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Zbtb34 is a novel zinc finger protein, which is revealed by biological software analysis to have 3 zinc fingers, but its functions remain unknown. In this study, mouseiZbtb34/icDNA was amplified by PCR and inserted into the plasmid pEGFP-N1 to generate Zbtb34-EGFP fusion protein. The upregulation of Zbtb34 in mouse embryonic stem cells promoted telomere elongation and increased cell proliferation. In order to understand the above phenomena, the telomere co-immunoprecipitation technique was employed to investigate the relationship between Zbtb34 and telomeres. The results indicated that Zbtb34 could bind to the DNA sequences of the telomeres. Alanine substitution of the third zinc finger abolished such binding. Since Pot1 is the only protein binding to the single-stranded DNA at the end of the telomeres, we further investigated the relationship between Zbtb34 and Pot1. The results revealed that the upregulation of Zbtb34 decreased the binding of Pot1b to the telomeres. Through the upregulation of Pot1b, the binding of Zbtb34 to the telomeres was also reduced. In conclusion, we showed that the main biological function of Zbtb34 was to bind telomere DNA via its third ZnF, competing with Pot1b for the binding sites, resulting in telomere elongation and cell proliferation.

With aging, iron will accumulate in the brain, catalyzing oxidative radicals that damage brain neurons and induceAlzheimer's disease. In this experiment, we observed that in the brains of senile mice, the iron-exporting protein ferriportin was decreased. Further investigation indicated that H3K27 of the slc40a1 gene was methylated and that the methyltransferase Ezh2 was activated. To discharge the excessive iron in the brains of senile mice, we developed the YP peptide, and with it, we demethylated H3K27me of Slc40a1 by phosphorylation, activating the demethylase Kdm6a and inhibiting methyltransferase Ezh2. Consequently, the transcription of Slc40a1 was enhanced,and ferriportin was resumed. Thesenile brain reacquired the function of iron excretion, and as a result, the radicals in the brain weredecreased,and neuron damage was reduced, which finally restored the intelligence of dementia senile mice. Thus, YP could be a potential drug in the prevention of Alzheimer's disease