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人 SerpinA6 基因ORF全长cDNA克隆(表达载体), N-Flag 标签

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表达宿主: Human Cells  
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10998-H08H-50
10998-H08H-100
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100 µg 
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表达宿主: Human Cells  
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50314-M08H-50
50314-M08H-100
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100 µg 
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反应性: Human  
应用 : ELISA  
    10998-R037-50
    10998-R037-100
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    100 µg 
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    反应性: Human  
    应用 : ELISA  
      10998-RP01-400
      10998-RP01-200
      10998-RP01-100
      400 µg 
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      100 µg 
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      反应性: Human  
      应用 : ELISA  
        10998-RP02-50
        10998-RP02-200
        10998-RP02-100
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        200 µg 
        100 µg 
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        反应性: Mouse  
        应用 : ELISA  
          50314-RP02-50
          50314-RP02-200
          50314-RP02-100
          50 µg 
          200 µg 
          100 µg 
          Add to Cart
          反应性: Mouse  
          应用 : ELISA  
            50314-RP01-400
            50314-RP01-200
            50314-RP01-100
            400 µg 
            200 µg 
            100 µg 
            Add to Cart
            反应性: Mouse  
            应用 : ELISA  
              50314-R014-50
              50314-R014-100
              50 µg 
              100 µg 
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              SerpinA6 cdna-clone 研究背景

              Corticosteroid-binding globulin (CBG), also known as SerpinA6, is a non-inhibitory member of the serine proteinase inhibitor (serpin) superfamily. It is the high-affinity transport protein for glucocorticoids in vertebrate blood. CBG is specifically cleaved by this protease at a precise site close to its carboxy-terminus. This induces a conformation change and disrupts the binding between glucocorticoids and CBG, and promotes a significant and local release of glucocorticoids (over 90% of them are bound to CBG in human plasma). In this context, CBG directs glucocorticoids to sites of inflammation, and plays in consequence a crucial role in efficient glucocorticoid action in physiology. The SerpinA6 protein is mainly secreted by the liver. This negative acute phase protein regulates free cortisol levels in the blood and distributes cortisol to its target tissues. SerpinA6 deficiency is an extremely rare hereditary disorder characterized by reduced corticosteroid-binding capacity with normal or low plasma corticosteroid-binding globulin concentration, and normal or low basal cortisol levels associated with hypo-/hypertension and muscle fatigue. There are three heritable, human CBG gene mutations that can reduce CBG-cortisol binding affinity and/or reduce circulating CBG levels.

               SerpinA6 cdna-clone 参考资料
            • Seralini GE. (1991) A new role for corticosteroid binding globulin (CBG), member of SERPIN superfamily. C R Seances Soc Biol Fil. 185(6): 500-9.
            • Buss C, et al. (2007) Haploinsufficiency of the SERPINA6 gene is associated with severe muscle fatigue: A de novo mutation in corticosteroid-binding globulin deficiency. J Neural Transm. 114(5): 563-9.
            • Torpy DJ, et al. (2007) Corticosteroid-binding globulin gene polymorphisms: clinical implications and links to idiopathic chronic fatigue disorders. Clin Endocrinol (Oxf). 67(2): 161-7.
            • Braun BC, et al. (2010) Effect of mutations of the human serpin protein corticosteroid-binding globulin on cortisol-binding, thermal and protease sensitivity. J Steroid Biochem Mol Biol. 120(1): 30-7.
            • Lin HY, et al. (2010) Molecular and structural basis of steroid hormone binding and release from corticosteroid-binding globulin. Mol Cell Endocrinol. 316(1): 3-12.
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