Camk1d, or calcium/calmodulin-dependent protein kinase ID, is involved in multiple biological processes. It participates in intracellular signaling pathways [1,2,3,4]. In addition, it has been associated with important physiological functions and diseases, making it a key gene for understanding various biological phenomena. Genetic models, such as knockout mouse models, have been crucial in studying its functions [1].

Global Camk1d-knockout male mice are resistant to ghrelin, gain less body weight and are protected against high-fat-diet-induced obesity. Deletion of Camk1d in AgRP/NPY neurons, but not in POMC neurons, recapitulates these phenotypes. In response to ghrelin, lack of CaMK1D attenuates phosphorylation of CREB and CREB-dependent expression of orexigenic neuropeptides in fibre projections to the paraventricular nucleus, suggesting its role in mediating ghrelin-dependent food intake [1]. In glioma, knockdown of Camk1D promotes the proliferation, invasion and migration of glioma cells, while overexpression has the opposite effect, indicating its inhibitory role on glioma through the PI3K/AKT/mTOR pathway [2].

In conclusion, Camk1d plays a significant role in regulating food intake via its action in AgRP neurons and is also involved in glioma development. The study of Camk1d-knockout mouse models has provided valuable insights into its functions in these disease-related biological processes, which are crucial for understanding the underlying mechanisms and potentially developing new therapeutic strategies.