human, Cynomolgus/ Rhesus macaque, rat, mouse sprouty homolog 1, antagonist of FGF signaling (Drosophila) (SPRY1) for cell curture,in vitro study, in vivo study,benchmark, drug discovery & MOA research and positive control for the diagnosis.

Genemedi produces human, Cynomolgus/ Rhesus macaque, rat, mouse sprouty homolog 1, antagonist of FGF signaling (Drosophila) (SPRY1) His+Avi (Biotinylated) for cell curture, in vitro study, in vivo study, benchmark, drug discovery & MOA research and positive control for the diagnosis. A number of MAPK modulators have been identified, including Sprouty (Spry) proteins. The Spry family members are products of four genes located on different chromosomes and differ in their tissue distribution, activity, and interaction partners. Sprouty (Spry) was first identified in a genetic screen in Drosophila to be an antagonist of fibroblast growth factor and epidermal growth factor (EGF) signaling, seemingly by inhibiting the Ras/MAP kinase pathway.  Spry proteins are not able to fully complement each other, and their biological function is likely to be dependent on tissue and cell type context. Although Spry proteins have been found to interact with several Ras–MAPK pathway components. Sprouty 1 (SPRY1) modulates the microenvironment to enable proper mammary branching morphogenesis. This process occurs through negative regulation of epidermal growth factor receptor (EGFR) signaling in mammary stroma. Spry1 was initially identified as an inhibitor of the Ras–MAPK pathway in Drosophila melanogaster. Surprisingly, subsequent studies demonstrated that Spry proteins not only inhibited Ras–MAPK pathway but also enhanced the activation of this pathway. Spry1 function in cancer has proven elusive, and it is likely dependent on tumor type, and genetic context. In fact, although a reduced expression of Spry1 was found in sarcoma, liver, ovarian, and prostate cancers, accumulating evidence indicate that up-regulation of Spry proteins, including Spry1, can promote the growth of various tumors harboring Raf or Ras mutations where they act as enhancers rather than as inhibitors of the Ras–MAPK pathway.