C10782: TEM1 (CD164L1/ endosialin) Knockout Mice
Value Proposition:
JHU scientists have generated a mouse model with a targeted null mutation in the Tem1 gene. They demonstrate that Tem1 is not required for angiogenesis during fetal development, postnatal growth, or wound healing; however, Tem1 plays a critical role in determining tumor behavior in clinically relevant anatomical sites.
Technical Details:
Tumor endothelial markers (TEMs) are genes that were found to be significantly up-regulated during angiogenesis and neoangiogenesis that are crucial for the growth of solid tumors. TEM1, also termed CD164L1 and endosialin is a single-pass transmembrane glycoprotein that has multiple extracellular domains, including three EGF-like domains, a sushi-like domain, and a C lectin-like domain. While TEM1 is not required for angiogenesis during fetal development, postnatal growth or wound healing, it plays a role in tumor growth, invasion, and metastasis.
Looking for Partners:
These knockout mice are useful for studies to understand the importance of TEM gene products as potential therapeutic targets and for studies to gain new insights into angiogenesis.
Publications/Associated Cases:
Nanda, A., Karim, B., Peng, Z., Liu, G., Qiu, W., Gan, C., et al. (2006). Tumor endothelial marker 1 (Tem1) functions in the growth and progression of abdominal tumors. Proceedings of the National Academy of Sciences of the United States of America, 103(9), 3351-3356.
