Caln1, a gene encoding a neuron-specific protein, is a member of the calmodulin superfamily. It has two conserved EF-hand motifs, indicating a potential role in signal transduction. Located on chromosome 7q11 in humans, Caln1 may be involved in membrane remodeling as it interacts with proteins like APOL3 to control PI(4)P synthesis, which is crucial for infection-induced inflammation processes [4,7]. In neurons, its high expression in regions like the cerebellum, hippocampus, and cortex, along with its developmental-stage-specific expression, suggests a significant role in neuronal physiology, potentially in memory and learning [8].

In bladder cancer, CALN1 hypomethylation is associated with advanced tumor stage, high histological grade, and is an independent risk factor for intravesical recurrence in non-muscle-invasive bladder cancer, indicating its potential as a biomarker [1]. In schizophrenia, experimental evidence shows that CALN1 is a target of miR-137, with SNPs in CALN1 associated with the disease [2]. In glioma, CALN1 expression is decreased, positively correlated with prognosis, and its abnormal decrease may lead to the invasion of tumor-promoting immune cells [3]. In aldosterone-producing adenoma, increased CALN1 expression is associated with elevated Ca2+ storage in the endoplasmic reticulum and aldosterone overproduction, suggesting it as a potential therapeutic target [5]. In metastatic osteosarcoma, exosomal miR-675 down-regulates CALN1 expression in recipient cells, promoting cell migration and invasion [6].

In conclusion, Caln1 plays diverse roles in multiple biological processes and disease conditions. Its functions in membrane remodeling, neuronal physiology, and its associations with various cancers and schizophrenia highlight its importance. Studies on Caln1 using different genetic models contribute to understanding the mechanisms of these diseases, providing potential biomarkers and therapeutic targets.

References:

1. Takagi, Kimiaki, Naruse, Azumi, Akita, Kazutoshi, Horie, Masanobu, Kikuchi, Arizumi. 2022. CALN1 hypomethylation as a biomarker for high-risk bladder cancer. In BMC urology, 22, 176. doi:10.1186/s12894-022-01136-y. https://pubmed.ncbi.nlm.nih.gov/36352401/

2. Xia, Shihui, Zhou, Xinyao, Wang, Teng, He, Lin, Zhao, Xinzhi. 2015. Experimental validation of candidate schizophrenia gene CALN1 as a target for microRNA-137. In Neuroscience letters, 602, 110-4. doi:10.1016/j.neulet.2015.07.001. https://pubmed.ncbi.nlm.nih.gov/26163462/

3. Zhang, Han, Zhang, Jinhao, Wang, Tao. . [Bioinformatic analysis of the clinical significance of calneuron 1 (CALN1) in glioma and its correlation with immune cell infiltration]. In Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology, 39, 205-212. doi:. https://pubmed.ncbi.nlm.nih.gov/36946344/

4. Pays, Etienne. 2024. Apolipoprotein-L Functions in Membrane Remodeling. In Cells, 13, . doi:10.3390/cells13242115. https://pubmed.ncbi.nlm.nih.gov/39768205/

5. Kobuke, Kazuhiro, Oki, Kenji, Gomez-Sanchez, Celso E, Yoneda, Masayasu, Hattori, Noboru. 2017. Calneuron 1 Increased Ca2+ in the Endoplasmic Reticulum and Aldosterone Production in Aldosterone-Producing Adenoma. In Hypertension (Dallas, Tex. : 1979), 71, 125-133. doi:10.1161/HYPERTENSIONAHA.117.10205. https://pubmed.ncbi.nlm.nih.gov/29109191/

6. Gong, Liangzhi, Bao, Qiyuan, Hu, Chuanzhen, Zhang, Weibin, Shen, Yuhui. 2018. Exosomal miR-675 from metastatic osteosarcoma promotes cell migration and invasion by targeting CALN1. In Biochemical and biophysical research communications, 500, 170-176. doi:10.1016/j.bbrc.2018.04.016. https://pubmed.ncbi.nlm.nih.gov/29626470/

7. Pays, Etienne. 2024. The Janus-faced functions of Apolipoproteins L in membrane dynamics. In Cellular and molecular life sciences : CMLS, 81, 134. doi:10.1007/s00018-024-05180-9. https://pubmed.ncbi.nlm.nih.gov/38478101/

8. Wu, Y Q, Lin, X, Liu, C M, Jamrich, M, Shaffer, L G. . Identification of a human brain-specific gene, calneuron 1, a new member of the calmodulin superfamily. In Molecular genetics and metabolism, 72, 343-50. doi:. https://pubmed.ncbi.nlm.nih.gov/11286509/