Factor XIIIa (F13A1) Mouse Monoclonal Antibody [Clone ID: LBI8E2]

Factor XIIIa (F13A1) Mouse Mon

oclonal Antibody [Clone ID: LBI8E2]
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  • ¥3300
  • Leading Biology
  • 美国
  • 2025年07月14日
  • WB 1:2000
  • Mouse
  • Human, Mouse, Rat
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    • 详细信息
    • 技术资料
    • 靶点

      F13A1

    • 应用范围

      WB 1:2000

    • 宿主

      Mouse

    • 适应物种

      Human, Mouse, Rat

    • 保质期

      1-2年

    • 供应商

      安诺伦(北京)生物科技有限公司

    • 标记物

      Unconjugated

    • 克隆性

      Monoclonal Antibody

    • 保存条件

      Stable for 1 year at -20°C from date of shipment. For long-term storage, aliquot and store at -20°C or below. Stable for 12 months at -20°C. Avoid repeated freeze-thaw cycles.

    • 形态

      Lyophilized powder (original buffer 1X PBS, pH 7.3, 8% trehalose)

    • 亚型

      IgG2b

    • 免疫原

      Full length human recombinant protein of human F13A1 (NP_000120) produced in HEK293T cell.

    • 规格

      100 ug

    别名:F13A

    产品概述:Carrier-free (BSA/glycerol-free) F13A1 mouse monoclonal antibody, clone LBI8E2

    总结:This gene encodes the coagulation factor XIII A subunit. Coagulation factor XIII is the last zymogen to become activated in the blood coagulation cascade. Plasma factor XIII is a heterotetramer composed of 2 A subunits and 2 B subunits. The A subunits have catalytic function, and the B subunits do not have enzymatic activity and may serve as plasma carrier molecules. Platelet factor XIII is comprised only of 2 A subunits, which are identical to those of plasma origin. Upon cleavage of the activation peptide by thrombin and in the presence of calcium ion, the plasma factor XIII dissociates its B subunits and yields the same active enzyme, factor XIIIa, as platelet factor XIII. This enzyme acts as a transglutaminase to catalyze the formation of gamma-glutamyl-epsilon-lysine crosslinking between fibrin molecules, thus stabilizing the fibrin clot. It also crosslinks alpha-2-plasmin inhibitor, or fibronectin, to the alpha chains of fibrin. Factor XIII deficiency is classified into two categories: type I deficiency, characterized by the lack of both the A and B subunits; and type II deficiency, characterized by the lack of the A subunit alone. These defects can result in a lifelong bleeding tendency, defective wound healing, and habitual abortion. [provided by RefSeq]

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