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Hyaluronan synthase 3 (HAS3) and tumor necrosis factor-alpha (TNF-alpha (zeige TNF Proteine)) formed an inter-regulation loop to enhance tumorigenesis in oral cancer.
The study describes novel regulatory mechanisms governed by UDP-sugars in hyaluronan synthesis, i.e. the intracellular trafficking and extracellular shedding of HAS3. The control mechanisms reveal the significance of these glucose metabolites in hyaluronan synthesis, which is particularly important in the interactions of malignant cells with their microenvironment, and hence the progression of tumors, like melanoma.
Overexpression of HAS3 decreased ERK1/2 phosphorylation suggesting that inhibition of MAP-kinase (zeige MAPK1 Proteine) signaling was responsible for decreased melanoma cell adhesion, migration and proliferation.
HAS3 underexpression is associated with advanced tumor stage and adverse pathological features, as well as implies inferior clinical outcomes for both groups of patients with UTUCs and UBUCs, suggesting its critical role in tumor progression
Hyaluronan accumulation by HAS3 favors pancreatic cancer growth.
Transcriptional factor binding analysis indicated that HAS3 gene promoter lacks of canonical TATA box, but contains classical GC box as well as other putative binding sites for transcriptional factors
HAS3 mRNA expression level increases in atopic dermatitis lesions compared with healthy and non-lesional skin
Rab10 (zeige RAB10 Proteine) silencing increased the plasma membrane residence of HAS3, resulting in a significant increase of hyaluronan secretion and an enlarged cell surface HA coat, whereas Rab10 (zeige RAB10 Proteine) overexpression suppressed hyaluronan synthesis.
Hyaluronan (HA) produced by HAS3 is a ubiquitous component of the extracellular matrix and plays an active role in tissue remodeling. In addition, HA is known to reduce reactive oxygen species (ROS (zeige ROS1 Proteine)) -induced cardiac injury.
Data indicate that oxLDL doubled the transcripts of hyaluronan synthases HAS2 (zeige HAS2 Proteine) and HAS3 and hyaluronan deposition via the scavenger receptor LOX-1 (zeige OLR1 Proteine).
These gene expression patterns suggested that Has3 is the main control factor for prenatal and postnatal HA synthesis of the tooth germ, and may in part regulate crown and root formation of the tooth germ, maintenance of stem cell niches in the apical bud as well as mineral transport in PL.
HAS3-mediated HA synthesis after vessel injury supports seminal signaling pathways in activation of VSMC, increases platelet-derived growth factor BB-mediated migration, and in turn enhances neointimal hyperplasia in vivo.
This study demonstrates that the ablation of Has3-dependent HA causes reduced ECS volume in the CA1 (zeige CA1 Proteine) stratum pyramidale, epileptiform activity in the CA1 (zeige CA1 Proteine) region, and epileptic seizures in the mutant mouse.
Selective loss of Has1 (zeige HAS1 Proteine) and Has3 leads to a proinflammatory milieu that favors recruitment of neutrophils and other inflammation-related changes in the dermis.
sequence of xlHAS3(hyaluronan synthase 3) mRNA, its genomic organization and expression in adult tissues as well as during embryonic development; in situ hybridization indicates that expression is restricted to the developing inner ear and cement gland
hyaluronan synthase 3 is expressed by the porcine endosalpinx epithelium and the levels of expression do not vary during the critical periods of sperm transport and fertilization
The protein encoded by this gene is involved in the synthesis of the unbranched glycosaminoglycan hyaluronan, or hyaluronic acid, which is a major constituent of the extracellular matrix. This gene is a member of the NODC/HAS gene family. Compared to the proteins encoded by other members of this gene family, this protein appears to be more of a regulator of hyaluronan synthesis. Alternative splicing results in multiple transcript variants.
hyaluronan synthase 3
, hyaluronan synthase 3-like
, HA synthase 3
, hyaluronate synthase 3
, hyaluronic acid synthase 3