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产品信息 >> 蛋白相关 >> 重组蛋白;
Recombinant MouseEDAR, C-Fc, Human Cells

产品描述

概述

Recombinant Mouse Ectodysplasin Receptor is produced by our Mammalian expression system and the target gene encoding Glu27-Ile189 is expressed with a Fc tag at the C-terminus.

使用说明

This material is offered by Novin Biotech for research, laboratory or further evaluation purposes. NOT FOR HUMAN USE.

技术规格

TagC-Fc
种属Mouse
表达系统Human Cells
Accession#Q9R187
SourceHuman Cells
Formulation_DescriptionLyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.
StorageLyophilized protein should be stored at < -20°C, though stable at room temperature for 3 weeks.Reconstituted protein solution can be stored at 4-7°C for 2-7 days.Aliquots of reconstituted samples are stable at < -20°C for 3 months.
ReconstitutionDissolve the lyophilized protein in distilled water.
PurityGreater than 95% as determined by reducing SDS-PAGE.
EndotoxinLess than 0.1 ng/μg (1 EU/μg) as determined by LAL test.
BackgroundEctodysplasin A receptor (EDAR) is a type I transmembrane protein of the TNF-α receptor superfamily which plays a key role in ectodermal differentiation. EDAR was encoded by the mouse downless gene and defective in human dominant and recessive forms of autosomal hypohidrotic ectodermal dysplasia (EDA) syndrome. The extracellular domain of EDAR contains 14 cysteine residues, six of which approximate the TNFRSF cysteine-rich region, the cytoplasmic domain contains a region with homology to the death domains found in other TNFRSF members. EDAR has been suggested to be an early and important promoter of placode development in all ectodermal organs, such as uch as hair follicles, teeth and sweat glands. EDA-A1, the A1 isoform of EDA, is the EDAR ligand. EDA and EDA are implicated in appendage development by the cloning of a gene underlying hypohidrotic ectodermal dysplasia (HED) in mouse and human. HED is characterized by agenesis or malformation of ectoderm-derived appendages, such as teeth, sweat glands and hair follicles, while the skin itself develops normally.
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