An in-depth review on the structure and functionality of the zinc finger protein ZFP36L and its role in gene regulation

Zinc finger proteins are one of the most structurally diverse protein domains and this includes the Zinc finger protein like 1 (ZFP36L1) also known as Butyrate response factor 1 (BRF1). It has been postulated that ZFP36L1 is involved in both proliferation and angiogenesis. ZFP36L1 has both a negative and positive regulation of cellular protein processes (such as transcription) depending on external and internal stimulations. ZFP36L1 mechanism functions by binding on the Adenylate-Uridylate rich elements (AREs) regions found within the 3’ untranslated regions (3’UTRs) within the mRNA, attenuating expression for mRNA degradation. Degradation can remove essential cell regulators such as cytokines, transcriptional factors as well as protein-signalling cells. ZFP36L1 is still considered a novel protein in the field, its structure as well as its mRNA targets is yet to be fully realised. It is postulated that ZFP36L1 may function as a tumour suppressor gene, by interacting with cells during cell replication and arresting cells in the G0 phase, keeping the cells in a state of Quiescence. A key question is to unravel the role of ZFP36L1 in the immune system. ZFP36L1 seems to interact and control the development of T and B lymphocytes. ZFP36L1 may act to ensure that B lymphocytes progress through the cell cycle, to mature B cells and possible plasma cells engaged in antibody synthesis. Mice deficient in ZFP36L1 and its paralogue, ZFP36L2 had B lymphocyte development blocked. ZFP36L1 and ZFP36L2 are seen to create a thymic β-selection checkpoint, which stopped damaged thymocytes undergoing thymopoeisis. Upregulation of ZFP36L1 and ZFP36L2 regulated the DNA damage response and halted cell cycle progression. Thymocytes were found to be reduced or arrested in the G0 phase. Taken together, ZFP36L1 might be an important regulator step in various processes including the immune system and cancer cell proliferation.