胶质细胞源性神经营养因子抗体英文名称 Anti-GDNF
中文名称 胶质细胞源性神经营养因子抗体
别 名 glial cell line derived neurotrophic factor; Astrocyte derived trophic factor 1; Astrocyte derived trophic factor; ATF 1; ATF 2; ATF1; ATF2; Glial cell derived neurotrophic factor; Glial derived neurotrophic factor; HFB1 GDNF.
浓 度 1mg/1ml
规 格 0.1ml/100μg 0.2ml/200μg
纯化的抗体可通过不同的途径获取,有些胶质细胞源性神经营养因子抗体可通过下述方法制备或从商家购买。从商家购买的抗体,通常附有正确的储存方法。
1)工作液应在4℃下融化并存放,可能稳定达数月。
2)如果没有特殊原因而避免使用叠氮钠,亦可加入叠氮钠,浓度为0.02%。将纯化的抗体样本分装成合适的体积,于-20℃保存。
3)纯化的抗体溶液应以较高的浓度(如lmg/m1)在中性pH下保存。:常用的抗体储存浓度高达l0mg/ml。较低浓度的抗体冻存前应浓缩。所有标准的浓缩方法(如超滤法),皆可使用。还有一个简单的方法是用蛋白A或蛋白G亲和柱来浓缩溶液。如果纯化的抗体不是用于标记,可将它们以较低浓度储存于加有1%BSA的溶液中。
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,对胶质细胞源性神经营养因子抗体能有损害。如果没有其他说明.律议用PBS或50mmol/LTris(DH8.0)溶液长期存放抗体。
抗体来源 Rabbit
克隆类型 polyclonal
交叉反应 Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Horse, Rabbit
产品类型 一抗
研究领域 神经生物学 细胞凋亡 生长因子和激素
蛋白分子量 predicted molecular weight: 15kDa
性 状 Lyophilized or Liquid
免 疫 原 KLH conjugated synthetic peptide derived from human GDNF C-terminus
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide
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.
胶质细胞源性神经营养因子抗体产品介绍 Neurobiology. Neurotrophins. Neuroscience.
This gene encodes a highly conserved neurotrophic factor. The recombinant form of this protein was shown to promote the survival and differentiation of dopaminergic neurons in culture, and was able to prevent apoptosis of motor neurons induced by axotomy. The encoded protein is processed to a mature secreted form that exists as a homodimer. The mature form of the protein is a ligand for the product of the RET (rearranged during transfection) protooncogene. In addition to the transcript encoding GDNF, two additional alternative transcripts encoding distinct proteins, referred to as astrocyte-derived trophic factors, have also been described. Mutations in this gene may be associated with Hirschsprung disease.
Function : Neurotrophic factor that enhances survival and morphological differentiation of dopaminergic neurons and increases their high-affinity dopamine uptake.
Subunit : Homodimer; disulfide-linked.
Subcellular Location : Secreted.
Tissue Specificity : In the brain, predominantly expressed in the striatum with highest levels in the caudate and lowest in the putamen. Isoform 2 is absent from most tissues except for low levels in intestine and kidney. Highest expression of isoform 3 is found in pancreatic islets. Isoform 5 is expressed at very low levels in putamen, nucleus accumbens, prefrontal cortex, amygdala, hypothalamus and intestine. Isoform 3 is up-regulated in the middle temporal gyrus of Alzheimer disease patients while isoform 2 shows no change.
DISEASE : Defects in GDNF may be a cause of Hirschsprung disease type 3 (HSCR3) [MIM:613711]. In association with mutations of RET gene, defects in GDNF may be involved in Hirschsprung disease. This genetic disorder of neural crest development is characterized by the absence of intramural ganglion cells in the hindgut, often resulting in intestinal obstruction.
Defects in GDNF are a cause of congenital central hypoventilation syndrome (CCHS) [MIM:209880]; also known as congenital failure of autonomic control or Ondine curse. CCHS is a rare disorder characterized by abnormal control of respiration in the absence of neuromuscular or lung disease, or an identifiable brain stem lesion. A deficiency in autonomic control of respiration results in inadequate or negligible ventilatory and arousal responses to hypercapnia and hypoxemia.
Similarity : Belongs to the TGF-beta family. GDNF subfamily.
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