Dnajc5b, also known as cysteine-string protein beta, is a member of the DnaJ heat shock protein family. It is involved in maintaining cellular homeostasis, with potential roles in pathways related to autophagy and mitochondrial function [1]. Heat shock proteins, to which Dnajc5b belongs, are evolutionarily conserved and play diverse physiological functions [3].

In germ-cell knockout Dnajc5b mice, male fertility declines with an increased ratio of abnormal spermatozoa. The absence of Dnajc5b leads to mitochondrial damages like oxidative stress, mitochondrial stress in testes, and lower mitochondrial membrane potential of spermatozoa. Also, Dnajc5b mitigates excessive cellular autophagy and mitophagy via its DNAJ domain under stress conditions [1]. In the context of HCV, Dnajc5b shows antiviral activity similar to HSPB8, affecting HCV replication [2]. In esophageal squamous cell carcinoma, Dnajc5b could serve as a promising target for prognostic prediction [3].

In summary, Dnajc5b is crucial for maintaining mitochondrial functions and autophagic homeostasis, especially during spermiogenesis, thus contributing to male fertility. Its role in antiviral activity against HCV and as a prognostic target in esophageal squamous cell carcinoma further highlights its significance in different disease areas. The use of Dnajc5b knockout mouse models has been instrumental in uncovering its role in male fertility-related biological processes [1,2,3].