Polyclonal Wnt10A; Anti-WNT10A; WntAA 10; WntAA-10; Wnt 10a; Wnt10AA; WNT-10A; wnt10a

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

Wnt10A antibody was purified by affinity chromatography.

Purified by Immunoaffinity Chromatography and supplied in PBS with 0.1% NaN3.

1.0 mg/ml (lot specific)

Store at 4 degree C for short term storage. Aliquot and store at -70 degree C for long term storage. Avoid repeated freeze/thaw cycles.

Small volumes of anti-Wnt10A antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Rabbit polyclonal Wnt10A antibody

Cytokines & Growth Factors

Immunohistochemistry (IHC) Paraffin

IHC-P: 10 ug/ml

46,454 Da

wingless-type MMTV integration site family, member 10A

protein Wnt-10a

Protein Wnt-10a

WN10A_MOUSE

WNT10A: Ligand 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. Defects in WNT10A are a cause of ectodermal dysplasia anhidrotic (EDA); 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. 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). 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). 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 *****hood. 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. Belongs to the Wnt family.

Protein type: Secreted, signal peptide; Secreted

Cellular Component: extracellular space; proteinaceous extracellular matrix; extracellular region

Molecular Function: frizzled binding; receptor binding

Biological Process: skin development; tongue development; Wnt receptor signaling pathway; hair follicle morphogenesis; cell fate commitment; multicellular organismal development; sebaceous gland development; signal transduction; odontogenesis; neuron differentiation; organ morphogenesis; cell-cell signaling; hair follicle development; epidermis morphogenesis; neural crest cell differentiation; regulation of odontogenesis of dentine-containing teeth

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