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 (KO) and conditional knockout (CKO) mouse models, can be used to study its functions in vivo [2].

In neonatal sepsis (NS), elevated serum Prkch levels have diagnostic value for NS, suggesting its potential as a non-invasive biomarker for NS prognosis and diagnosis [1]. In glioma, Prkch overexpression promotes tumorigenesis, influences glioma stem cell properties, and is an independent prognostic factor for poor prognosis in glioma patients [2]. In osteoarthritis (OA), knockdown of circ-Prkch alleviates IL-1β-treated chondrocyte cell phenotypic changes through modulating the miR-502-5p/ADAMTS5 axis, indicating a potential biomarker for OA treatment [3]. Also, Prkch 1425G/A polymorphism may be a biomarker for predicting ischemic stroke recurrence in a Chinese population [4]. Moreover, the rs3783782 polymorphism in Prkch is associated with rheumatoid arthritis susceptibility in a Chinese population [5]. In acute myeloid leukemia (AML), Prkch is highly expressed in mouse and human hematopoietic stem cells (HSCs) and leukemia stem cells (LSCs), and its deletion in mice impairs HSC function, while high expression in AML patients correlates with poor overall survival [6].

In conclusion, Prkch plays crucial roles in cell proliferation, differentiation, and is involved in various disease conditions including neonatal sepsis, glioma, osteoarthritis, ischemic stroke, rheumatoid arthritis, and acute myeloid leukemia. Studies using KO or CKO mouse models have provided insights into its functions in these disease-related biological processes, highlighting its potential as a biomarker and therapeutic target in these diseases.

References:

1. Zhang, Yue, Li, JingYa, Qi, HaiLian, Kong, XiangYong. . Mechanisms of PALLD, PRKCH, AKAP12, PDK4, and CHIT1 Proteins in Serum Diagnosis of Neonatal Sepsis. In Clinical laboratory, 68, . doi:10.7754/Clin.Lab.2022.210917. https://pubmed.ncbi.nlm.nih.gov/36377982/

2. Pang, Fangning, He, Wei, Liu, Xuantong, Li, Mingyang, Xu, Jin. 2022. Overexpression of PRKCH promotes tumorigenesis in patients with glioma and influences glioma stem cell properties. In Pathology, research and practice, 240, 154236. doi:10.1016/j.prp.2022.154236. https://pubmed.ncbi.nlm.nih.gov/36434855/

3. Liu, Zhongxing, Cao, Jian, Zhang, Limin, Zhou, Peng, Zhang, Sidi. 2022. Knockdown of circ-PRKCH alleviates IL-1β-treated chondrocyte cell phenotypic changes through modulating miR-502-5p/ADAMTS5 axis. In Autoimmunity, 55, 179-191. doi:10.1080/08916934.2022.2027918. https://pubmed.ncbi.nlm.nih.gov/35352613/

4. Zhang, Zhizhong, Xu, Gelin, Zhu, Wusheng, Yan, Bernard, Liu, Xinfeng. 2014. PRKCH 1425G/A Polymorphism Predicts Recurrence of Ischemic Stroke in a Chinese Population. In Molecular neurobiology, 52, 1648-1653. doi:10.1007/s12035-014-8964-6. https://pubmed.ncbi.nlm.nih.gov/25370935/

5. Zhuang, Yue, Di, Yanan, Huang, Lulin, Zhu, Jing. 2019. PRKCH polymorphism is associated with rheumatoid arthritis in a Chinese population. In Bioscience trends, 13, 556-561. doi:10.5582/bst.2019.01247. https://pubmed.ncbi.nlm.nih.gov/31875586/

6. Porter, Shaina N, Magee, Jeffrey A. 2017. PRKCH regulates hematopoietic stem cell function and predicts poor prognosis in acute myeloid leukemia. In Experimental hematology, 53, 43-47. doi:10.1016/j.exphem.2017.05.006. https://pubmed.ncbi.nlm.nih.gov/28596089/