Asb10, also known as Ankyrin and SOCS Box-containing protein-10, is a member of the ASB family of proteins. It has a structure with a unique N-terminus, ankyrin (ANK) repeat domains, and a suppressor of cytokine signaling (SOCS) box at the C-terminus. Asb10 functions in ubiquitin-mediated degradation pathways, where the ANK repeats bind proteins for degradation, and the SOCS box recruits ubiquitin ligase proteins to form a complex for ubiquitin transfer [2].

Evidence from multiple studies suggests its association with glaucoma. In a Pakistani cohort, certain variants in Asb10 were significantly associated with sporadic primary open-angle glaucoma (POAG), indicating 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]. Additionally, 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 TNBC 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 plays a crucial role in ubiquitin-mediated protein degradation pathways. Its variants are associated with glaucoma in some ethnic populations, and it also has an impact on the development of triple-negative breast cancer by regulating the degradation of key proteins. The study of Asb10 in these disease models helps to understand the molecular mechanisms underlying these diseases and may provide potential targets for treatment.