Catalog Number: |
EZC-RS1-M1 |
Synonym: |
RSPO1, RSPO-1, CRISTIN3, CRISTIN-3, FLJ40906, RP11-566C13.1, RSPO, R-spondin-1, Rspondin-1, Rspondin1 |
Source: |
Recombinant mouse RSPO1 mFc Chimera (rmRSPO1-mFc), Met1-Asn 932 (Accession # P08069) was produced in human HEK293 cells. |
Molecular
Characterization: |
rmRSPO1-mFc was fused with the mouse Fc region of at the C-terminus, the reduced monomer has a calculated molecular mass of 58.5 kDa. In SDS-PAGE under reducing conditions, the apparent molecular mass of rmRSPO1-mFc monomer is approximately 67-75kDa due to the glycosylation. |
Purity: |
>95% as determined by SDS-PAGE. All lots are greater than 95% pure. |
Endotoxin: |
Less than 1.0 EU per 1 µg of the rmRSPO1-mFc by the LAL method. |
Formulation: |
Bulk protein in a 0.22 µm filtered solution of PBS, pH 7.4 and delivered as liquid formulation or lyophilized powder.Normally 5-8% trehalose and mannitol are added as protectants before lyophilization. |
Storage: |
Store at -20? in lyophilized state after receipt. For long term storage, upon reconstitution rmRSPO1-mFc should be aliquot and store at -20? or -80?. Avoid repeated freeze-thaw cycles. |
Background: |
Mouse R-Spondin 1 ( Roof plate-specific Spondin 1 ), also known as RSPO1 and CRISTIN3, FLJ40906 or RP11-566C13.1, Which is a secreted activator protein with two cystein-rich, furin-like domains and one thrombospondin type 1 domain, which belongs to the R-Spondin family. In mice, the protein induces the rapid onset of crypt cell proliferation and increases intestinal epithelial healing, providing a protective effect against chemotherapy-induced adverse effects. R-Spondin1 activity critically depends on the presence of canonical Wnt ligands and LRP6. R-Spondin1 does not directly activate LRP6, it interferes with DKK1 / Kremen-mediated internalization of LRP6 through an interaction with Kremen, resulting in increased LRP6 levels on the cell surface. Mouse R-Spondin1 shares 89%, 87%, 92%, 91%, 91%, and 89% aa identity with human R-Spondin1. Defects in RSPO1 are the cause of palmoplantar keratoderma with squamous cell carcinoma of skin and sex reversal (PKKSCC)[1]. This recessive syndrome is characterized by XX (female to male) SRY-independent sex reversal, palmoplantar hyperkeratosis and predisposition to squamous cell carcinoma of the skin. |
Research Use Only. Not for use in diagnostic or therapeutic procedures. |
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Reference |
(1) Parma, P. et al., 2006, Nature genetics. 38 (11): 1304-9
(2) Capel, B., 2006, Nature genetics. 38 (11) :1233-4
(3) Binnerts, ME. et al., 2007, Proc Natl Acad Sci. 104 (37): 14700-5
(4) Zhao, J. et al., 2009, Proc Natl Acad Sci. 106 (7) :2331-6 |
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