Zfp143, also known as ZNF143, is a zinc-finger protein that serves as a transcription factor. It plays crucial roles in multiple biological processes such as the maintenance of embryonic stem (ES) cell self-renewal, regulation of nuclear-encoded mitochondrial genes, and is involved in the development of non-alcoholic fatty liver disease. Its functions are associated with various signaling pathways [1,2,3]. Genetic models, like gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable tools to study Zfp143's functions.

In ES cells, depletion of Zfp143 by RNA interference leads to loss of self-renewal. Zfp143 directly binds to the Nanog proximal promoter and regulates Nanog expression through modulating Oct4 binding. Co-immunoprecipitation experiments showed that Zfp143 and Oct4 physically interact [1]. In mouse embryonic stem cells, Zfp143 degradation has no effect on chromatin looping, but it specifically activates nuclear-encoded mitochondrial genes, and its loss leads to severe mitochondrial dysfunction. Using an in vitro embryo model, Zfp143 was found to be an essential regulator of organismal development [2]. In hepatocytes, knockdown of Zfp143 inhibits lipid droplets formation and promotes mitophagy, while overexpression of related factors can reverse these effects, suggesting Zfp143 promotes non-alcoholic fatty liver disease by inhibiting mitophagy via the ROCK2 pathway [3].

In conclusion, Zfp143 is essential for maintaining ES cell self-renewal, regulating mitochondrial gene expression for organismal development, and has an impact on the development of non-alcoholic fatty liver disease. Studies using KO/CKO mouse models have provided important insights into these functions, helping to understand the underlying mechanisms of related biological processes and disease conditions.