Key features and details
- Rabbit polyclonal to Wnt10a
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Wnt10a antibody
See all Wnt10a primary antibodies
DescriptionRabbit polyclonal to Wnt10a
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat, Cow
- MOLT4, Raji lysates
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Storage instructionsShipped at 4°C. Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.00
Preservative: 0.01% Thimerosal (merthiolate)
Constituents: 1.21% Tris, 0.75% Glycine, 10% Glycerol (glycerin, glycerine)
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab97469 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/3000. Predicted molecular weight: 46 kDa.|
FunctionLigand for members of the frizzled family of seven transmembrane receptors. Probable developmental protein. May be a signaling molecule important in CNS development. Is likely to signal over only few cell diameters.
Involvement in diseaseDefects in WNT10A 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. Note=Most patients carrying WNT10A mutations present with sweating anomalies. However, comparison with EDA cases harboring mutations in the ectodysplasin pathway identifies some phenotypic differences. Dermatological features (anomalies of hair and sweat glands) are less severe in patients carrying WNT10A mutations and facial dysmorphism can be absent. The dental phenotype consists in microdontia, whereas teeth agenesis is more frequent in patients carrying mutations in the ectodysplasin pathway.
Defects in WNT10A are a cause of odonto-onycho-dermal dysplasia (OODD) [MIM:257980]. OODD is a rare autosomal recessive ectodermal dysplasia in which the presenting phenotype is dry hair, severe hypodontia, smooth tongue with marked reduction of fungiform and filiform papillae, onychodysplasia, keratoderma and hyperhidrosis of palms and soles, and hyperkeratosis of the skin.
Defects in WNT10A are a cause of Schopf-Schulz-Passarge syndrome (SSPS) [MIM:224750]. SSPS is rare ectodermal dysplasia, characterized chiefly by cysts of the eyelid margins, palmoplantar keratoderma, hypodontia, hypotrichosis and nail dystrophy. Multiple eyelid apocrine hidrocystomas are the hallmark of this condition, although they usually appear in adulthood. The concomitant presence of eccrine syringofibroadenoma in most patients and of other adnexal skin tumors in some affected subjects indicates that Schopf-Schulz-Passarge syndrome is a genodermatosis with skin appendage neoplasms.
Sequence similaritiesBelongs to the Wnt family.
Cellular localizationSecreted > extracellular space > extracellular matrix.
- Information by UniProt
- FLJ14301 antibody
- OODD antibody
- Protein Wnt-10a antibody
ab97469 has been referenced in 1 publication.
- Richards MH et al. Porcupine is not required for the production of the majority of Wnts from primary human astrocytes and CD8+ T cells. PLoS One 9:e92159 (2014). WB . PubMed: 24647048