RANBP10, also known as RAN binding protein 10, is an evolutionarily conserved and ubiquitously expressed protein. It functions as a RAN-GTP exchange factor (GEF) regulating factors involved in cellular progression. It is associated with pathways like the FBXW7/c-Myc pathway and may also be involved in the DNA Damage Response (DDR) due to protein similarities with RANBP9 [1,2]. It has been implicated in multiple biological processes, such as cell proliferation, migration, and invasion, making it biologically important. Genetic models, like gene knockout mouse models, can be valuable for studying its functions.

In glioblastoma (GBM), downregulation of RANBP10 significantly inhibited cell proliferation, migration, invasion, and tumor growth. RANBP10 was found to suppress the promoter activity of FBXW7, increasing the protein stability of c-Myc in GBM cells. Silencing of FBXW7 in RANBP10-knockdown GBM cells could partly reverse the effects of RANBP10 downregulation [1]. In mice lacking RanBP10, stable thrombus formation was impaired, platelet shape change was attenuated, and there was increased β1-tubulin protein driving microtubule polymerization, suggesting RanBP10 inhibits premature microtubule polymerization and is pivotal in thrombus stabilization [3].

In conclusion, RanBP10 plays essential roles in processes like cell growth and microtubule-related functions. The gene knockout mouse models have revealed its significance in glioblastoma progression and thrombus stability, providing insights into these disease-related areas. This research helps understand the biological functions of RanBP10 and its potential as a therapeutic target in relevant diseases.