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Recombinant Human Wnt-7a (RMPP-00231627)

Cat. No.: RMPP-00231627

Category: Growth Factors & Cytokines

INQUIRY 3 μg 15 μg
Wnt-7a belongs to the Wnt family of signaling proteins that play a key role in maintaining the integrity of embryonic and adult tissues. It is expressed in placenta, kidney, testis, uterus, fetal lung, and fetal and adult brain. Most Wnt proteins can signal tho μgh a mechanism called the canonical Wnt pathway, in which Wnt proteins bind to and activate seven-pass transmembrane receptors of the Frizzled family, ultimately leading to the disruption of β-catenin degradation. Intracellular accumulation of β-catenin increases translocation of the protein into the nucleus, where it binds to TCF/LEF transcription factors to induce the expression of numerous genes. Increased Wnt/β-catenin signaling is associated with tumorigenesis in a diverse set of human cancers. However, Wnt-7a/Frizzled-9 signaling has been shown to act as a tumor suppressor in non-small cell lung cancers. Recombinant Human Wnt-7a is a 35.5 kDa glycoprotein containing 318 amino acids. Due to glycosylation, Wnt-7a migrates between 40-55 kDa by SDS-PAGE gel under unreduced conditions.

Product Features

Source HEK293 cells
Purity ≥ 80% by SDS-PAGE gel and HPLC analyses.
Nature Recombinant
Endotoxin Level < 1 Eu/μg
Cross Reactivity Chicken, Human

Protein Information

UniProt ID O00755
Molecular Weight 35.5 kDa
Sequence Similarities Belongs to the Wnt family.
Protein Length Full length protein
Cellular Localization Secreted > extracellular space > extracellular matrix.
Tissue Specificity Expression is restricted to placenta, kidney, testis, uterus, fetal lung, and fetal and adult brain.
Function Ligand for members of the frizzled family of seven transmembrane receptors. Probable developmental protein. Signaling by Wnt-7a allows sexually dimorphic development of the mullerian ducts.
Involvement in Disease Defects in WNT7A are the cause of limb/pelvis-hypoplasia/aplasia syndrome (LPHAS); also known as absence of ulna and fibula with severe limb deficiency. LPHAS is a limb-malformation disorder characterized by various degrees of limb aplasia/hypoplasia and joint dysplasia.Defects in WNT7A are a cause of Fuhrmann syndrome (FUHRS); also known as fibular aplasia or hypoplasia femoral bowing and poly- syn- and oligodactyly. Fuhrmann syndrome is a distinct limb-malformation disorder characterized also by various degrees of limb aplasia/hypoplasia and joint dysplasia.

Storage & Shipping

Shipping and Storage Shipped on Dry Ice.

For research use only. Not for clinical use.