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Literature summary for 2.4.1.212 extracted from

  • Garoby-Salom, S.; Rouahi, M.; Mucher, E.; Auge, N.; Salvayre, R.; Negre-Salvayre, A.
    Hyaluronan synthase-2 upregulation protects smpd3-deficient fibroblasts against cell death induced by nutrient deprivation, but not against apoptosis evoked by oxidized LDL (2015), Redox Biol., 4, 118-126.
    View publication on PubMedView publication on EuropePMC
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Cloned(Commentary)

Cloned (Comment) Organism
gene has2, quantitative real time PCR enzyme expression analysis, HAS2 expression is dependent on ceramide generated by neutral type 2 sphingomyelinase, nSMase2, as shown by treatment with C2-ceramide that decreases HAS2 expression in murine fro/fro fibroblasts Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
ceramide
-
 Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus P70312 isozyme HAS2, gene has2
-
Mus musculus 129/Sv P70312 isozyme HAS2, gene has2
-

Source Tissue

Source Tissue Comment Organism Textmining
fibroblast
-
 Mus musculus
-

Synonyms

Synonyms Comment Organism
Has2
-
 Mus musculus
hyaluronan synthase-2
-
 Mus musculus

General Information

General Information Comment Organism
physiological function recombinant hyaluronan synthase-2 upregulation protects smpd3-deficient fibroblasts against cell death induced by nutrient deprivation, but not against apoptosis evoked by human oxidized LDL. Resistance of fro/fro cells to starvation-induced apoptosis is associated with an increased expression of hyaluronan synthase 2 (HAS2) mRNAs and protein, which is inhibited by ceramide. The protective mechanism of HAS2 involves an increased expression of the heat-shock protein Hsp72, a chaperone with antiapoptotic activity. Antiapoptotic properties of HAS2 , overview Mus musculus