Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA326260 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA
2010-11-03 | GSE18906 | GEO
Project description:B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA CD36+ EPCs were generated from CD34+ stem cells, and transduced with B19V NS1 or control-lentivirus for 12, 24,and 48 hours. Each sample has triplicates. There are 18 samples analyzed.
2010-11-03 | E-GEOD-18906 | biostudies-arrayexpress
Project description:After severe renal injury, renal tubular epithelial cells (TECs) will be arrested in G2/M phase, and the arrested cells will be aging, showing senescence related secretory phenotype (SASP), which mediates renal fibrosis by secreting fibrogenic cytokines. Cyclin B1 is an important protein that promotes G2/M phase transition of cell cycle. Its role in renal fibrosis mediated by G2/M arrest of TECs is unknown. The aim of this study was to investigate the role of cyclin B1 in renal fibrosis induced by TECs G2/M arrest and its mechanism
2024-01-01 | GSE224039 | GEO
Project description:We construct two stable UT7/Epo-S1 cell lines which could be inducible expressing B19 NS1 and NS1 TAD2 domain mutation proteins. After treated with or without doxycycline induction, we extract the total RNA for RNA-seq analysis.
2017-03-01 | GSE83525 | GEO
Project description:The goal of our present work was to understand the influence parvovirus B19 infection may have on the thyroid hormone signaling pathway, as well as the nuclear receptors (NR) pathway overall. We demonstrated that B19 infection of CD36+ erythroid progenitor cells leads to downregulation of the thyroid hormone receptor α isoform. In addition to that we have shown that B19 infection modulates the expression of other members of the NR superfamily such as estrogen and retinoid receptors.
2012-11-04 | GSE42005 | GEO
Project description:Cell size and the cell cycle are intrinsically coupled and abnormal increases in cell size are associated with senescence and permanent cell cycle arrest. The mechanism by which overgrowth primes cells to withdraw from the cell cycle remains unknown. We investigate this here using CDK4/6 inhibitors that arrest cell cycle progression during G0/G1 and are used in the clinic to treat ER+/HER2- metastatic breast cancer. We demonstrate that CDK4/6 inhibition promotes cellular overgrowth during G0/G1, causing p38MAPK-p53-p21-dependent cell cycle withdrawal. We find that cell cycle withdrawal is triggered by two waves of p21 induction. First, overgrowth during a long-term G0/G1 arrest induces an osmotic stress response. This stress response produces the first wave of p21 induction. Second, when CDK4/6 inhibitors are removed, a fraction of cells escape long term G0/G1 arrest and enter S-phase where overgrowth-driven replication stress results in a second wave of p21 induction that causes cell cycle withdrawal from G2, or the subsequent G1. We propose a model whereby both waves of p21 induction contribute to promote permanent cell cycle arrest. This model could explain why cellular hypertrophy is associated with senescence and why CDK4/6 inhibitors have long-lasting effects in patients.
2023-11-27 | PXD036519 | Pride
Project description:NO effects on gene expression, independent of cGMP, were examined globally. Differentiated human U937 cells that lack soluble guanylate cyclase were exposed to Snitrosoglutathione, a NO donor, or glutathione without or with dibutyryl-cAMP (Bt2cAMP). NO regulated 110 transcripts that annotated disproportionately to the cell cycle and cell proliferation (47/110, 43%) and more frequently than expected contained AU-rich, post-transcriptional regulatory elements (ARE). Bt2cAMP regulated 106 genes; cell cycle gene enrichment did not reach significance. Like NO, Bt2cAMP was associated with ARE-containing transcripts. Cell cycle genes induced by NO were G1/S phase associated (7/8) including E2F1 and p21/Waf1/Cip1; 6 of these 7 were E2F target genes involved in G1/S transition. Repressed genes were G2/M associated (24/27); 8 of 27 were known targets of p21. E2F1 mRNA and protein were increased by NO, as was E2F1 binding to E2F promoter elements. NO activated p38 MAPK, stabilizing p21 mRNA and increasing p21 protein. Subsequent increases in protein binding to CDE/CHR sites repressed key G2/M phase genes and increased the proportion of cells in G2/M. Thus, NO triggers a specific and coordinated program of cell cycle arrest independent of cGMP. Stress kinase pathways and mRNA stability are major mechanisms by which NO regulates the transcriptome.
2007-09-11 | E-GEOD-2649 | biostudies-arrayexpress
Project description:The goal of our present work was to understand the influence parvovirus B19 infection may have on the thyroid hormone signaling pathway, as well as the nuclear receptors (NR) pathway overall. We demonstrated that B19 infection of CD36+ erythroid progenitor cells leads to downregulation of the thyroid hormone receptor α isoform. In addition to that we have shown that B19 infection modulates the expression of other members of the NR superfamily such as estrogen and retinoid receptors. CD36+ cells (StemCell Technologies) were mock-infected or infected with B19, 48 hours post infection cells were collected, total RNA was isolated, and cDNA was obtained as described above. TaqMan® array human nuclear receptors fast 96-well plates obtained from Applied Biosystems (Carlsbad, CA) were utilized in order to assess the differences of 92 nuclear receptors’ expression in mock- and B19-infected CD36+ cells. Relative quantity (RQ) values were calculated using the 2-ΔΔCt method.
2012-11-04 | E-GEOD-42005 | biostudies-arrayexpress
Project description:Human parvovirus B19 (B19V) infection can cause transient aplastic crisis, persistent viremia, and pure red-cell aplasia. In fetuses, B19V infection can result in non-immune hydrops fetalis and fetal death. To systematically investigate the interaction between B19V and erythoid progenetor cells (EPC), microarray was applied to systematically analyze the dynamic transcriptome of CD36+ EPCs during B19V infection.
2017-12-07 | GSE103460 | GEO
Project description:The actin-related proteins (ARPs) comprise a conserved protein family. Arp4p is found in large multisubunits of the INO80 and SWR1 chromatin remodeling complexes and in the NuA4 histone acetyltransferase complex. Here we show that arp4 (arp4S23AD159A) temperature-sensitive cells are defective in G2/M phase function. arp4 mutants are sensitive to the microtubule depolymering agent benomyl and arrest at G2/M phase at restrictive temperature. Arp4p is associated with centromeric and telomeric regions throughout cell cycle. Ino80p, Esa1p, and Swr1p, components of the INO80, NuA4, and SWR1 complexes, respectively, also associate with centromeres. The association of many kinetochore components including Cse4p, a component of the centromere nucleosome, Mtw1p, and Ctf3p is partially impaired in arp4 cells, suggesting that the G2/M arrest of arp4 mutant cells is due to a defect in formation of the chromosomal segregation apparatus. Keywords: ChIP-chip
2007-03-16 | GSE7276 | GEO