Tumor necrosis factor receptor superfamily member EDAR; Anhidrotic ectodysplasin receptor 1; Downless; Ectodermal dysplasia receptor; Ectodysplasin-A receptor; Edar; Dl

For Research Use Only. Not for use in diagnostic procedures.

For long term storage, please store the entire kit at -20 degree C.

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Small volumes of Edar elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS2888090 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Tumor necrosis factor receptor superfamily member EDAR, ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing Edar. The ELISA analytical biochemical technique of the MBS2888090 kit is based on Edar antibody-Edar antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect Edar antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, Edar. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

51,690 Da

ectodysplasin A receptor

tumor necrosis factor receptor superfamily member EDAR

Tumor necrosis factor receptor superfamily member EDAR

DL??[Similar Products]

EDAR_HUMAN

This gene encodes a member of the tumor necrosis factor receptor family. The encoded transmembrane protein is a receptor for the soluble ligand ectodysplasin A, and can activate the nuclear factor-kappaB, JNK, and caspase-independent cell death pathways. It is required for the development of hair, teeth, and other ectodermal derivatives. Mutations in this gene result in autosomal dominant and recessive forms of hypohidrotic ectodermal dysplasia. [provided by RefSeq, Jul 2008]

EDAR: Receptor for EDA isoform A1, but not for EDA isoform A2. Mediates the activation of NF-kappa-B and JNK. May promote caspase-independent cell death. Defects in EDAR are a cause of ectodermal dysplasia anhidrotic (EDA); also known ectodermal dysplasia hypohidrotic autosomal recessive (HED). Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. EDA is characterized by sparse hair (atrichosis or hypotrichosis), abnormal or missing teeth and the inability to sweat due to the absence of sweat glands. Defects in EDAR are the cause of ectodermal dysplasia type 3 (ED3); also known as ectodermal dysplasia hypohidrotic autosomal dominant or EDA3. ED3 is an autosomal dominant condition characterized by hypotrichosis, abnormal or missing teeth, and hypohidrosis due to the absence of sweat glands.

Protein type: Membrane protein, integral; Receptor, misc.

Chromosomal Location of Human Ortholog: 2q13

Cellular Component: plasma membrane

Molecular Function: protein binding; receptor activity

Biological Process: epidermis development; positive regulation of I-kappaB kinase/NF-kappaB cascade; positive regulation of JNK cascade; tumor necrosis factor-mediated signaling pathway

Disease: Ectodermal Dysplasia 10a, Hypohidrotic/hair/nail Type, Autosomal Dominant; Ectodermal Dysplasia 10b, Hypohidrotic/hair/tooth Type, Autosomal Recessive; Hair Morphology 1

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