Prkch, encoding protein kinase C eta, is a member of the PKC family. It has the potential to regulate cell proliferation and differentiation, and is involved in multiple biological processes. Genetic models such as gene knockout could potentially be used to further explore its functions [2].

In neonatal sepsis, elevated serum Prkch levels were found, suggesting its diagnostic value for this condition [1]. In glioma, overexpression of Prkch promotes tumorigenesis and influences glioma stem cell properties, and its expression level is an independent prognostic factor [2]. Knockdown of circ-Prkch alleviates IL-1β-treated chondrocyte cell phenotypic changes in osteoarthritis via the miR-502-5p/ADAMTS5 axis [3]. Also, the Prkch 1425G/A polymorphism may be a biomarker for predicting ischemic stroke recurrence [4]. In a Chinese population, the rs3783782 polymorphism in Prkch is associated with rheumatoid arthritis susceptibility [5]. Prkch deletion in mice impairs hematopoietic stem cell function, and its high expression in acute myeloid leukemia correlates with poor overall survival [6].

In summary, Prkch is crucial in regulating cell proliferation and differentiation. Studies using genetic models like gene knockout in mice have revealed its role in various diseases such as neonatal sepsis, glioma, osteoarthritis, ischemic stroke, rheumatoid arthritis, and acute myeloid leukemia, contributing to our understanding of disease mechanisms and potential biomarker discovery.