EDAR Antibody (F-5): sc-398337

EDAR Antibody (F-5) is a mouse monoclonal IgG1 antibody that detects ectodermal dysplasia receptor (EDAR) in human samples through applications such as western blotting (WB), immunoprecipitation (IP), immunofluorescence (IF), and enzyme-linked immunosorbent assay (ELISA). EDAR plays a crucial role in ectodermal differentiation and is essential for the development of structures such as hair, teeth, and sweat glands. This receptor is activated by its ligand, Ectodysplasin A (EDA), which is produced in various splice variants, with EDA-A1 being the primary form that binds to EDAR. Mutations in the EDAR gene can lead to ectodermal dysplasia syndromes, resulting in significant developmental issues. EDAR′s structure includes an extracellular domain containing cysteine-rich repeats that facilitate ligand binding, and an intracellular death domain involved in signaling pathways that regulate cell survival and apoptosis. Understanding EDAR′s structural features helps researchers comprehend functional implications in cellular signaling and developmental biology, making anti-EDAR antibody (F-5) a valuable tool for studying these processes in human tissues.

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EDAR Antibody (F-5) References:

1. Ectodysplasin, Edar and TNFRSF19 are expressed in complementary and overlapping patterns during mouse embryogenesis.  |  Pispa, J., et al. 2003. Gene Expr Patterns. 3: 675-9. PMID: 12972005
2. Edar and Troy signalling pathways act redundantly to regulate initiation of hair follicle development.  |  Pispa, J., et al. 2008. Hum Mol Genet. 17: 3380-91. PMID: 18689798
3. Two novel mutations in the gene EDAR causing autosomal recessive hypohidrotic ectodermal dysplasia.  |  Naqvi, SK., et al. 2011. Orthod Craniofac Res. 14: 156-9. PMID: 21771270
4. Hair shaft structures in EDAR induced ectodermal dysplasia.  |  Stecksén-Blicks, C., et al. 2015. BMC Med Genet. 16: 79. PMID: 26336973
5. Generation of Cashmere Goats Carrying an EDAR Gene Mutant Using CRISPR-Cas9-Mediated Genome Editing.  |  Hao, F., et al. 2018. Int J Biol Sci. 14: 427-436. PMID: 29725264
6. Sequence variants in the EDAR gene causing hypohidrotic ectodermal dysplasia.  |  Ahmad, F., et al. 2019. Congenit Anom (Kyoto). 59: 145-147. PMID: 30079503
7. EDAR, LYPLAL1, PRDM16, PAX3, DKK1, TNFSF12, CACNA2D3, and SUPT3H gene variants influence facial morphology in a Eurasian population.  |  Li, Y., et al. 2019. Hum Genet. 138: 681-689. PMID: 31025105
8. Functional studies for a dominant mutation in the EDAR gene responsible for hypohidrotic ectodermal dysplasia.  |  Okita, T., et al. 2019. J Dermatol. 46: 710-715. PMID: 31245878
9. Missense mutations in EDA and EDAR genes cause dominant syndromic tooth agenesis.  |  Andreoni, F., et al. 2021. Mol Genet Genomic Med. 9: e1555. PMID: 33205897
10. Different degree of loss-of-function among four missense mutations in the EDAR gene responsible for autosomal recessive hypohidrotic ectodermal dysplasia may be associated with the phenotypic severity.  |  Yagi, S., et al. 2023. J Dermatol. 50: 349-356. PMID: 36258277

The preferred EDAR antibody is EDAR Antibody (G-1): sc-271627.