Prkcb-flox Mouse

Prkcb, Protein kinase C beta, is a member of the classical PRKCs. It plays a role in negatively modulating the mitochondrial energy status and inhibiting autophagy [6]. It is also involved in pathways like T cell receptor-NF-κB signaling and T cell trafficking, as well as immunosurveillance [5].

In lung adenocarcinoma (LUAD), Prkcb expression is related to prognosis through methylation and immune infiltration. It is lowly expressed in LUAD patients and involved in cancer-related Kyoto Encyclopedia of Genes and Genomes pathway and immune infiltration [1]. In Ewing sarcoma, Prkcb is significantly overexpressed and its immunohistochemistry is sensitive and specific for diagnosing Ewing sarcoma with EWSR1 rearrangement [2].

In intestinal ischemia/reperfusion, a circRNA transcribed from the Prkcb gene, circ-Prkcb, acts as an endogenous miR-339-5p sponge to regulate p66Shc expression, which is related to oxidative stress [3]. In the study of crosstalk between periodontitis and osteoporosis, Prkcb was identified as a key gene involved in neutrophil extracellular trap formation and MAPK signaling pathway [4]. In Nano NiO-induced collagen formation in BEAS-2B cells, Prkcb DNA methylation is regulated by lncRNA AP000487.1, affecting the TLR4/MyD88/NF-κB pathway [7]. Zuojin capsule may inhibit colorectal cancer by targeting Prkcb [8].

In conclusion, Prkcb plays essential roles in various biological processes and diseases. Studies on Prkcb contribute to understanding the mechanisms of autophagy, tumorigenesis, oxidative stress, and the crosstalk between different diseases. The findings from different research models help to explore potential biomarker and therapeutic targets related to Prkcb in multiple disease areas.