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Mouse Anti-EDA Recombinant Antibody (4B3) (CBMAB-A2440-LY)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
4B3
Antibody Isotype
IgG2b, κ
Application
WB, ELISA

Basic Information

Immunogen
EDA (aa245-391) partial recombinant protein.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG2b, κ
Clonality
Monoclonal Antibody
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS
Preservative
None
Concentration
Batch dependent
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
ectodysplasin A
Introduction
The protein encoded by this gene is a type II membrane protein that can be cleaved by furin to produce a secreted form. The encoded protein, which belongs to the tumor necrosis factor family, acts as a homotrimer and may be involved in cell-cell signaling during the development of ectodermal organs. Defects in this gene are a cause of ectodermal dysplasia, anhidrotic, which is also known as X-linked hypohidrotic ectodermal dysplasia. Several transcript variants encoding many different isoforms have been found for this gene. [provided by RefSeq]
Entrez Gene ID
1896
UniProt ID
Q92838
Alternative Names
ED1; ED1-A1; ED1-A2; EDA1; EDA2; HED; XHED; XLHED
Research Area
Cytokine which is involved in epithelial-mesenchymal signaling during morphogenesis of ectodermal organs. Functions as a ligand activating the DEATH-domain containing receptors EDAR and EDA2R (PubMed:8696334, PubMed:11039935, PubMed:27144394).

May also play a role in cell adhesion (By similarity).

Isoform 1:
Binds only to the receptor EDAR, while isoform 3 binds exclusively to the receptor EDA2R.

Isoform 3:
Binds only to the receptor EDA2R.
Biological Process
Animal organ development Source: GO_Central
Cell differentiation Source: UniProtKB-KW
Cell-matrix adhesion Source: Ensembl
Cytokine-mediated signaling pathway Source: UniProtKB
Gene expression Source: Ensembl
Hair follicle placode formation Source: Ensembl
Immune response Source: InterPro
Odontogenesis of dentin-containing tooth Source: UniProtKB
Pigmentation Source: Ensembl
Positive regulation of canonical Wnt signaling pathway Source: Ensembl
Positive regulation of gene expression Source: Ensembl
Positive regulation of I-kappaB kinase/NF-kappaB signaling Source: Ensembl
Positive regulation of NF-kappaB transcription factor activity Source: HGNC-UCL
Positive regulation of NIK/NF-kappaB signaling Source: Ensembl
Regulation of NIK/NF-kappaB signaling Source: UniProtKB
Salivary gland cavitation Source: Ensembl
Trachea gland development Source: Ensembl
Cellular Location
Cell membrane
Ectodysplasin-A, secreted form: Secreted
Involvement in disease
Ectodermal dysplasia 1, hypohidrotic, X-linked (XHED):
A form of ectodermal dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. Characterized by sparse hair (atrichosis or hypotrichosis), abnormal or missing teeth and the inability to sweat due to the absence of sweat glands. It is the most common form of over 150 clinically distinct ectodermal dysplasias.
Tooth agenesis, selective, X-linked, 1 (STHAGX1):
A form of selective tooth agenesis, a common anomaly characterized by the congenital absence of one or more teeth. Selective tooth agenesis without associated systemic disorders has sometimes been divided into 2 types: oligodontia, defined as agenesis of 6 or more permanent teeth, and hypodontia, defined as agenesis of less than 6 teeth. The number in both cases does not include absence of third molars (wisdom teeth).
Topology
Cytoplasmic: 1-41
Helical: 42-62
Extracellular: 63-391
PTM
N-glycosylated.
Processing by furin produces a secreted form.
More Infomation

Yang, R., Mei, Y., Jiang, Y., Li, H., Zhao, R., Sima, J., & Yao, Y. (2022). Ectodysplasin A (EDA) Signaling: From Skin Appendage to Multiple Diseases. International Journal of Molecular Sciences, 23(16), 8911.

Capuzzello, G., Jacinto, J. G. P., Häfliger, I. M., Chapman, G. E., Martin, S. S., Viora, L., ... & Drögemüller, C. (2022). A large deletion encompassing exon 2 of the ectodysplasin A (EDA) gene in a British blue crossbred calf with hypohidrotic ectodermal dysplasia. Acta Veterinaria Scandinavica, 64(1), 1-8.

Wagner, M., Bračun, S., Duenser, A., Sturmbauer, C., Gessl, W., & Ahi, E. P. (2022). Expression variations in ectodysplasin-A gene (eda) may contribute to morphological divergence of scales in haplochromine cichlids. Bmc ecology and evolution, 22(1), 1-16.

Marrero, E., Attal, N., Nimeri, A., McGee, R. M., Benbow, J. H., Thompson, K. J., ... & McKillop, I. H. (2022). Ectodysplasin-A mRNA in exosomes released from activated hepatic stellate cells stimulates macrophage response. Experimental Cell Research, 113297.

Ahmed, H. A., El-Kamah, G. Y., Rabie, E., Mostafa, M. I., Abouzaid, M. R., Hassib, N. F., ... & Sayed, I. S. (2021). Gene Mutations of the Three Ectodysplasin Pathway Key Players (EDA, EDAR, and EDARADD) Account for More than 60% of Egyptian Ectodermal Dysplasia: A Report of Seven Novel Mutations. Genes, 12(9), 1389.

Bayliss, J., Ooi, G. J., De Nardo, W., Shah, Y. J. H., Montgomery, M. K., McLean, C., ... & Watt, M. J. (2021). Ectodysplasin a is increased in non-alcoholic fatty liver disease, but is not associated with type 2 diabetes. Frontiers in Endocrinology, 12, 642432.

Körber, I., Klein, O. D., Morhart, P., Faschingbauer, F., Grange, D. K., Clarke, A., ... & Schneider, H. (2020). Safety and immunogenicity of Fc‐EDA, a recombinant ectodysplasin A1 replacement protein, in human subjects. British journal of clinical pharmacology, 86(10), 2063-2069.

Yang, J., Zhou, W., Zhu, J., Wu, Y., Xu, L., Wang, Y., ... & Yang, Y. (2019). Circulating ectodysplasin A is a potential biomarker for nonalcoholic fatty liver disease. Clinica chimica acta, 499, 134-141.

Kuony, A., Ikkala, K., Kalha, S., Magalhães, A. C., Pirttiniemi, A., & Michon, F. (2019). Ectodysplasin-A signaling is a key integrator in the lacrimal gland–cornea feedback loop. Development, 146(14), dev176693.

He, F., Wang, H., Zhang, X., Gao, Q., Guo, F., & Chen, C. (2018). Conservation analysis and pathogenicity prediction of mutant genes of ectodysplasin a. BMC Medical Genetics, 19(1), 1-7.

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For research use only. Not intended for any clinical use.

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