CREBRF, short for cyclic-adenosine-monophosphate-response-element-binding protein 3 regulatory factor, is a key regulator involved in multiple biological processes. It has been linked to pathways related to energy metabolism, apoptosis, hormonal synthesis, and glucocorticoid signaling, and is of great biological importance in areas such as metabolism, reproduction, and cancer [1,2,4,5]. Genetic models, especially mouse models, have been crucial in studying its functions.

In mouse models, Crebrf knockout mice showed reduced epithelial proliferation and increased apoptosis in the prostate, suggesting its role in prostate tissue homeostasis and potentially in limiting prostate tumorigenesis [4]. Male Crebrf knockout mice also had a trend towards increased lean mass and reduced insulin sensitivity [3]. Additionally, global loss of CREBRF in male and female mice led to reduced anxiety-like behaviors and lower plasma corticosterone after restraint stress, indicating its impact on stress-related responses [5].

In conclusion, CREBRF is essential in regulating muscle energy metabolism, apoptosis, estradiol synthesis, and stress-related behaviors. Mouse knockout models have been instrumental in revealing its functions in prostate tumorigenesis, metabolism, and anxiety-like behaviors, providing valuable insights into related disease mechanisms.