Camk1d, also known as calcium/calmodulin-dependent protein kinase ID, is involved in multiple intracellular signaling pathways. It has been associated with the PI3K/AKT/mTOR pathway and is important in various biological processes. It is widely expressed in many tissues and plays a role in cell growth, making it relevant in understanding disease mechanisms [2].

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 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 PVN, indicating its role in ghrelin-mediated food intake [1]. In glioma, knockdown of CamK1D promotes cell proliferation, invasion and migration, while overexpression has the opposite effects, suggesting its tumor-inhibitory role through the PI3K/AKT/mTOR pathway [2].

In conclusion, Camk1d is crucial in regulating ghrelin-mediated food intake and body weight, as shown by knockout mouse models. In addition, it plays a role in tumor-related processes such as glioma cell function. These findings from Camk1d KO models contribute to understanding the mechanisms of obesity-related diseases and glioma, providing potential targets for treatment.