent fibroblasts
MDAMB-231 and HS578T breast cancer cell line express higher levels of hyaluronan synthase 2 mRNA and synthesize higher amounts of hyaluronan than breast cancer cell lines with a less aggressive phenotype, like MCF-7
reduced HAS 2 gene expression and increased excreted urinary hyaluronidase activity during dehydration contribute to the reduced amount of hyaluronan and to antidiuretic response
the enzyme expression is decreased in transcriptional regulation by estradiol, 4-methylumbelliferone, and TGF-beta1
transforming grwoth factor 1beta significantly inhibits HAS3 expression and protein formation