4)经纯化制备的抗体在常用的缓冲液中是稳定的。其DH应保持在中性左右。如果pH在7-8之间,即使保存多年,对抗体也无损害。多数情况下,盐浓度适于保持在0-150mmol/L之间,但在长期存放的抗体中,盐溶液浓度高达500mmol/L时,对
抗体来源 Rabbit
克隆类型 polyclonal
交叉反应 Human, Mouse, Rat, Chicken, Dog, Cow, Horse
产品类型 一抗
研究领域 细胞生物 发育生物学 转录调节因子 表观遗传学
蛋白分子量 predicted molecular weight: 57kDa
性 状 Lyophilized or Liquid
免 疫 原 KLH conjugated synthetic peptide derived from human FOXC1/FREAC3
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4
产品应用 WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500
(石蜡切片需做抗原修复)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
保存条件 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.
Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
叉头相关转录因子3抗体产品介绍 Binding of FREAC-3 and FREAC-4 to their cognate sites results in bending of the DNA at an angle of 80-90 degrees.
Involvement in disease; Defects in FOXC1 are the cause of Axenfeld-Rieger syndrome type 3 (RIEG3); also known as Axenfeld-Rieger syndrome (ARS) or Axenfeld syndrome or Axenfeld anomaly. It is characterized by posterior corneal embryotoxon, prominent Schwalbe line and iris adhesion to the Schwalbe line. Other features may be hypertelorism (wide spacing of the eyes), hypoplasia of the malar bones, congenital absence of some teeth and mental retardation. When associated with tooth anomalies, the disorder is known as Rieger syndrome. Glaucoma is a progressive blinding condition that occurs in approximately half of patients with Axenfeld-Rieger malformations.
Subunit : Monomer.
Subcellular Location : Nucleus.
Tissue Specificity : Expressed in all tissues and cell lines examined.
Similarity : Contains 1 fork-head DNA-binding domain.
[DISEASE] Defects in FOXC1 are the cause of iridogoniodysgenesis anomaly (IGDA) [MIM:601631]. IGDA is an autosomal dominant phenotype characterized by iris hypoplasia, goniodysgenesis, and juvenile glaucoma.
[DISEASE] Defects in FOXC1 are a cause of Peters anomaly (PAN) [MIM:604229]. Peters anomaly consists of a central corneal leukoma, absence of the posterior corneal stroma and Descemet membrane, and a variable degree of iris and lenticular attachments to the central aspect of the posterior cornea.