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Fgf signaling is required early, from 6 to 10h pf,for has2 activation. Loss of has2 results inthe loss of the chondrogenic program resulting in postchordal neurocranial defects in Fgf loss-of-function embryos. Shh (show SHH Proteins) is not essential for this early activation of has2.
propose here a rather unique role of Med10 (show MED10 Proteins) in orchestrating cardiac valve formation by mediating Foxn4 (show FOXN4 Proteins) dependent tbx2b transcription, expression of Has2 and subsequently proper development of the cardiac jelly
identify Npnt (show NPNT Proteins) as a novel upstream regulator of Bmp4 (show BMP4 Proteins)-Has2 signaling that plays a crucial role in AV canal differentiation
MiR-23 is both necessary and sufficient for restricting the number of endocardial cells that differentiate into endocardial cushion cells by inhibiting Has2 and extracellular hyaluronic acid production.
data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5 (show TBX5 Proteins), tbx20 (show TBX20 Proteins), and has2 in the hear
allergen-challenged mice that overexpress HAS2 in myofibroblasts and smooth muscle cells develop increased airway fibrosis, which lessens airway hyperresponsiveness to bronchoconstrictors.
Expression of the innate immune receptor Toll-like receptor 4 (TLR4 (show TLR4 Proteins)) and the extracellular matrix glycosaminoglycan hyaluronan (HA) on type 2 alveolar epithelial cells (AEC@2) are important for AEC2 renewal, repair of lung injury and limiting the extent of fibrosis. Either deletion of TLR4 (show TLR4 Proteins) or HA synthase 2 in surfactant-protein-C (show SFTPC Proteins)-positive AEC2s leads to impaired renewal capacity, severe fibrosis and mortality.
Has2 mRNA was expressed in the surrounding mesenchyme from E12.0 to 18.0 in both molar and incisor tooth germs, but disappeared after birth.
the ineffective repair of injured cartilage in Has1 (show HAS1 Proteins)(-/-) joints can be at least partly explained by the markedly enhanced expression of particular genes in pathways linked to ECM (show MMRN1 Proteins) turnover, IL-17 (show IL17A Proteins)/IL-6 (show IL6 Proteins) cytokine signaling, and apoptosis.
these results highlight the role of nSMase2 in apoptosis evoked by nutrient starvation that could contribute to the delayed apoptosis of hypertrophic chondrocytes in the growth plate, and emphasize the antiapoptotic properties of HAS2
mir (show MLXIP Proteins)-23a-3p causes cellular senescence by targeting hyaluronan synthase 2: possible implication for skin aging.
Has2 expression and hyaluronan produced at the tips of epithelial cells play a critical role in driving tubulogenesis and branching in vitro.
Hyaluronan synthase 2 has a role in protecting skin fibroblasts against apoptosis induced by environmental stress
Stimulation with LPS (show TLR4 Proteins) caused rapid increases in versican (show Vcan Proteins) mRNA and protein, a rapid increase in Has1 (show HAS1 Proteins) mRNA, and concomitant inhibition of hyaluronidases 1 and 2, the major hyaluronan degrading enzymes
This study demonistrated that Has2 expression in adult mouse subventricular zone and rostral migratory stream and in ischemic cortex.
HAS2 may be a critical regulator of the fate of pulmonary fibrosis and we propose a model where over-expression of HAS2 promotes an invasive phenotype resulting in severe fibrosis and down-regulation of HAS2 promotes resolution.
GNPDA1 (show GNPDA1 Proteins) siRNA induced GFAT2 which was hardly measurable in these cells under standard culture conditions, GNPDA2 (show GNPDA2 Proteins) siRNA increased GFAT1 (show GFPT1 Proteins), and GFAT1 (show GFPT1 Proteins) siRNA increased the expression of hyaluronan synthase 2 (HAS2). Silencing of GFAT1 (show GFPT1 Proteins) stimulated GNPDA1 (show GNPDA1 Proteins) and GDPDA2, and inhibited cell migration.
Results show that cancer-associated fibroblasts (CAFs (show TBX1 Proteins)) expresses higher levels of HAS2 and suggest that HAS2 is one of the key regulators responsible for CAF (show KAT2B Proteins)-mediated oral squamous cell carcinoma progression by modulating the balance of MMP1 (show MMP1 Proteins) and TIMP1 (show TIMP1 Proteins).
stable hyaluronate synthase 2 (HAS2) overexpression in estrogen receptor alpha (ERalpha (show ESR1 Proteins)) -positive MCF7 cells oppositely altered estrogen dependence of cell growth and its sensitivity towards antiestrogens.
Reduced expression of HAS1 (show HAS1 Proteins) and HAS2 is associated with melanoma progression and suggests that HAS1 (show HAS1 Proteins) and HAS2 have a prognostic significance in cutaneous melanoma.
Results demonstrate that hypoxia induces HAS2 expression and thereby HA production, which contributes to EMT (show ITK Proteins) of oral squamous cell carcinoma. This process is mediated by HAS2-AS1 (show PTGDR Proteins), which can bind to HAS2 gene inducing its transcription.
We identified HAS2, tumor cell-derived hyaluronic acid (HA) and ZEB1 to form a positive feedback loop as ZEB1, elevated by HA, directly activates HAS2 expression in breast cancer
The present data reveal a selective up-regulation of HAS2 expression by extracellular Uridine Triphosphate, which is likely to contribute to the previously reported rapid activation of hyaluronan metabolism in response to tissue trauma or ultraviolet radiation.
HAS2 and HAS3 (show HAS3 Proteins) were the only hyaluronan synthases detected, the expression of which was almost similar in NPs (show NPS Proteins) and NM.
HAS2 has been proposed to be a target for therapeutic intervention in cancer. Our findings suggested a possible antagonistic role of androgen receptor (AR (show AR Proteins)) pathway on HAS2 function.
In the absence of XHas2, early myoblasts underwent apoptosis, failing to complete their muscle differentiation programme. XHas2 activity is also required for migration of hypaxial muscle cells and trunk neural crest cells (NCC (show SLC12A3 Proteins)).
Hyaluronan or hyaluronic acid (HA) is a high molecular weight unbranched polysaccharide synthesized by a wide variety of organisms from bacteria to mammals, and is a constituent of the extracellular matrix. It consists of alternating glucuronic acid and N-acetylglucosamine residues that are linked by beta-1-3 and beta-1-4 glycosidic bonds. HA is synthesized by membrane-bound synthase at the inner surface of the plasma membrane, and the chains are extruded through pore-like structures into the extracellular space. It serves a variety of functions, including space filling, lubrication of joints, and provision of a matrix through which cells can migrate. HA is actively produced during wound healing and tissue repair to provide a framework for ingrowth of blood vessels and fibroblasts. Changes in the serum concentration of HA are associated with inflammatory and degenerative arthropathies such as rheumatoid arthritis. In addition, the interaction of HA with the leukocyte receptor CD44 is important in tissue-specific homing by leukocytes, and overexpression of HA receptors has been correlated with tumor metastasis. HAS2 is a member of the newly identified vertebrate gene family encoding putative hyaluronan synthases, and its amino acid sequence shows significant homology to glycosaminoglycan synthetase (DG42) from Xenopus laevis, and human and murine hyaluronan synthase 1.
hyaluronan synthase 2
, hyaluronic acid synthase 2
, HA synthase 2
, hyaluronan synthase homolog
, hyaluronate synthase 2