Blood: P53 activation during the occurrence of nuclear glycosome organisms regulates normal red system differentiation.

Central point: During the transition period between early and late alkaline erythrine cells, nuclear glycosome organisms stagnate, and in immature red blood cell presupposes, p53 is activated and drives red blood cell transcription procedures, suggesting that p3 interacts with GATA1.
: In Diamond-Blackfan anemia and 5q-syndrome, understanding of red system defects in kerucose disorders supports the role of kerucleosome organisms in red line development.
, it is not clear whether the occurrence of nuclear glycosome organisms has a regulatory function for normal red line development.
In this study, detailed characteristics of the dynamics of nuclear glycosome biogenesis during human and mouse red blood cell production showed that the occurrence of cyldosome organisms was suddenly interrupted by rDNA transcription and the collapse of the new synthesis of UC Protein.
the proliferation of immature maturing red blood cells by prematurely blocking the proliferation of RNA po/I inhibitors CX-5461 prematurely.
the study also found that p53 was activated spontaneously or stimulated by CX-5461, accompanied by stagnant nuclear glycosome organisms, and driven by transcription of genes involved in cell cycle blocking, negative regulation of apoptosis, and increased response to DNA damage.
RNA po/I transcription stress causes nuclear kernel damage and atR-CHK1-p53 path activation.
(effects of CX-5461 treatment on the structure of human red blood cell prescellular nuclei) suggests that the time when nuclear glycosome organisms stop and p53 is activated is critical to red line development.
In CYTs, the imbalance of ICOs can change the utilization rate of UCOs, prematurely reaching the threshold of reduction of ICOs, and p53 pathological activation together hinder the normal amplification of red line ancestral cells.
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