Hyaluronan Synthase 2 (HAS2) Antibody
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Description
Catalyzes the addition of GlcNAc or GlcUA monosaccharides to the nascent hyaluronan polymer. Therefore, it is essential to hyaluronan synthesis a major component of most extracellular matrices that has a structural role in tissues architectures and regulates cell adhesion, migration and differentiation. This is one of the isozymes catalyzing that reaction and it is particularly responsible for the synthesis of high molecular mass hyaluronan. Required for the transition of endocardial cushion cells into mesenchymal cells, a process crucial for heart development. May also play a role in vasculogenesis. High molecular mass hyaluronan also play a role in early contact inhibition a process which stops cell growth when cells come into contact with each other or the extracellular matrix.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Hyaluronan Synthase 2 (HAS2) |
| Host | Mouse |
| Reactivity | Human |
| Recommended Dilution | ELISA: 1/10000, WB: 1/500 - 1/2000, IHC: 1/200 - 1/1000, IF/ICC: 1/100 - 1/500. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Monoclonal |
| Conjugation | Unconjugated |
| Isotype | IgG1 |
| Clone ID | H010 |
| Purification | Purified from ascites by Protein G chromatography. |
| Size 1 | 100 µl |
| Form | Liquid |
| Tested Applications | ELISA, WB, IHC, IF/ICC |
| Buffer | PBS, containing 0.05% sodium azide. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q92819 |
| Gene ID | 3037 |
| OMIM | 601636 |
| Background | Antibody anti-HAS2 |
| Status | RUO |
| Note | Concentration: 1 mg/ml - |
Descripción
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Human HAS2 (Hyaluronan synthase 2) ELISA Kit
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Hyaluronan Synthase 2 (HAS2) Antibody
Catalyzes the addition of GlcNAc or GlcUA monosaccharides to the nascent hyaluronan polymer. Therefore, it is essential to hyaluronan synthesis a major component of most extracellular matrices that has a structural role in tissues architectures and regulates cell adhesion, migration and differentiation. This is one of the isozymes catalyzing that reaction and it is particularly responsible for the synthesis of high molecular mass hyaluronan. Required for the transition of endocardial cushion cells into mesenchymal cells, a process crucial for heart development. May also play a role in vasculogenesis. High molecular mass hyaluronan also play a role in early contact inhibition a process which stops cell growth when cells come into contact with each other or the extracellular matrix.
Ver Producto
Hyaluronan Synthase 2 (HAS2) Antibody
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.
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