https://www.selleckchem.com/btk.html
In vitro, the overexpression of FBXW7 in glioblastoma cells induced apoptosis, whereas, its knockdown displayed the opposite effect. Mechanistically, FBXW7 interacted with HDAC7 to promote HDAC7 ubiquitination, however, the overexpression of HDAC7 in glioblastoma cells blocked FBXW7-induced apoptosis. Finally, FBXW7 and HDAC7 displayed an inverse correlation in glioblastoma tissues in vivo. Therefore, our data demonstrated an important function of FBXW7 in promoting glioblastoma apoptosis by interacting with HDAC7 and promoting HDAC7 ubiquitination.
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