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Merck
CN

HPA000647

Sigma-Aldrich

Anti-FAM109B antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

别名:

Anti-Protein FAM109B antibody produced in rabbit

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关于此项目

UNSPSC代码:
12352203
人类蛋白质图谱编号:
NACRES:
NA.41
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生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

产品线

Prestige Antibodies® Powered by Atlas Antibodies

表单

buffered aqueous glycerol solution

种属反应性

human

技术

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:50-1:200

免疫原序列

AWVKVLSRASFGYMRLVVRELESQLQDARQSLALQRRSSWKSVASRCKPQAPNHRAAGLENGHCLSKDSSPVGLVEEAGSRSAGWGLAEWELQGPASLLLGKGQSPVSPETSCFSTLHDWYGQEIVELRQCWQKRAQGSHSKCEEQ

运输

wet ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... FAM109B(150368)

免疫原

Protein FAM109B recombinant protein epitope signature tag (PrEST)

应用

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

生化/生理作用

The gene FAM109B is also known as Ses2 and IPIP27B. It is localized on endosomes along with APPL1 and Ses1 but resides on different endosomal subpopulations. The gene is a key player in endocytic trafficking and defects in this process are responsible for the pathology of Lowe syndrome and Dent disease.

特点和优势

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

外形

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

其他说明

Corresponding Antigen APREST73442

法律信息

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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储存分类代码

10 - Combustible liquids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)

法规信息

新产品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Laura E Swan et al.
Proceedings of the National Academy of Sciences of the United States of America, 107(8), 3511-3516 (2010-02-06)
Mutations of the inositol 5' phosphatase oculocerebrorenal syndrome of Lowe (OCRL) give rise to the congenital X-linked disorders oculocerebrorenal syndrome of Lowe and Dent disease, two conditions giving rise to abnormal kidney proximal tubule reabsorption, and additional nervous system and
Christopher J Noakes et al.
Molecular biology of the cell, 22(5), 606-623 (2011-01-15)
Mutation of the inositol polyphosphate 5-phosphatase OCRL1 results in two disorders in humans, namely Lowe syndrome (characterized by ocular, nervous system, and renal defects) and type 2 Dent disease (in which only the renal symptoms are evident). The disease mechanisms

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