EDAR cDNA ORF Clone in Cloning Vector, Human

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EDAR cDNA ORF Clone in Cloning Vector, Human: General Information

Gene
Species
Human
NCBI Ref Seq
RefSeq ORF Size
1347 bp
Sequence Description
Identical with the Gene Bank Ref. ID sequence except for two point mutations: 750 C/T, 1056 C/T not causing the amino acid variation.
Description
ORF Clone of Human ectodysplasin A receptor DNA.
Plasmid
Quality Control
The plasmid is confirmed by full-length sequencing.
Screening
Antibiotic in E.coli
Ampicillin
Storage & Shipping
Shipping
Each tube contains lyophilized plasmid.
Storage
The lyophilized plasmid can be stored at ambient temperature for three months.

EDAR cDNA ORF Neucleotide Sequence and Amino Acid Sequence Information

**Sino Biological guarantees 100% sequence accuracy of all synthetic DNA constructs we deliver, but we do not guarantee protein expression in your experimental system. Protein expression is influenced by many factors that may vary between experiments or laboratories.**

EDAR cDNA ORF Clone in Cloning Vector, Human: Alternative Names

DL cDNA ORF Clone, Human; ECTD10A cDNA ORF Clone, Human; ECTD10B cDNA ORF Clone, Human; ED1R cDNA ORF Clone, Human; ED3 cDNA ORF Clone, Human; ED5 cDNA ORF Clone, Human; EDA-A1R cDNA ORF Clone, Human; EDA1R cDNA ORF Clone, Human; EDA3 cDNA ORF Clone, Human; HRM1 cDNA ORF Clone, Human

EDAR Background Information

Tumor necrosis factor receptor superfamily member EDAR is a Single-pass type I membrane protein. Edar was expressed reiteratively in signaling centers regulating key steps in morphogenesis. activin signaling from mesenchyme induces the expression of the TNF receptor edar in the epithelial signaling centers, thus making them responsive to Wnt-induced ectodysplasin from the nearby ectoderm. This is the first demonstration of integration of the Wnt, activin, and TNF signaling pathways. 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.
Full Name
ectodysplasin A receptor
References
  • Elomaa O, et al. (2001) Ectodysplasin is released by proteolytic shedding and binds to the EDAR protein. Hum Mol Genet. 10 (9): 953-62.
  • Koppinen P, et al. (2001) Signaling and subcellular localization of the TNF receptor Edar. Exp Cell Res. 269 (2): 180-92.
  • Chassaing N, et al. (2006) Mutations in EDAR account for one-quarter of non-ED1-related hypohidrotic ectodermal dysplasia. Hu. Mutat. 27 (3): 255-9.
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