The CALM-3 gene, along with the protein of calmodulin, has been included in different types of experiments such as DNA isolation that is most common in laboratory animals such as rats. This gene can be detected in animals and humans, mainly through our genomes, and its specific polymorphisms can be found through different types of restriction enzymes.7 In hospital settings, a process named whole exome sequencing are used and are beneficial in determining whether CALM-3 is a cause of a certain disease.8 Because the protein calmodulin consists of 3 different genes, it may be difficult to determine exactly how the gene can cause a certain disease to occur and potentially worsen.9 However, there have been few mutations that were detected in the genes of the calmodulin protein such as in long QT syndrome.10
There is significant evidence that Calmodulin-3 may be associated with certain diseases, however there are few evidence that this particular gene contributes to diseases that can cause a sudden death as a result. In the lab experiment with rats, lambda rCB1 or hCE1 underwent DNA isolation as both of the genes included the CALM-3 gene, and was compared with 2 different genes that are more common among rats such as genes lambda SC4 and lambda SC8.11 As a result, although the lambda rCB1 or hCE1 gene may have different structures from the other genes that rats contain in their genomes, its coding strands were fairly similar.12 As the process of whole exome sequencing was used for patients with long QT syndrome, there was a certain criteria that had to be met in order to fully go through WES such as the patient having a stable or normal medical family history.13 Based on an electrocardiogram, the rhythms and waves can be detected and if irregular, it could lead to the pathway of long QT syndrome.14
"CALM3 - Calmodulin-3 - Homo sapiens (Human) - CALM3 gene & protein". www.uniprot.org. Retrieved 2022-05-18. https://www.uniprot.org/uniprot/P0DP25 ↩
"CALM3 - Calmodulin-3 - Homo sapiens (Human) - CALM3 gene & protein". www.uniprot.org. Retrieved 2022-04-16. https://www.uniprot.org/uniprot/P0DP25 ↩
Zhang M, Yuan T (2011-01-24). "Molecular mechanisms of calmodulin's functional versatility". Biochemistry and Cell Biology. 76 (2–3): 313–323. doi:10.1139/o98-027. PMID 9923700. /wiki/Doi_(identifier) ↩
Koller M, Schnyder B, Strehler EE (October 1990). "Structural organization of the human CaMIII calmodulin gene". Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression. 1087 (2): 180–189. doi:10.1016/0167-4781(90)90203-E. PMID 2223880. /wiki/Doi_(identifier) ↩
Friedrich FW, Bausero P, Sun Y, Treszl A, Krämer E, Juhr D, et al. (July 2009). "A new polymorphism in human calmodulin III gene promoter is a potential modifier gene for familial hypertrophic cardiomyopathy". European Heart Journal. 30 (13): 1648–1655. doi:10.1093/eurheartj/ehp153. PMID 19429631. https://doi.org/10.1093%2Feurheartj%2Fehp153 ↩
SenGupta B, Friedberg F, Detera-Wadleigh SD (December 1987). "Molecular analysis of human and rat calmodulin complementary DNA clones. Evidence for additional active genes in these species". The Journal of Biological Chemistry. 262 (34): 16663–16670. doi:10.1016/S0021-9258(18)49306-4. PMID 2445749. https://doi.org/10.1016%2FS0021-9258%2818%2949306-4 ↩
Reed GJ, Boczek NJ, Etheridge SP, Ackerman MJ (February 2015). "CALM3 mutation associated with long QT syndrome". Heart Rhythm. 12 (2): 419–422. doi:10.1016/j.hrthm.2014.10.035. PMC 4907373. PMID 25460178. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4907373 ↩