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产品介绍/ PRODUCT PRESENTATION产品编号 yb-14656R
英文名称 Anti-EXDL1抗体
中文名称 EXDL1蛋白抗体
别 名 exd1; EXD1_HUMAN; MGC33637; OTTHUMP00000160721.
Anti-EXDL1抗体
说 明 书 0.2ml
研究领域 细胞生物 神经生物学
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Rabbit, Sheep,
产品应用 WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=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.
分 子 量 58kDa
性 状 Lyophilized or Liquid
浓 度 1mg/1ml
免 疫 原 KLH conjugated synthetic peptide derived from human EXDL1
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
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.
PubMed PubMed
产品介绍 background:
EXDL1 is a 514 amino acid protein that belongs to the EXD1 family and contains one 3'-5' exonuclease domain. Existing as two alternatively spliced isoforms, the gene encoding EXDL1 maps to human chromosome 15q15.1 and mouse chromosome 2 E5. Encoding more than 700 genes, chromosome 15 is made up of approximay 106 million base pairs and is about 3% of the human genome. Angelman and Prader-Willi syndromes are associated with loss of function or deletion of genes in the 15q11-q13 region. In the case of Angelman syndrome, this loss is due to inactivity of the maternal 15q11-q13 encoded UBE3A gene in the brain by either chromosomal deletion or mutation. In cases of Prader-Willi syndrome, there is a partial or complete deletion of this region from the paternal copy of chromosome 15.
Similarity:
Belongs to the EXD1 family.
Contains 1 3'-5' exonuclease domain.
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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