Asb13, an ankyrin repeat and suppressor of cytokine signaling (SOCS) box-containing protein, is a ubiquitin E3 ligase. It may be involved in regulating compartment size, such as the size of the brain and muscle compartment, and is thought to be related to the differences in brain size between humans and apes. It also plays a role in canonical Notch signaling and mitochondrial function [2].

In breast cancer, ASB13 knockout in cells promoted cell migration and decreased F-actin polymerization, while overexpression suppressed lung metastasis. ASB13 acts as an E3 ubiquitin ligase that targets SNAI2 for ubiquitination and degradation. ASB13 knockout decreased YAP expression, which is regulated by an increased SNAI2 protein level that represses YAP transcription. Clinical data shows ASB13 expression is positively correlated with improved overall survival in breast cancer patients [1]. In young women with breast cancer, the mutated CNA status in gene ASB13 was associated with a higher gene expression, which predicted patient survival outcome [3].

In acute myocardial infarction with cardiogenic shock under extracorporeal membrane oxygenation treatment, ASB13 was identified as a prognostic marker, and its co-expressed proteins are related to post-translational protein modification, cullin-RING ubiquitin ligase complex, etc., with ubiquitin-mediated proteolysis as the most enriched pathway. Immune cell infiltration analysis revealed ASB13 was positively correlated with natural killer cell, monocyte, and gamma delta T cell [4].

In conclusion, Asb13 is an important E3 ubiquitin ligase involved in multiple biological processes. Its function in diseases, especially in breast cancer and acute myocardial infarction, has been revealed through gene knockout-related studies. These findings contribute to understanding the mechanisms of these diseases and may provide potential therapeutic targets.