MsrB3, short for methionine sulfoxide reductase B3, is a protein repair enzyme. It specifically catalyzes the reduction of methionine-R-sulfoxide residues and has an antioxidant function [2,4]. It is involved in multiple biological processes, with its location in the endoplasmic reticulum (ER) suggesting a role in ER-related redox regulation [3,5].

MsrB3 deficiency in cancer cells has been studied. It induces apoptosis through p53-independent and ER stress-dependent pathways. MsrB3 depletion leads to post-transcriptional down-regulation of p53, and apoptosis occurs to a similar extent in p53 wild-type and null cancer cells. It also significantly increases ER stress, activates the pro-apoptotic Bim molecule, and disturbs calcium homeostasis in the ER [1]. In clear cell renal cell carcinoma, knockdown of MSRB3 arrests cell proliferation, migration, and invasion, while promoting apoptosis and inducing ER stress marker changes [2]. In zebrafish, down-regulation of msrb3 causes hair cell apoptosis, leading to abnormal auditory system development [6]. In cattle, polymorphisms in the MSRB3 gene are associated with growth traits [7].

In conclusion, MsrB3 plays a crucial role in multiple biological processes and disease conditions. Its deficiency-induced apoptosis in cancer cells, its impact on the development of the auditory system in zebrafish, and its association with growth traits in cattle, as revealed through functional studies, provide important insights. Understanding MsrB3 helps in grasping the underlying mechanisms of these biological processes and diseases, potentially offering new strategies for treatment and breeding improvement.