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  • Katacalcin TFA
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Katacalcin TFA

KatacalcinTFA(PDN21TFA)是一种有效的具有降低血钙效应的多肽激素。

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¥1737-13887
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1390-11110
Katacalcin TFA的二维码

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  • 库存: 现货
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  • 货号: ajcx13640
  • CAS: N/A
  • 别名: PDN 21 TFA
  • 分子式: C99H155F3N34O38S2
  • 分子量: 2550.62
  • 纯度: >98%
  • 溶解度: Soluble in Water
  • 储存: Store at -20°C
  • 库存: 现货

Background

Katacalcin TFA (PDN 21 TFA) is a potent plasma calcium-lowering peptide[1].


Katacalcin is a potent plasma calcium lowering peptide. Katacalcin belongs to the calcitonin family, that causes a rapid but short-lived drop in the level of calcium and phosphate in blood by promoting the incorporation of these ions in the bones[1]. Katacalcin (KC) belongs to a small family of polypeptides that are encoded by the calc-1 gene and also include calcitonin (CT) and procalcitonin NH2-terminal cleavage peptide (N-ProCT). Katacalcin pretreatment leads to a concentration-dependent decrease at concentrations between 1 amol/liter and 10 fmol/liter and is a more potent inhibitor of fMLP-induced chemotaxis than CT or procalcitonin (PCT). Katacalcin deactivates CD14+ peripheral blood mononuclear cell (PBMC) chemotaxis not only toward N-formyl-Met-Leu-Phe (fMLP) but also toward other attractants of the chemokine family (heterologous deactivation) as well as toward PCT and CT. Pretreatment of CD14+ PBMCs with Katacalcin also deactivates subsequent chemotaxis toward Katacalcin itself. Katacalcin elicites concentration-dependent migration of CD14+ PBMC at concentrations from the atomolar to the micromolar range and deactivates attractant-induced chemotaxis. Katacalcin regulates human CD14+ PBMC migration via signaling events involving protein kinase A-dependent cAMP pathways[2].


[1]. Hillyard CJ, et al. Katacalcin: a new plasma calcium-lowering hormone. Lancet. 1983 Apr 16;1(8329):846-8. [2]. Kaneider NC, et al. Involvement of cyclic adenosine monophosphate-dependent protein kinase A and pertussis toxin-sensitive G proteins in the migratory response of human CD14+ mononuclear cells tokatacalcin. J Bone Miner Res. 2002 Oct;17(10):1872-82.

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