Pelo, a ribosome rescue factor, is involved in multiple biological processes. It plays a crucial role in cell meiotic division and mice embryonic development. It is also associated with translational quality control pathways [1,2].

Knockdown of PELO increased hemin-induced erythroid differentiation of K562 and HEL cells, inhibited cell proliferation and cell cycle progression, and promoted apoptosis of K562 cells. PELO regulates erythroid differentiation by interacting with MYC to upregulate KLF10 [1]. PELO also catalyzes the oligomeric assembly of NOD-like receptor family proteins via activating their ATPase enzymatic activity [2]. In prostate cancer, PELO facilitates PLK1-induced the ubiquitination and degradation of Smad4, promoting the progression of prostate cancer [3]. In Drosophila, pelo deficiency limits the high-level synthesis of the Drosophila C virus capsid proteins, and in Aedes aegypti, pelo is upregulated during DENV replication and its silencing leads to reduced DENV virion production [4,5].

In conclusion, Pelo has diverse functions in biological processes such as erythroid differentiation, innate immune response, and viral replication. In disease-related contexts, it is involved in the progression of prostate cancer and the replication of certain viruses. Studies on Pelo, especially through loss-of-function experiments, help to understand its role in these biological processes and diseases, providing potential targets for therapeutic strategies.