| First Author | Bogomolovas J | Year | 2020 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 318 |
| Issue | 6 | Pages | H1509-H1515 |
| PubMed ID | 32383995 | Mgi Jnum | J:292812 |
| Mgi Id | MGI:6450348 | Doi | 10.1152/ajpheart.00249.2020 |
| Citation | Bogomolovas J, et al. (2020) Atypical ALPK2 kinase is not essential for cardiac development and function. Am J Physiol Heart Circ Physiol 318(6):H1509-H1515 |
| abstractText | Protein kinases play an integral role in cardiac development, function, and disease. Recent experimental and clinical data have implied that protein kinases belonging to a family of atypical alpha-protein kinases, including alpha-protein kinase 2 (ALPK2), are important for regulating cardiac development and maintaining function via regulation of WNT signaling. A recent study in zebrafish reported that loss of ALPK2 leads to severe cardiac defects; however, the relevance of ALPK2 has not been studied in a mammalian animal model. To assess the role of ALPK2 in the mammalian heart, we generated two independent global Alpk2-knockout (Alpk2-gKO) mouse lines, using CRISPR/Cas9 technology. We performed physiological and biochemical analyses of Alpk2-gKO mice to determine the functional, morphological, and molecular consequences of Alpk2 deletion at the organismal level. We found that Alpk2-gKO mice exhibited normal cardiac function and morphology up to one year of age. Moreover, we did not observe altered WNT signaling in neonatal Alpk2-gKO mouse hearts. In conclusion, Alpk2 is dispensable for cardiac development and function in the murine model. Our results suggest that Alpk2 is a rapidly evolving gene that lost its essential cardiac functions in mammals.NEW & NOTEWORTHY Several studies indicated the importance of ALPK2 for cardiac function and development. A recent study in zebrafish report that loss of ALPK2 leads to severe cardiac defects. In contrast, murine Alpk2-gKO models developed in this work display no overt cardiac phenotype. Our results suggest ALPK2, as a rapidly evolving gene, lost its essential cardiac functions in mammals. |
