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p53 activation during ribosome biogenesis regulates normal erythroid differentiation.
PubMed Similar studies Analyze with GEO2R
p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]
PubMed Similar studies SRA Run Selector
p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]
Murine Proerythroblasts (ProEs): WT vs. Bmi1-/-
PubMed Full text in PMC Similar studies
Murine Myeloid-Erythroid Progenitors (MEPs): WT vs. Bmi1-/-
Analysis of gene expression change in cancer cells induced by nucleolar stress
PubMed Full text in PMC Similar studies Analyze with GEO2R
Surveillance of rRNA synthesis by an RNA helicase mediates tissue-specific developmental disorders
PubMed Full text in PMC Similar studies SRA Run Selector
The mechanistic studies of GATA1 regulation of SREBP2 in G1-ER4 cells
Quantitative Analysis of erythroblast cells Transcriptomes treated with cholesterol or not
Runx1 deficiency decreases ribosome biogenesis and confers stress resistance to hematopoietic stem and progenitor cells
RNAseq comparison of Whole crypt mRNA levels between Control, conditional Notchless KO, Apc KO and Notchless-Apc KO mice 24h or 48h after induction
Epo-Induced Erythroid Maturation Is Dependent on Plcγ1 Signaling
RNA-Seq analysis of Rpl22l1-deficient murine CD4-CD-CD44-CD25+ (DN3) thymocytes
Expression data from HCT116 cell transduced with lentivirus encoding PNO1 shRNA (sh-PNO1) or Control shRNA (sh-Ctrl)
Rb Intrinsically Promotes Erythropoiesis by Coupling Cell Cycle Exit with Mitochondrial Biogenesis
Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis
Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation ofcomplement pathway in to prevent craniosynostosis [Ribo-seq]
Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis [RNA-seq]
RNA exosome mutations in pontocerebellar hypoplasia alter ribosome biogenesis and p53 levels
A p53-dependent translational program directs tissue-selective phenotypes in a model of ribosomopathies
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