Mybbp1a, also known as MYB binding protein 1A or p160, acts as a co-repressor of multiple transcription factors. It is involved in many physiological processes such as mitosis, cellular senescence, epigenetic regulation, cell cycle, metabolism plasticity and stemness [2]. It also participates in pathways like the NAT10/Mybbp1a/p53 axis in cardiomyocyte ferroptosis [1], and is associated with herpes simplex virus 1 replication and gene expression [3]. Genetic models like gene knockout (KO) are valuable for studying its functions.

In a KO mouse model-related study, cardiomyocyte-specific knockout of NAT10, which affects Mybbp1a through ac4C modification, alleviated cardiomyocyte ferroptosis and cardiac ischemia-reperfusion (I/R) injury, indicating Mybbp1a's role in exacerbating this injury [1]. In pancreatic cancer (PANC1) cell lines, MYBBP1A KO cells showed lower proliferation capacity, higher asparaginase sensitivity, and other cellular changes, while in lymphoblastic leukemia (NALM6) cell lines, MYBBP1A KO displayed resistance to asparaginase, showing its tissue-specific role in drug response [4]. In hepatocellular carcinoma (HCC), suppression of Mybbp1a reduced HCC cell proliferation and migration by inhibiting the IGF1/AKT signaling pathway [5].

In conclusion, Mybbp1a is crucial in various biological processes and disease conditions. Model-based research, especially KO/CKO mouse models, has revealed its role in cardiac I/R injury, drug sensitivity in different cancer cell lines, and HCC progression. Understanding Mybbp1a provides insights into disease mechanisms and potential therapeutic targets.