EDAR Antibodies

Structure of EDAR

The protein encoded by the EDAR gene is a type I transmembrane receptor with a molecular weight of approximately 40 kDa. The molecular weight of this protein varies slightly among different mammals, mainly due to interspecific variations in the amino acid sequence of the cysteine-rich domain in its extracellular region. The following table shows the molecular weight and main structural characteristics of EDAR proteins in different species:

This protein is composed of 448 amino acids, and its primary structure includes a signal peptide sequence, an extracellular ligand-binding domain, a transmembrane domain, and an intracellular death domain. Its secondary structure is mainly composed of β -folds, which form specific spatial conformations in the extracellular region and are responsible for the recognition and binding to the ligand EDN. Intracellular death domains initiate cascade reactions of downstream NF-κB and other signaling pathways through specific protein-protein interactions.

Fig. 1 Domain structure of EDAR.¹

Key structural properties of EDAR:

• Extracellular ligand binding domains rich in cysteine
• Single transmembrane helical structure
• Intracellular death domains mediate signal transduction

Functions of EDAR

The core function of the EDAR gene is to regulate the development of ectodermal organs during the embryonic period. However, it also plays a role in various physiological and evolutionary processes.

Unlike the extensive pleiotropic effects of most genes, the function of EDAR is highly concentrated in ectodermal derivatives, and the strength of its signaling pathway directly determines heritable physical characteristics such as hair thickness and tooth crown shape.

Applications of EDAR and EDAR Antibody in Literature

1. Gao, Yanzi, et al. "The EDA/EDAR/NF-κB pathway in non-syndromic tooth agenesis: A genetic perspective." Frontiers in genetics 14 (2023): 1168538. https://doi.org/10.3389/fgene.2023.1168538

The article indicates that non-syndromic tooth loss (NSTA) is a common dental developmental malformation, mainly caused by genetic factors. As a key member of the EDA/EDAR/NF-κB signaling pathway, mutations in the EDAR gene play a significant role in the pathogenesis of NSTA and ectodermal dysplasia. This article focuses on the tooth development defects caused by EDAR mutations.

2. Williams, Rebecca, et al. "Elevated EDAR signalling promotes mammary gland tumourigenesis with squamous metaplasia." Oncogene 41.7 (2022): 1040-1049. https://doi.org/10.1038/s41388-021-01902-6

Research has found that EDAR is a death receptor associated with certain types of breast cancer. In estrogen receptor-negative breast cancer with squamous differentiation, the expression of EDAR is significantly elevated. Animal experiments have confirmed that the enhanced EDAR signaling can drive the occurrence of breast tumors by activating the β-catenin pathway, thereby revealing that EDAR is a new oncogene for breast cancer.

3. Wegner, Kyle A., et al. "Edar is a downstream target of beta-catenin and drives collagen accumulation in the mouse prostate." Biology Open 8.3 (2019): bio037945. https://doi.org/10.1242/bio.037945

This study explored the role of EDAR in prostate development. It was found that β-catenin can transcriptionally activate the expression of Edar in the prostate. Functional experiments have shown that although Edar does not affect the morphogenesis of prostate branches, its overexpression can lead to abnormal thickening of the prostate matrix and collagen deposition in adult mice, revealing a new function of EDAR in endodermal organs.

4. Kim, Youn Jung, et al. "Critical Considerations in Calling Disease-Causing EDAR Mutations in Nonsyndromic Oligodontia." Journal of Clinical Medicine 13.23 (2024): 7328. https://doi.org/10.3390/jcm13237328

This study identified recessive inherited EDAR gene mutations in families with non-syndromic oligodontic malformations (NSO). The luciferase reporter gene assay confirmed that these novel missense mutations led to impaired function of the EDAR protein and reduced the transcriptional activity of the EDA signaling pathway, thereby clarifying the molecular mechanism of its pathogenicity.

5. Sadier, Alexa, et al. "Modeling Edar expression reveals the hidden dynamics of tooth signaling center patterning." PLoS biology 17.2 (2019): e3000064. https://doi.org/10.1371/journal.pbio.3000064

This study, by analyzing the expression dynamics of the Edar gene during the development of molars in mice, reveals that the formation of dental signal centers follows a "activation-inhibition" reaction-diffusion model. Research has found that the extensive activation of Edar precedes spatial constraints, and this process is malleable. Reducing the activity of Edar can actually "save" the R2 signal center that was about to disappear, indicating that the pattern formation is a dynamic adjustment rather than a predestined result.

Creative Biolabs: EDAR Antibodies for Research

Creative Biolabs specializes in the production of high-quality EDAR antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom EDAR Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our myoglobin antibodies, custom preparations, or technical support, contact us at email.