Akap5, also known as AKAP79/150, is a member of the A-kinase anchoring proteins (AKAPs) family. It plays a crucial role in regulating the spatial and temporal organization of cellular signal transduction. Akap5 can bind to various molecules such as β2-adrenergic receptor, protein kinases, protein phosphatases and cytoskeletal elements, and is involved in multiple pathways [1]. It is originally identified in neurons but later detected in other tissues, participating in diverse biological processes. Genetic models like Akap5-null mice are valuable for studying its functions.

In Akap5-null mice, ECG analysis showed a normal sinus rhythm but decreased responsiveness to isoproterenol compared to wild-type mice. Heart rate variability analysis indicated an unstable R-R interval and decreased low-frequency components, suggesting an affected sympathetic nervous system tonus. The atrium also showed a decreased positive inotropic response to isoproterenol, indicating Akap5's involvement in a PKA-dependent pathway [2]. In addition, amylase secretion from acinar cells of Akap5 knockout (KO) mice treated with the β-adrenergic agonist isoproterenol was reduced by 30-40% compared with wild-type mice, suggesting Akap5's role in this process [3].

In conclusion, Akap5 is essential for regulating sympathetic nerve activities and amylase secretion. The use of Akap5 KO mouse models has revealed its importance in these specific physiological processes, providing insights into potential mechanisms underlying related diseases, such as those involving abnormal sympathetic regulation or glandular secretion disorders.

References:

1. Guo, Yanjing, Bo, Tao, Zhou, Xinli, Wang, Yong, Zhao, Jiajun. . AKAP5 signaling complexes: focal points and functional properties. In Neuro endocrinology letters, 36, 7-14. doi:. https://pubmed.ncbi.nlm.nih.gov/25789584/

2. Han, Chong, Tomita, Hirofumi, Ohba, Takayoshi, Okumura, Ken, Murakami, Manabu. 2015. Modified sympathetic nerve regulation in AKAP5-null mice. In Biochemical and biophysical research communications, 469, 897-902. doi:10.1016/j.bbrc.2015.12.057. https://pubmed.ncbi.nlm.nih.gov/26713362/

3. Wu, Ching-Yi, DiJulio, Dennis H, Jacobson, Kerry L, McKnight, G Stanley, Watson, Eileen L. 2010. The contribution of AKAP5 in amylase secretion from mouse parotid acini. In American journal of physiology. Cell physiology, 298, C1151-8. doi:10.1152/ajpcell.00382.2009. https://pubmed.ncbi.nlm.nih.gov/20164376/