|Other Names||WNT1-inducible-signaling pathway protein 3, WISP-3, CCN family member 6, WISP3, CCN6|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP6257a was selected from the Center region of human WISP2. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Appears to be required for normal postnatal skeletal growth and cartilage homeostasis.|
|Tissue Location||Predominant expression in adult kidney and testis and fetal kidney. Weaker expression found in placenta, ovary, prostate and small intestine. Also expressed in skeletally- derived cells such as synoviocytes and articular cartilage chondrocytes|
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Provided below are standard protocols that you may find useful for product applications.
Wisp2 encodes a member of the WNT1 inducible signaling pathway (WISP) protein subfamily, which belongs to the connective tissue growth factor (CTGF) family. WNT1 is a member of a family of cysteine-rich, glycosylated signaling proteins that mediate diverse developmental processes. The CTGF family members contain four well-conserved cysteine-rich domains: insulin-like growth factor-binding domain, von Willebrand factor type C module, thrombospondin domain and the C-terminal cysteine knot-like (CT) domain. Human Wisp2 is 72% identical to the mouse Wisp2 protein. Wisp2 is abundantly expressed in bone tissue, and may play an important role in modulating bone turnover. Wisp2 expression in colon tumors is often reduced while the other two Wisp members (Wisp1 and 3) are overexpressed in these tumors.
Clark, H.F., et al., Genome Res. 13(10):2265-2270 (2003).Tanaka, S., et al., Gastroenterology 123(1):392-393 (2002).Kleer, C.G., et al., Oncogene 21(20):3172-3180 (2002).Hurvitz, J.R., et al., Nat. Genet. 23(1):94-98 (1999).Pennica, D., et al., Proc. Natl. Acad. Sci. U.S.A. 95(25):14717-14722 (1998).
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