Mrto4-flox Mouse

Mrto4, also known as MRT4 Homolog, Ribosome Maturation Factor, is involved in ribosome biogenesis [4]. It contains a C-terminal extension similar to ribosomal P proteins, and its phosphorylation by CK2 kinase at serines S229, S233, and S235 within the acidic C-termini affects its molecular behavior during ActD-induced nucleolar stress, suggesting its role in connecting ribosome biogenesis with cellular metabolism [4].

Mrto4 has been implicated in multiple diseases. In hepatocellular carcinoma (HCC), it is an independent prognostic risk factor. It accelerates glycolysis of HCC cells, promotes proliferation and invasion, and suppresses apoptosis by inhibiting ALDOB [1]. In HCC, its overexpression is also associated with poor prognosis, and is positively correlated with the stage and grade of HCC patients. It is related to the tumor microenvironment, immune checkpoint gene expressions, and drug sensitivity [2]. In colorectal cancer, Mrto4 is highly expressed and may influence its progression [3]. In buccal mucosa squamous cell carcinoma, it may serve as a putative therapeutic target and potential biomarker [5]. Moreover, in male mice, abnormal expression of Mrto4 due to Tripterygium wilfordii treatment, Trichinella spiralis infection, or Neospora caninum infection is associated with reproductive injury [6,7,8].

In conclusion, Mrto4 is crucial in ribosome biogenesis and stress response. Its dysregulation is linked to various cancers and male reproductive injury. Studies on Mrto4, especially through in vivo models like mouse models, help in understanding disease mechanisms in these areas, potentially paving the way for new therapeutic strategies.