Aimp1-KO Mouse

AIMP1, also known as p43, is a non-catalytic component of the multi-tRNA synthetase complex that not only participates in translation but also has diverse functions [4]. It is involved in various pathways including cell-cycle control, tumor suppression, and immune regulation [4]. It also plays a role in processes like adipogenesis, chondrogenesis, and hair growth, highlighting its overall biological importance. Genetic models, such as gene knockout (KO) mouse models, have been crucial in understanding its functions.

In multiple myeloma, AIMP1 expression is increased and is associated with unfavorable outcomes. It promotes cell proliferation in vitro and in vivo via the mitogen-activated protein kinase (MAPK) signaling pathway by interacting with ANP32A to regulate histone H3 acetylation [1]. In hair follicle stem cells, an AIMP1-derived peptide activates dermal papilla cells and promotes hair growth [2]. In T cells, AIMP1 inhibits TCR-dependent activation and proliferation of CD4 T cells, reduces lipid raft association and phosphorylation of related proteins, and enhances regulatory T cell differentiation [3]. AIMP1 deficiency in mice leads to enhanced airway hyperreactivity via increased TH2 immune responses [5]. In chondrocytes, downregulation of AIMP1 restores chondrogenic characteristics by enhancing TGF-β signaling [6].

In conclusion, AIMP1 has a wide-ranging impact on biological processes. Through model-based research, especially KO mouse models, its roles in diseases like multiple myeloma, as well as in normal physiological processes such as hair growth and T-cell regulation, have been revealed. Understanding AIMP1 provides insights into disease mechanisms and potential therapeutic targets for conditions related to abnormal cell proliferation, immune dysregulation, and tissue-specific disorders.

References:

1. Wei, Rongfang, Zhu, Yan, Zhang, Yuanjiao, Gu, Xiaosong, Yang, Ye. 2022. AIMP1 promotes multiple myeloma malignancy through interacting with ANP32A to mediate histone H3 acetylation. In Cancer communications (London, England), 42, 1185-1206. doi:10.1002/cac2.12356. https://pubmed.ncbi.nlm.nih.gov/36042007/

2. Kim, YounHa, Kim, Sang Bum, Lee, Ho, Sung, Young Kwan, Kim, Sunghoon. 2024. AIMP1-Derived Peptide Secreted from Hair Follicle Stem Cells Promotes Hair Growth by Activating Dermal Papilla Cells. In International journal of biological sciences, 20, 5764-5778. doi:10.7150/ijbs.101127. https://pubmed.ncbi.nlm.nih.gov/39494335/

3. Kim, Myun Soo, Lee, Arim, Cho, Daeho, Kim, Tae Sung. 2019. AIMP1 regulates TCR signaling and induces differentiation of regulatory T cells by interfering with lipid raft association. In Biochemical and biophysical research communications, 514, 875-880. doi:10.1016/j.bbrc.2019.05.040. https://pubmed.ncbi.nlm.nih.gov/31084930/

4. Liang, D, Halpert, M M, Konduri, V, Decker, W K. 2015. Stepping Out of the Cytosol: AIMp1/p43 Potentiates the Link Between Innate and Adaptive Immunity. In International reviews of immunology, 34, 367-81. doi:10.3109/08830185.2015.1077829. https://pubmed.ncbi.nlm.nih.gov/26325028/

5. Hong, Hye-Jin, Kim, Eugene, Jung, Mi Young, Kim, Sunghoon, Kim, Tae Sung. 2012. AIMP1 deficiency enhances airway hyperreactivity in mice via increased TH2 immune responses. In Clinical immunology (Orlando, Fla.), 143, 256-65. doi:10.1016/j.clim.2012.02.004. https://pubmed.ncbi.nlm.nih.gov/22472603/

6. Ahn, J, Kumar, H, Cha, B-H, Park, S G, Lee, S-H. 2016. AIMP1 downregulation restores chondrogenic characteristics of dedifferentiated/degenerated chondrocytes by enhancing TGF-β signal. In Cell death & disease, 7, e2099. doi:10.1038/cddis.2016.17. https://pubmed.ncbi.nlm.nih.gov/26890138/