Anti-EDAR antibody (ab198168)
- Datasheet
- References
- Protocols
Overview
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Product name
Anti-EDAR antibody
See all EDAR primary antibodies -
Description
Rabbit polyclonal to EDAR -
Host species
Rabbit -
Specificity
This antibody detects endogenous levels of total EDAR protein. -
Tested applications
Suitable for: IHC-Pmore details -
Species reactivity
Reacts with: Human -
Immunogen
Synthetic peptide corresponding to Human EDAR (internal sequence).
Database link: Q9UNE0 -
Positive control
- Human lung cancer tissue.
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. -
Storage buffer
pH: 7.3
Preservative: 0.05% Sodium azide
Constituents: 49% PBS, 50% Glycerol -
Concentration information loading... -
Purity
Immunogen affinity purified -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Recombinant Protein
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Related Products
Applications
Our Abpromise guarantee covers the use of ab198168 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Abreviews | Notes |
|---|---|---|
| IHC-P | 1/10 - 1/50. |
Target
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Function
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. -
Tissue specificity
Detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. Not detected in lymphoblast and fibroblast cell lines. -
Involvement in disease
Defects in EDAR are a cause of ectodermal dysplasia anhidrotic (EDA) [MIM:224900]; 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) [MIM:129490]; 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. -
Sequence similarities
Contains 1 death domain.
Contains 3 TNFR-Cys repeats. -
Developmental stage
Found in craniofacial tissues from embryonic day 42-53. Expressed in fetal skin 11 and 15 weeks after gestation. -
Cellular localization
Membrane. - Information by UniProt
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Database links
- Entrez Gene: 10913 Human
- Omim: 604095 Human
- SwissProt: Q9UNE0 Human
- Unigene: 171971 Human
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Alternative names
- Anhidrotic ectodysplasin receptor 1 antibody
- DL antibody
- Downless (mouse) homolog antibody
see all
Images
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Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-EDAR antibody (ab198168)Immunohistochemical analysis of paraffin-embedded human lung cancer tissue labeling EDAR with ab198168 at a 1/15 dilution.
Protocols
Datasheets and documents
References
ab198168 has not yet been referenced specifically in any publications.
