Zbtb20, or zinc finger and BTB domain-containing protein 20, is a transcription factor with a zinc finger DNA-binding domain and a BTB domain for protein-protein interaction. It is involved in multiple biological processes, regulating genes in various pathways. Its study via gene knockout models, like KO or CKO mouse models, has been crucial in understanding its functions [2].

In KO mouse models, specific ablation of Zbtb20 in cardiomyocytes led to increased basal myocardial contractile parameters but impaired cardiac reserve and exercise capacity, by reducing PLN expression and enhancing SERCA2a activity [1]. Cochlear-specific deletion caused profound deafness due to arrested postnatal development of cochlear epithelial cells [3]. Conditional deletion in mature lactotropes led to decreased PRL levels and impaired lactation [4]. Zbtb20-null mice also showed hypotension, reduced heart size, and impaired cardiac contractility, along with decreased cardiac ATP and mitochondrial complex I enzyme activity [5]. In cardiac allograft rejection, ZBTB20 gene knockdown prolonged allograft survival [6]. Small-diameter primary sensory neuron-specific ZBTB20 knockout mice had diminished itch behaviors [7].

In conclusion, Zbtb20 is essential for normal development and function in multiple systems including the heart, cochlea, and lactotropes. Gene knockout mouse models have revealed its role in cardiac contractility, cochlear maturation, lactation, blood pressure regulation, cardiac allograft rejection, and itch sensation, providing insights into related disease mechanisms [1,3,4,5,6,7].