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Human Monoclonal HAS2 Primary Antibody für ICC, IHC - ABIN1098124
Okuda, Kobayashi, Xia, Watabe, Pai, Hirota, Xing, Liu, Pandey, Fukuda, Modur, Ghosh, Wilber, Watabe: Hyaluronan synthase HAS2 promotes tumor progression in bone by stimulating the interaction of breast cancer stem-like cells with macrophages and stromal cells. in Cancer research 2012
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Human Polyclonal HAS2 Primary Antibody für FACS, IHC (p) - ABIN651874
Simpson, Wilson, Furcht, Spicer, Oegema, McCarthy: Manipulation of hyaluronan synthase expression in prostate adenocarcinoma cells alters pericellular matrix retention and adhesion to bone marrow endothelial cells. in The Journal of biological chemistry 2002
Show all 6 Pubmed References
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 is not essential for this early activation of has2.
propose here a rather unique role of Med10 in orchestrating cardiac valve formation by mediating Foxn4 dependent tbx2b transcription, expression of Has2 and subsequently proper development of the cardiac jelly
identify Npnt as a novel upstream regulator of Bmp4-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, tbx20, 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) 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 or HA synthase 2 in surfactant-protein-C-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(-/-) joints can be at least partly explained by the markedly enhanced expression of particular genes in pathways linked to ECM turnover, IL-17/IL-6 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-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 caused rapid increases in versican mRNA and protein, a rapid increase in Has1 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.
This study identifies Has2 as a novel downstream target of Shh signaling required for joint patterning and chondrogenesis.
HAS2 was significantly upregulated at the level of gene expression during muscle hypertrophy.
analysis of changes in cervical glycosaminoglycan composition during normal pregnancy and preterm birth: Has1 is expressed in preterm birth, while Has2 is induced at term
NSMase2/Cer are the key mediators of the regulation of HA synthesis, via microdomains and the Akt/mTOR pathway
repression of HA-accumulation by both COX-2 selective and non-selective COX inhibition implicates COX-2 in the regulation of HA synthesis via stimulation of HAS1 and HAS2 expression in vivo
Inhibition of Has2 expression and extracellular hyaluronic acid production requires MiR23 in the embryonic heart to restrict endocardial cushion formation.
Data show that Has2 knockout mice died near birth and displayed severe abnormality in skeletal development.
PDGF-BB stimulates cultured cardiomyocytes to synthesize the extracellular matrix component hyaluronan via HAS2
Data suggest that hyaluronan production by Has2 in chondrocytes is not only essential for formation of an organized growth plate and subsequent long bone growth but also for normal modeling of the diaphyseal bone.
hyaluronan synthase 2 activity is regulated by dimerization and ubiquitination
This study indicates that elevated expression of HAS2 is associated with glioma progression
hyaluron synthase 2 has a role in stem cell senescence
COX-2, GREM1, and HAS2 are cumulus cell genes that potentially determine oocyte and embryo developmental competence. (Review)
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 siRNA induced GFAT2 which was hardly measurable in these cells under standard culture conditions, GNPDA2 siRNA increased GFAT1, and GFAT1 siRNA increased the expression of hyaluronan synthase 2 (HAS2). Silencing of GFAT1 stimulated GNPDA1 and GDPDA2, and inhibited cell migration.
Results show that cancer-associated fibroblasts (CAFs) expresses higher levels of HAS2 and suggest that HAS2 is one of the key regulators responsible for CAF-mediated oral squamous cell carcinoma progression by modulating the balance of MMP1 and TIMP1.
stable hyaluronate synthase 2 (HAS2) overexpression in estrogen receptor alpha (ERalpha) -positive MCF7 cells oppositely altered estrogen dependence of cell growth and its sensitivity towards antiestrogens.
Reduced expression of HAS1 and HAS2 is associated with melanoma progression and suggests that HAS1 and HAS2 have a prognostic significance in cutaneous melanoma.
Results demonstrate that hypoxia induces HAS2 expression and thereby HA production, which contributes to EMT of oral squamous cell carcinoma. This process is mediated by HAS2-AS1, 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 were the only hyaluronan synthases detected, the expression of which was almost similar in NPs 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) pathway on HAS2 function.
HAS-2 gene silencing may inhibit proliferation and promote apoptosis in the MCF-7 human breast cancer cell line.
Our study establishes HAS2-mediated HA synthesis as a driver of growth of bladder cancer with low AGL and provides preclinical rationale for personalized targeting of HAS2/HA signaling in patients with low amylo-alpha-1-6-glucosidase-4-alpha-glucanotransferase -expressing tumors.
HAS2-HA system influences the biological characteristics of human breast cancer cells
Regulation of Hyaluronan (HA) Metabolism Mediated by HYBID (Hyaluronan-binding Protein Involved in HA Depolymerization, KIAA1199) and HA Synthases in Growth Factor-stimulated Fibroblasts.
Our study identified HAS2 as a novel candidate gene for susceptibility to adult asthma.
In contrast to other carcinoma subtypes, HAS2 expression was observed in up to 72.7% of metaplastic carcinomas of breast, a carcinoma subtype related to the epithelial-mesenchymal transition.
transcriptional regulation of the HAS and HAS2-antisense RNA 1 genes, was analyzed.
Direct targeting of hyaluronan synthase 2 by miR-574 negatively impacts oocyte quality during in vitro maturation and inhibiting miR-574 derepresses HAS2 expression and subsequently improves oocyte maturation.
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).
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