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Rabbit Anti-Factor X heavy chain/APC Conjugated antibody (bs-7762R-APC)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-7762R-APC
英文名稱 Rabbit Anti-Factor X heavy chain/APC Conjugated antibody
中文名稱 APC標(biāo)記的凝血因子10抗體
別    名 Activated factor Xa heavy chain; Coagulation factor; Coagulation factor X; EC 3.4.21.6; F10 antibody FA10_HUMAN; Factor Xa; FX; FXA; Prothrombinase; Stuart factor; Stuart Prower factor; Stuart-Prower factor.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 心血管  細(xì)胞生物  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Dog, Cow, )
產(chǎn)品應(yīng)用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 28kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human factor Xa heavy chain
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產(chǎn)品介紹 background:
This gene encodes the vitamin K-dependent coagulation factor X of the blood coagulation cascade. This factor undergoes multiple processing steps before its preproprotein is converted to a mature two-chain form by the excision of the tripeptide RKR. Two chains of the factor are held together by 1 or more disulfide bonds; the light chain contains 2 EGF-like domains, while the heavy chain contains the catalytic domain which is structurally homologous to those of the other hemostatic serine proteases. The mature factor is activated by the cleavage of the activation peptide by factor IXa (in the intrisic pathway), or by factor VIIa (in the extrinsic pathway). The activated factor then converts prothrombin to thrombin in the presence of factor Va, Ca+2, and phospholipid during blood clotting. Mutations of this gene result in factor X deficiency, a hemorrhagic condition of variable severity. Alternative splicing results in multiple transcript variants encoding different isoforms that may undergo similar proteolytic processing to generate mature polypeptides. [provided by RefSeq, Aug 2015]

Function:
Factor Xa is a vitamin K-dependent glycoprotein that converts prothrombin to thrombin in the presence of factor Va, calcium and phospholipid during blood clotting.

Subunit:
The two chains are formed from a single-chain precursor by the excision of two Arg residues and are held together by 1 or more disulfide bonds. Forms heterodimer with SERPINA5.

Subcellular Location:
Secreted.

Tissue Specificity:
Plasma; synthesized in the liver.

Post-translational modifications:
The vitamin K-dependent, enzymatic carboxylation of some glutamate residues allows the modified protein to bind calcium.
N- and O-glycosylated. O-glycosylated with core 1 or possibly core 8 glycans.
The activation peptide is cleaved by factor IXa (in the intrinsic pathway), or by factor VIIa (in the extrinsic pathway).
The iron and 2-oxoglutarate dependent 3-hydroxylation of aspartate and asparagine is (R) stereospecific within EGF domains.

DISEASE:
Defects in F10 are the cause of factor X deficiency (FA10D) [MIM:227600]. A hemorrhagic disease with variable presentation. Affected individuals can manifest prolonged nasal and mucosal hemorrhage, menorrhagia, hematuria, and occasionally hemarthrosis. Some patients do not have clinical bleeding diathesis.

Similarity:
Belongs to the peptidase S1 family.
Contains 2 EGF-like domains.
Contains 1 Gla (gamma-carboxy-glutamate) domain.
Contains 1 peptidase S1 domain.

Database links:

Entrez Gene: 2159 Human

Omim: 227600 Human

SwissProt: P00742 Human

Unigene: 361463 Human

 



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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