Gene name: | EZH2 |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | HSCs,JS1,LX-2 |
Experiment: | Western blot//Flow cytometry//SA-β-gal activity assay//RT-qPCR//GO analysis |
Description: | Treatment of primary HSCs with DZNep, or transient transfection with potent siRNAs for Ezh2 silencing, resulted in more quiescent HSCs-phenotype and pronounced growth retardation, remarkably weakened H3K27me2/3, and significantly downregulated α-SMA and COL1A.EZH2 inhibition by DZNep in mouse JS1 cells resulted in cell cycle arrest in S and G2 phases, lowered cell viability, increased cell senescence (in dose dependent mode), and higher percent of early apoptotic cells.DZNep treatment in rat primary HSCs, JS1 and LX-2 cells significantly lowered the transcriptional expression of cell proliferation marker protein Ki-67 coding gene MKI67 (marker of proliferation Ki-67).Key signaling pathways involved in cell cycle, DNA replication, mitotic cell cycle and spindle organization, and cytoplasmic ribosomal proteins were significantly inactivated. Some positive regulators of cell cycle including cyclins, cyclin-dependent kinases and E2F transcription factors, and of mitosis were pervasively downregulated; while the key negative regulators of cell cycle, Cdkn1a (cyclin dependent kinase inhibitor 1A), Gadd45a (growth arrest and DNA damage inducible alpha) and Gadd45b, the target genes of p53 and primary inhibitors of G2/M transition) were upregulated.(不知道用了什么实验) |
Regulatory pathway: | TGF-β-SMAD |
R-AG-Pathway: | Downregulation |
Pathway experiment: | RNA-seq |
Pathway description: | 154 out of the 351 associated DEGs in knowledgebase have measurement direction consistent with Tgfβ1 inhibition (P = 9.96E-30, Z-score = -2.087), the majority (127) of which are downregulated activator or effector genes, while a few (27) are upregulated inhibitor genes. |
Annotation:
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