کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1963665 | 1058487 | 2012 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Dickkopf-1 (DKK-1) interrupts FAK/PI3K/mTOR pathway by interaction of carbonic anhydrase IX (CA9) in tumorigenesis Dickkopf-1 (DKK-1) interrupts FAK/PI3K/mTOR pathway by interaction of carbonic anhydrase IX (CA9) in tumorigenesis](/preview/png/1963665.png)
Recently, we found that carbonic anhydrase IX (CA9) modulates tumor-associated cell migration and invasion, and then identified dickkopf-1 (DKK-1) as a novel CA9-interacting protein. In this study, we have determined the binding regions that are required for interaction between CA9 and DKK-1 through in vitro and in vivo. The N-terminal domain of CA9 is participated to interact with the Val60–Tyr168 site of DKK-1. We also observed that DKK-1 inhibits endothelial cell angiogenesis of CA9 in tumorigenesis. Furthermore, induction of CA9-mediated mTOR phosphorylation and angiogenesis was significantly inhibited by over-expression of DKK-1. Taken together, these findings identify DKK-1 as a potential factor in the regulation of CA9 cellular homeostasis and also suggest a new possible role for DKK1-1 in tumorigenesis.
► The N-terminal domain of CA9 interacts with the Val60–Tyr168 site of DKK-1.
► DKK-1 inhibits endothelial cell angiogenesis of CA9 in tumorigenesis.
► Identified DKK-1 as a potential factor in the regulation of CA9 cellular homeostasis.
Journal: Cellular Signalling - Volume 24, Issue 7, July 2012, Pages 1406–1413