Hyaluronic acid (HA) stimulates the in vitro expression of CD44 proteins but not HAS1 proteins in normal human epidermal keratinocytes (NHEKs) and is HA molecular weight dependent.
Epigenome-wide association study in healthy individuals identifies significant associations with DNA methylation and PBMC extract VEGF-A concentration.
There was a higher HAS1 and HAS2 reactivity and lower HAS3 reactivity in the PCOS endometrium compared to women with regular menstrual cycles in the proliferative phase.
These results demonstrate that miR-125a could constrain cell migration invasion and regulate HAS1 expression in renal cell carcinoma cells by targeting STAT3.
Reduced expression of HAS1 and HAS2 is associated with melanoma progression and suggests that HAS1 and HAS2 have a prognostic significance in cutaneous melanoma.
Regulation of Hyaluronan (HA) Metabolism Mediated by HYBID (Hyaluronan-binding Protein Involved in HA Depolymerization KIAA1199) and HA Synthases in Growth Factor-stimulated Fibroblasts.
The minor allele genotypes of HAS1 SNPs are significantly more frequent in MM WM CLL and in affected members of a monoclonal gammopathy-prone family than they are in breast cancer sporadic MGUS or healthy donors
The HAS1-dependent coat is induced by inflammatory agents and glycemic stress mediated by altered presentation of either CD44 or hyaluronan and can offer a rapid cellular response to injury and inflammation.
aberrant intronic HAS1 splicing in multiple myeloma patients may rely on intronic HAS1 deletions and mutations that are frequent in MM patients but absent from healthy donors
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