Human Protein Wnt-10a ELISA Kit | WNT10A elisa kit

Human Protein Wnt-10a ELISA Kit

Cat. Num. AAA762854

• Gene Names: WNT10A; OODD; SSPS; STHAG4
• Reactivity: Human
• Synonyms: Protein Wnt-10a; Human Protein Wnt-10a ELISA Kit; WNT10A; WNT10A elisa kit

• Reactivity: Human
• Specificity: This assay has high sensitivity and excellent specificity for detection of WNT10A. No significant cross-reactivity or interference between WNT10A and analogues was observed.
• Sequence Length: 417

• Samples: Serum, plasma, tissue homogenates and other biological fluids
• Assay Type: Quantitative Sandwich
• Detection Range: 0.156-10ng/ml
• Sensitivity: 0.094ng/ml
• Intra-assay Precision: CV<8%
• Inter-assay Precision: CV<10%
• Preparation and Storage: Store at 4 degree C if kit is to be used within 1 week. Stable for 6 months (if micro ELISA Plate, Lyophilized Standard and Concentrated Biotinylated Detection Protein stored at-20 degree C. Other components at 2-8 degree C). Stable for 12 months (if the entire kit is stored at-20 degree C).

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for WNT10A elisa kit

Principle of the Assay: This kit was based on sandwich enzyme-linked immune-sorbent assay technology. Capture antibody was pre-coated onto 96-well plates. And the biotin conjugated antibody was used as detection antibodies. The standards, test samples and biotin conjugated detection antibody were added to the wells subsequently, and washed with wash buffer. HRP-Streptavidin was added and unbound conjugates were washed away with wash buffer. TMB substrates were used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the target amount of sample captured in plate. Read the O.D. absorbance at 450nm in a microplate reader, and then the concentration of target can be calculated.

NCBI and Uniprot Product Information

• NCBI GI #: 16936520
• NCBI GeneID: 80326
• NCBI Accession #: NP_079492.2
• NCBI GenBank Nucleotide #: NM_025216.2
• Molecular Weight: 46,444 Da
• NCBI Official Full Name: protein Wnt-10a
• NCBI Official Synonym Full Names: wingless-type MMTV integration site family member 10A
• NCBI Official Symbol: WNT10A
• NCBI Official Synonym Symbols: OODD; SSPS; STHAG4
• NCBI Protein Information: protein Wnt-10a
• UniProt Protein Name: Protein Wnt-10a
• Protein Family: Protein
• UniProt Gene Name: WNT10A
• UniProt Entry Name: WN10A_HUMAN

NCBI Description

The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It is strongly expressed in the cell lines of promyelocytic leukemia and Burkitt's lymphoma. In addition, it and another family member, the WNT6 gene, are strongly coexpressed in colorectal cancer cell lines. The gene overexpression may play key roles in carcinogenesis through activation of the WNT-beta-catenin-TCF signaling pathway. This gene and the WNT6 gene are clustered in the chromosome 2q35 region. [provided by RefSeq, Jul 2008]

Uniprot Description

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 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. Belongs to the Wnt family.

Protein type: Secreted, signal peptide; Secreted

Chromosomal Location of Human Ortholog: 2q35

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

Molecular Function: frizzled binding

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

Disease: Odontoonychodermal Dysplasia; Schopf-schulz-passarge Syndrome; Tooth Agenesis, Selective, 4