SH3GLB1, also known as Bax-interacting factor 1 (Bif-1) and Endophilin B1, is a protein-coding gene involved in multiple biological processes. It is associated with autophagy and apoptosis pathways, and plays a crucial role in maintaining cellular homeostasis. SH3GLB1 can interact with BECN1 through UVRAG to regulate the post-Golgi trafficking of membrane-integrated ATG9A for autophagy [4].

In glioblastoma, high SH3GLB1 gene expression is associated with higher disease grading and worse survival. Downregulation of SH3GLB1 retains temozolomide (TMZ) susceptibility, as it promotes autophagy-mediated mitochondrial metabolism to acquire resistance against TMZ [1].

In bone homeostasis, Bif-1/Endophilin B1/SH3GLB1 is upregulated during osteoclastogenesis. Bif-1-deficient (Bif-1-/-) mice show increased trabecular bone volume and number, with accelerated osteoclastogenesis without affecting certain downstream signals. Unexpectedly, both bone formation rate and osteoblast surface increase in these mice, suggesting Bif-1 regulates bone homeostasis by controlling the differentiation and function of both osteoclasts and osteoblasts [2].

In radiation-induced hypertrophic cardiomyopathy, SH3GLB1 deficiency inhibits mitophagy activation, revealing its regulatory role in cardiac hypertrophy. IR promotes the interaction between SH3GLB1 and mitochondrial membrane proteins, indicating its function in cardiac hypertrophy might involve mitophagy [3].

In conclusion, SH3GLB1 is essential in regulating autophagy, apoptosis, and mitochondrial metabolism. Its role in glioblastoma, bone homeostasis, and cardiac hypertrophy is significant. Studies using gene-knockout mouse models, such as Bif-1-/-mice, have provided valuable insights into its functions in these specific disease-related biological processes, helping to understand disease mechanisms and potentially develop new therapeutic strategies.