Pou2af1-KO Mouse

POU2AF1, also known as OCA-B, is a transcription co-factor. It is involved in multiple biological processes. In the immune system, it has a role in Tfh cell formation and migration into germinal centers by regulating CXCR5 expression [3]. It also functions in promoting CD4+ T cell memory and can identify memory precursor cells [4]. In addition, it is implicated in adipogenesis of mesenchymal stem cells (MSCs) [2], and may regulate host defense genes in the human airway epithelium [5].

In overweight patients, the expression of POU2AF1 was upregulated in retroperitoneal adipose tissue, and its overexpression promoted MSCs adipogenesis, while silencing inhibited adipogenesis, suggesting its role in the HDAC1-related adipogenesis pathway [2]. In the context of hepatocellular carcinoma (HCC), POU2AF1 is considered a potential therapeutic target, with studies using WGCNA and molecular docking analysis to explore its role in HCC progression and treatment [1]. In multiple sclerosis patients receiving natalizumab, alterations in the miR-126-3p/POU2AF1/Spi-B axis are associated with JCPyV reactivation [6].

In conclusion, POU2AF1 is a multifunctional transcription co-factor involved in adipogenesis, immune-related processes, and host defense gene regulation. Its dysregulation is associated with diseases such as HCC, obesity-related adipose disorders, and multiple sclerosis. Research on POU2AF1, including through model-based studies, provides insights into disease mechanisms and potential therapeutic targets.

References:

1. Li, Xin, Zhou, Hongxu, Ma, Ruiyang, Zhong, Yifan, Jing, Zuoqian. 2024. Structure of POU2AF1 recombinant protein and it affects the progression and treatment of liver cancer based on WGCNA and molecular docking analysis. In International journal of biological macromolecules, 278, 134629. doi:10.1016/j.ijbiomac.2024.134629. https://pubmed.ncbi.nlm.nih.gov/39128756/

2. Wang, Yaqing, Wang, Luyang, Su, Zhongping, Jiang, Li, Kong, Xiangqing. . POU2AF1 promotes MSCs adipogenesis by inhibiting HDAC1 expression. In Adipocyte, 10, 251-263. doi:10.1080/21623945.2021.1918863. https://pubmed.ncbi.nlm.nih.gov/33949290/

3. Zhu, Xiaoliang, Chen, Xi, Cao, Yaqiang, Zhao, Keji, Zhu, Jinfang. 2024. Optimal CXCR5 Expression during Tfh Maturation Involves the Bhlhe40-Pou2af1 Axis. In bioRxiv : the preprint server for biology, , . doi:10.1101/2024.05.16.594397. https://pubmed.ncbi.nlm.nih.gov/38903096/

4. Sun, Wenxiang, Hughes, Erik P, Kim, Heejoo, Williams, Matthew A, Tantin, Dean. 2024. OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors. In Proceedings of the National Academy of Sciences of the United States of America, 121, e2309153121. doi:10.1073/pnas.2309153121. https://pubmed.ncbi.nlm.nih.gov/38386711/

5. Zhou, Haixia, Brekman, Angelika, Zuo, Wu-Lin, Crystal, Ronald G, Wang, Guoqing. 2016. POU2AF1 Functions in the Human Airway Epithelium To Regulate Expression of Host Defense Genes. In Journal of immunology (Baltimore, Md. : 1950), 196, 3159-67. doi:10.4049/jimmunol.1502400. https://pubmed.ncbi.nlm.nih.gov/26927796/

6. Mancuso, Roberta, Agostini, Simone, Hernis, Ambra, Scarpini, Elio, Clerici, Mario. 2022. Alterations of the miR-126-3p/POU2AF1/Spi-B Axis and JCPyV Reactivation in Multiple Sclerosis Patients Receiving Natalizumab. In Frontiers in neurology, 13, 819911. doi:10.3389/fneur.2022.819911. https://pubmed.ncbi.nlm.nih.gov/35359635/