ArticleAmerican journal of physiology. Heart and circulatory physiology2020
Atypical ALPK2 kinase is not essential for cardiac development and function.
Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- α Protein Kinase 3 Is Essential for Neonatal and Adult Cardiac Function.Journal of the American Heart Association · 2025Article
- Inhibition of circALPK2 enhances proliferation and therapeutic potential of human pluripotent stem cell-derived cardiomyocytes in myocardial infarction.Stem cell research & therapy · 2025Article
- Article
- ALPK2 prevents cardiac diastolic dysfunction in heart failure with preserved ejection fraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- CheekAge, a next-generation epigenetic buccal clock, is predictive of mortality in human blood.Frontiers in aging · 2024Article
- Automated quantification and statistical assessment of proliferating cardiomyocyte rates in embryonic hearts.American journal of physiology. Heart and circulatory physiology · 2023Article
- Expression Profile of New Marker Genes Involved in Differentiation of Canine Adipose-Derived Stem Cells into Osteoblasts.International journal of molecular sciences · 2021Article
- State-of-the-Art Technology of Model Organisms for Current Human Medicine.Diagnostics (Basel, Switzerland) · 2020Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
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 α-protein kinases, including α-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.