Zbtb5, short for zinc finger and BTB domain-containing 5, is a proto-oncogene that plays crucial roles in cell fate decisions and cell cycle regulation. It is involved in pathways related to cell proliferation, apoptosis, and interacts with key proteins such as p53, p300, and histone deacetylase complexes [1,2].

In the context of c-Myc-related cell fate decisions, c-Myc directly activates Zbtb5 transcription [1]. In p53-absent cells, Zbtb5 is acetylated at K597 by p300, leading to activation of NOXA transcription and apoptosis. In p53-present cells, Zbtb5 interacts with p53, blocking K597 acetylation. Non-acetylated Zbtb5 interacts with mSin3A/HDAC1 to repress p21/CDKN1A transcription, promoting cell proliferation [1]. Also, Zbtb5 can directly repress transcription of the cell cycle arrest gene p21 by binding to specific elements on its promoter and interacting with co-repressor-histone deacetylase complexes, stimulating cell proliferation and cell cycle progression [2].

In conclusion, Zbtb5 is a significant factor in regulating cell fate, cell cycle, and proliferation. Its interaction with p53 and p300 and subsequent acetylation-dependent functions are crucial in these processes. Understanding Zbtb5's role, especially through studies like those on its interaction with c-Myc, may provide insights into cancer-related cell behavior and potentially lead to new therapeutic strategies in cancer treatment [1,2].