- CITATIONS: 1
|Application ||WB, IHC-P, E|
|Calculated MW||39293 Da|
|Antigen Region||305-335 aa|
|Other Names||WNT1-inducible-signaling pathway protein 3, WISP-3, CCN family member 6, WISP3, CCN6|
|Target/Specificity||This WISP3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 305-335 amino acids from the Central region of human WISP3.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||WISP3 Antibody (Center) is for research use only and 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|
Provided below are standard protocols that you may find useful for product applications.
WISP3 is 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 are characterized by four conserved cysteine-rich domains: insulin-like growth factor-binding domain, von Willebrand factor type C module, thrombospondin domain and C-terminal cystine knot-like domain. WISP3 is overexpressed in colon tumors. It may be downstream in the WNT1 signaling pathway that is relevant to malignant transformation. Mutations of the WISP3 gene are associated with progressive pseudorheumatoid dysplasia, an autosomal recessive skeletal disorder, indicating that the gene is essential for normal postnatal skeletal growth and cartilage homeostasis.
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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