E3 ubiquitin ligase ASB8 promotes selinexor-induced proteasomal degradation of XPO1.

Nucleocytoplasmic transport meets CRISPR screening. We performed CRISPR screens to identify genes that affect selinexor sensitivity. We establish that our main hit, ASB8, is responsible for selinexor-induced degradation of XPO1. Additionally, we suggest that TGFβ-SMAD signaling may predict clinical benefit from selinexor treatment in patients with multiple myeloma.

More news

New insights into oncolytic virus selection for glioblastoma treatment

Our latest research is published in 𝘔𝘰𝘭𝘦𝘤𝘶𝘭𝘢𝘳 𝘛𝘩𝘦𝘳𝘢𝘱𝘺 𝘖𝘯𝘤𝘰𝘭𝘰𝘨𝘺:“𝐂𝐨𝐦𝐩𝐚𝐫𝐚𝐭𝐢𝐯𝐞 𝐞𝐯𝐚𝐥𝐮𝐚𝐭𝐢𝐨𝐧 𝐨𝐟 𝐨𝐧𝐜𝐨𝐥𝐲𝐭𝐢𝐜 𝐯𝐢𝐫𝐮𝐬𝐞𝐬 𝐫𝐞𝐯𝐞𝐚𝐥𝐬 𝐨𝐩𝐩𝐨𝐬𝐢𝐧𝐠 𝐩𝐫𝐞𝐟𝐞𝐫𝐞𝐧𝐜𝐞𝐬 𝐟𝐨𝐫 𝐠𝐥𝐢𝐨𝐛𝐥𝐚𝐬𝐭𝐨𝐦𝐚 𝐬𝐮𝐛𝐭𝐲𝐩𝐞𝐬” Glioblastoma

Read More »