Trim13-KO Mouse

TRIM13, a RING-type E3 ubiquitin ligase, is a member of the TRIM protein family. It participates in diverse cellular processes, such as autophagy, apoptosis, and immune responses. It is involved in multiple pathways, including those related to antiviral innate immunity, cholesterol metabolism, and cell cycle regulation, highlighting its overall biological importance. Genetic models, like KO mouse models, have been crucial in understanding its functions [1,2].

In atherosclerosis, TRIM13 KO mouse model studies showed that TRIM13 promotes the disease by reducing cholesterol efflux and increasing oxidized LDL uptake, leading to foam cell formation. Deletion of TRIM13 protects against diet-induced atherosclerosis [2]. In acute myeloid leukemia (AML), chromatin assembly factor CHAF1B represses TRIM13 expression. Overexpression of TRIM13 in AML cells initially causes a proliferative burst followed by exhaustion, while loss of TRIM13 enhances leukemogenesis in AML cell lines and patient-derived xenografts [3].

In conclusion, TRIM13 plays essential roles in various biological processes and diseases. The use of KO mouse models has revealed its significance in atherosclerosis and AML. Understanding TRIM13 functions can potentially lead to new therapeutic strategies for these and other related diseases.

References:

1. Zhou, Peng, Zhang, Qingxiang, Yang, Yueshan, Zhou, Hongbo, Luo, Rui. 2024. Avian TRIM13 attenuates antiviral innate immunity by targeting MAVS for autophagic degradation. In Autophagy, 21, 754-770. doi:10.1080/15548627.2024.2426114. https://pubmed.ncbi.nlm.nih.gov/39508267/

2. Govatati, Suresh, Kumar, Raj, Boro, Monoranjan, Lusis, Aldons J, Rao, Gadiparthi N. 2024. TRIM13 reduces cholesterol efflux and increases oxidized LDL uptake leading to foam cell formation and atherosclerosis. In The Journal of biological chemistry, 300, 107224. doi:10.1016/j.jbc.2024.107224. https://pubmed.ncbi.nlm.nih.gov/38537695/

3. Dean, Sarai T, Ishikawa, Chiharu, Zhu, Xiaoqin, Starczynowski, Daniel T, Volk, Andrew G. . Repression of TRIM13 by chromatin assembly factor CHAF1B is critical for AML development. In Blood advances, 7, 4822-4837. doi:10.1182/bloodadvances.2022009438. https://pubmed.ncbi.nlm.nih.gov/37205848/