Rnf24-KO Mouse

Rnf24, a membrane RING-H2 protein, has been shown to interact with the ankyrin-like repeat domain of TRPCs (transient receptor potential canonical channels). It is involved in the intracellular trafficking of TRPCs by interacting with them in the Golgi apparatus without affecting their activity [1]. Rnf24 may also be related to focal adhesion, as it was identified as a hub gene associated with focal adhesion in osteoporosis research. Its increased expression in monocytes was observed in both mouse and human blood samples, and anti-RNF24 was found to partially alleviate the progression of osteoporosis in mouse experiments [2].

In the context of pain-depression comorbidity, Rnf24 was identified as one of the five hub genes through bioinformatics analysis, suggesting its potential as a diagnostic and prognostic marker for patients with this comorbidity [3]. It was also among the differentially regulated genes in aged female skeletal muscle, indicating its possible role in sarcopenia-related processes [4]. In Parkinson's disease, Rnf24 was identified as a hub gene and was part of a 7-gene panel that could serve as a potential diagnostic signature [5]. In BRCA wild-type high-grade serous ovarian cancer, Rnf24 was in a ten-gene signature predictive of response to first-line chemotherapy and was defined as a cell-autonomous contributor to tumor resistance [6].

In summary, Rnf24 is involved in multiple biological processes and diseases. Its role in the intracellular trafficking of TRPCs, its association with osteoporosis, pain-depression comorbidity, sarcopenia, Parkinson's disease, and ovarian cancer highlights its importance. Research on Rnf24 using various models can help further understand its functions and potentially lead to new diagnostic and therapeutic strategies for these diseases.

References:

1. Lussier, Marc P, Lepage, Pascale K, Bousquet, Simon M, Boulay, Guylain. 2007. RNF24, a new TRPC interacting protein, causes the intracellular retention of TRPC. In Cell calcium, 43, 432-43. doi:. https://pubmed.ncbi.nlm.nih.gov/17850865/

2. Shi, Xiaojian, Fu, Qiang, Mao, Jianyu, Chen, Aimin, Lu, Nan. . Integration of single-cell and RNA-seq data to explore the role of focal adhesion-related genes in osteoporosis. In Journal of cellular and molecular medicine, 28, e18271. doi:10.1111/jcmm.18271. https://pubmed.ncbi.nlm.nih.gov/38534087/

3. Zhang, Tianyun, Geng, Menglu, Li, Xiaoke, Zhang, Huaxing, Zhang, Fan. 2024. Identification of Oxidative Stress-Related Biomarkers for Pain-Depression Comorbidity Based on Bioinformatics. In International journal of molecular sciences, 25, . doi:10.3390/ijms25158353. https://pubmed.ncbi.nlm.nih.gov/39125922/

4. Gharpure, Mohini, Chen, Jie, Nerella, Resheek, Adusumilli, Satish, Fulzele, Sadanand. 2023. Sex-specific alteration in human muscle transcriptome with age. In GeroScience, 45, 1303-1316. doi:10.1007/s11357-023-00795-5. https://pubmed.ncbi.nlm.nih.gov/37106281/

5. Wu, Zhaoping, Hu, Zhiping, Gao, Yunchun, Zhang, Xiaobo, Jiang, Zheng. 2023. A computational approach based on weighted gene co-expression network analysis for biomarkers analysis of Parkinson's disease and construction of diagnostic model. In Frontiers in computational neuroscience, 16, 1095676. doi:10.3389/fncom.2022.1095676. https://pubmed.ncbi.nlm.nih.gov/36704228/

6. Buttarelli, Marianna, Ciucci, Alessandra, Palluzzi, Fernando, Scambia, Giovanni, Gallo, Daniela. 2022. Identification of a novel gene signature predicting response to first-line chemotherapy in BRCA wild-type high-grade serous ovarian cancer patients. In Journal of experimental & clinical cancer research : CR, 41, 50. doi:10.1186/s13046-022-02265-w. https://pubmed.ncbi.nlm.nih.gov/35120576/