Asb10, or Ankyrin and SOCS Box-containing protein-10, is a member of the ASB family. It functions in ubiquitin-mediated degradation pathways. The ankyrin (ANK) repeats in Asb10 bind to proteins destined for degradation, while the suppressor of cytokine signaling (SOCS) box recruits ubiquitin ligase proteins to form a complex for ubiquitin transfer [2].

Mutations in Asb10 have been associated with glaucoma. In a Pakistani cohort, certain variants in Asb10 were found to be significantly associated with sporadic primary open-angle glaucoma (POAG), suggesting it may act as a risk factor [4]. However, in a Korean cohort, no significant association was found between Asb10 gene polymorphisms and normal-tension glaucoma (NTG) [3]. Also, in triple-negative breast cancer, Asb10, as an estrogen receptor ERα trans-activated E3 ligase, ubiquitylates tumor endothelial marker 8 (TEM8) for degradation. Its deficiency in this cancer type leads to a high homeostatic level of TEM8, which is involved in promoting stemness and vasculogenic mimicry capacity of breast cancer cells [1].

In conclusion, Asb10 is mainly involved in ubiquitin-mediated protein degradation. Studies on its gene variants in different ethnic groups have provided insights into its potential role in glaucoma. In triple-negative breast cancer, its function as an E3 ligase is crucial in regulating proteins related to cancer cell stemness and neovasculogenesis. These findings from various research models contribute to understanding disease mechanisms related to Asb10.