Plek, short for pleckstrin, is a gene whose functions are associated with various biological processes and diseases. It has been implicated in immune-related pathways, as its products are involved in processes like immune cell activation and cytokine-related functions [1,2,3,4,6]. Plek also seems to play a role in pathways relevant to conditions such as atherosclerosis, non-alcoholic steatohepatitis (NASH), and multiple sclerosis (MS), suggesting its importance in disease-related biological mechanisms [1,2,5,6,7].

In the context of psoriasis complicated with atherosclerosis, Plek was identified as one of the 16 important hub genes, indicating its potential role in the common pathogenesis of these two diseases [1]. In carotid atherosclerosis, higher expression of Plek was found, suggesting it could be a potential biomarker with worse prognosis when highly expressed [2]. In non-small cell lung cancer, the expression of Plek was associated with a better prognosis in lung adenocarcinoma among 13 differentiation-related genes in tumor-associated macrophages [3]. In addition, Plek was identified as a potential biomarker related to M2 macrophages in chronic rhinosinusitis with nasal polyps [4], and as a hub gene in the Turquoise module related to immune response in NASH [6]. Moreover, in MS, genetically predicted higher levels of Plek were associated with an increased risk of the disease, and it was identified as a druggable target gene [7].

In conclusion, Plek is involved in multiple biological processes and disease conditions, especially those related to the immune response and various disease-associated pathways. Its identification as a key gene in models of diseases like atherosclerosis, lung cancer, and MS provides valuable insights into the underlying mechanisms of these diseases, potentially paving the way for new diagnostic and therapeutic strategies.

References:

1. Su, Wenxing, Zhao, Ying, Wei, Yuqian, Ji, Jiang, Yang, Shun. 2021. Exploring the Pathogenesis of Psoriasis Complicated With Atherosclerosis via Microarray Data Analysis. In Frontiers in immunology, 12, 667690. doi:10.3389/fimmu.2021.667690. https://pubmed.ncbi.nlm.nih.gov/34122426/

2. Zhao, Man, Liu, Aixian, Mo, Linhong, Fu, Taozhu, Deng, Hongru. . Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis. In Medicine, 102, e34445. doi:10.1097/MD.0000000000034445. https://pubmed.ncbi.nlm.nih.gov/37861500/

3. Li, Zhaoxun, Zhou, Bin, Zhu, Xinsheng, Song, Xiao, Jiang, Gening. 2023. Differentiation-related genes in tumor-associated macrophages as potential prognostic biomarkers in non-small cell lung cancer. In Frontiers in immunology, 14, 1123840. doi:10.3389/fimmu.2023.1123840. https://pubmed.ncbi.nlm.nih.gov/36969247/

4. Zhu, Ying, Sun, Xiwen, Tan, Shaolin, Lin, Hai, Zhang, Weitian. 2022. M2 macrophage-related gene signature in chronic rhinosinusitis with nasal polyps. In Frontiers in immunology, 13, 1047930. doi:10.3389/fimmu.2022.1047930. https://pubmed.ncbi.nlm.nih.gov/36466903/

5. Li, Haobo, Zhang, Zhu, Qiu, Yuting, Zhai, Zhenguo, Wang, Chen. 2023. Proteome-wide mendelian randomization identifies causal plasma proteins in venous thromboembolism development. In Journal of human genetics, 68, 805-812. doi:10.1038/s10038-023-01186-6. https://pubmed.ncbi.nlm.nih.gov/37537391/

6. Zhang, Jun-Jie, Shen, Yan, Chen, Xiao-Yuan, Zhang, Jie, Xu, Fei. 2023. Integrative network-based analysis on multiple Gene Expression Omnibus datasets identifies novel immune molecular markers implicated in non-alcoholic steatohepatitis. In Frontiers in endocrinology, 14, 1115890. doi:10.3389/fendo.2023.1115890. https://pubmed.ncbi.nlm.nih.gov/37008925/

7. Liu, Yi, Wang, Qian, Zhao, Yuhui, Chen, Jinyi, Qin, Chao. 2024. Identification of novel drug targets for multiple sclerosis by integrating plasma genetics and proteomes. In Experimental gerontology, 194, 112505. doi:10.1016/j.exger.2024.112505. https://pubmed.ncbi.nlm.nih.gov/38964432/