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

BRENDA support

Literature summary for 2.4.1.212 extracted from

  • Homann, S.; Grandoch, M.; Kiene, L.S.; Podsvyadek, Y.; Feldmann, K.; Rabausch, B.; Nagy, N.; Lehr, S.; Kretschmer, I.; Oberhuber, A.; Bollyky, P.; Fischer, J.W.
    Hyaluronan synthase 3 promotes plaque inflammation and atheroprogression (2018), Matrix Biol., 66, 67-80 .
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
drug development inhibition of hyaluronan synthase 3-dependent synthesis of hyaluronan dampens systemic Th1 cell polarization and reduces plaque inflammation. Hyaluronan synthase 3 might be a promising therapeutic target in atherosclerosis. Because hyaluronan synthase 3 is regulated by IL-1beta, therapeutic anti-IL-1beta antibodies, may exert their beneficial effects on inflammation in post-myocardial infarction patients in part via effects on hyaluronan synthase 3 Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus O08650
-
-

Source Tissue

Source Tissue Comment Organism Textmining
vascular smooth muscle cell
-
Mus musculus
-

Synonyms

Synonyms Comment Organism
HA synthase 3
-
Mus musculus
Has3
-
Mus musculus
hyaluronan synthase 3
-
Mus musculus

Expression

Organism Comment Expression
Mus musculus Has3 expression is increased early during lesion formation when macrophages enter atherosclerotic plaques up

General Information

General Information Comment Organism
malfunction Has3/Apoe double deficient mice develop less atherosclerosis characterized by decreased Th1-cell responses, decreased IL-12 release, and decreased macrophage-driven inflammation Mus musculus
physiological function hyaluronan synthase 3 promotes plaque inflammation and atheroprogression. Hyaluronan synthase 3 expression in vascular smooth muscle cells is found to be regulated by interleukin 1 beta (IL-1beta) in an NFkappaB dependent manner Mus musculus