Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16503530_1.fastq.gz | Fastqsanger.gz | |||
| SRR16503530_2.fastq.gz | Fastqsanger.gz | |||
| SRR16503531_1.fastq.gz | Fastqsanger.gz | |||
| SRR16503531_2.fastq.gz | Fastqsanger.gz | |||
| SRR16503532_1.fastq.gz | Fastqsanger.gz |
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Project description:To identify signalling pathways altered by FUT8 in prostate cancer cells, we established luciferase-tagged CWR22Rv1 stable cell lines in which FUT8 was overexpressed (OE) and luciferase-tagged PC3 cell lines in which FUT8 was knocked down (KD). We then performed differential gene expression, Gene Ontology and GSEA analyses using data obtained from RNA-seq of the control and FUT8 overexpression, and the control and knockdown cell lines.
2025-05-19 | GSE280132 | GEO
Project description:Effect of Fut8 deletion in MEF Fut8MEF was cultured in 10cm dish (WT,KO n=3). The MEFs were submitted this microarray analysis to compare the gene expression between Fut8+/+ and Fut8-/- MEFs.
2013-07-31 | E-GEOD-49336 | biostudies-arrayexpress
Project description:Effect of Fut8 deletion in MEF
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Project description:The alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct mutagen and carcinogen, causing DNA damage and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiation, and cell death. Our previous study revealed that MNNG at different concentrations could induce extensive changes in gene expression at an early stage of exposure. To further understand the dynamic cellular responses and hazardous effects caused by this environmental carcinogen, we used a whole-genome time-course screening methods to find out the gene expression changes induced by a low concentration of MNNG in human normal amnion epithelial FL cells. The cells were exposed to 1.0 µM MNNG, and differential gene expression profiles at 3, 12, and 24 h after MNNG treatment were obtained by use of Affymetrix HG-U133 Plus 2.0 oligonucleotide microarray technology, followed by quantitative real-time RT-PCR validation. The results showed that the low-dose MNNG exposure triggered extensive but moderate changes in gene expression at these three experiment time points after exposure. The responsive genes encode important proteins, including cell cycle regulators, transcription factors and signal transducers that determine cell cycle progression, cell fate and other activities associate with pro-oncogenic potentials. The differential gene expression profiles at the three time points varied greatly, and generally reflected a cellular responsive process from initiation to progression and to recovery after MNNG exposure. These results will aid our understanding of the complicated mechanisms of MNNG-induced cellular responses. Keywords：N-methyl-N'-nitro-N-nitrosoguanidine; Cellular response; Temporal gene expression change; Oligonucleotide microarray; Quantitative real-time RT-PCR
2013-07-01 | GSE21270 | GEO
Project description:The alkylating agent N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) induces cellular DNA damages and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiations, and cell death. However, the molecular mechanism of MNNG-induced cellular stress remains unclear.We have genome-wide analyzed early transcriptional responses of human FL amnion epithelial cells after exposure to three relatively low doses of MNNG (0.2, 1.0, and 10.0µM),and differential gene expression profiles were obtained 4 h after exposure using oligonucleotide microarrays followed by validation with quantitative real-time RT-PCR. The results demonstrate that the MNNG-responsive genes are involved in multiple cellular biological processes including transcription regulation, signal transduction, cell cycle regulation, cytoskeleton organization, protein synthesis, immune response, metabolism, etc. The possible roles of these genes and their related pathways in MNNG-induced cellular responses were discussed. This study helps to draw the whole picture how cells respond to environmental chemical exposure via transcriptional regulation. Keywords: Dose response
2009-01-01 | GSE8602 | GEO
Project description:Investigation of whole genome gene expression level changes in human osteosarcoma cell line MNNG/HOS treated by TGF-beta1 for three days (mesophase) and five days (sarcospheres iOSCs), compared to non-treatment cells (residual adherent cells). A three chip study using total RNA cover from three cultures of non-treatment human osteosarcoma cell line MNNG/HOS (residual adherent cells), TGF-beta1 treated three days osteosarcoma cell line MNNG/HOS (mesophase) and TGF-beta1 treated five days osteosarcoma cell line MNNG/HOS ( only collected the suspending sarcospheres iOSCs). Each chip measures the expression level of 45033 genes from osteosarcoma cell line MNNG/HOS.
2012-05-22 | E-GEOD-38133 | biostudies-arrayexpress
Project description:The alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct mutagen and carcinogen, causing DNA damage and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiation, and cell death. Our previous study revealed that MNNG at different concentrations could induce extensive changes in gene expression at an early stage of exposure. To further understand the dynamic cellular responses and hazardous effects caused by this environmental carcinogen, we used a whole-genome time-course screening methods to find out the gene expression changes induced by a low concentration of MNNG in human normal amnion epithelial FL cells. The cells were exposed to 1.0 M-BM-5M MNNG, and differential gene expression profiles at 3, 12, and 24 h after MNNG treatment were obtained by use of Affymetrix HG-U133 Plus 2.0 oligonucleotide microarray technology, followed by quantitative real-time RT-PCR validation. The results showed that the low-dose MNNG exposure triggered extensive but moderate changes in gene expression at these three experiment time points after exposure. The responsive genes encode important proteins, including cell cycle regulators, transcription factors and signal transducers that determine cell cycle progression, cell fate and other activities associate with pro-oncogenic potentials. The differential gene expression profiles at the three time points varied greatly, and generally reflected a cellular responsive process from initiation to progression and to recovery after MNNG exposure. These results will aid our understanding of the complicated mechanisms of MNNG-induced cellular responses. KeywordsM-oM-<M-^ZN-methyl-N'-nitro-N-nitrosoguanidine; Cellular response; Temporal gene expression change; Oligonucleotide microarray; Quantitative real-time RT-PCR Human amnion epithelial FL cells were exposed to vehicle control (dimethyl sulfoxide) and a low concentration (1.0 M-BM-5M) MNNG for 2 h, respectively. The differential gene expression profiles at 3, 12 and 24 h post MNNG treatment were obtained using Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays. The transcriptomic changes at different time points post MNNG treatment would provide insight into the dynamic processes of cellular response to this genotoxic agent.
2013-07-01 | E-GEOD-21270 | biostudies-arrayexpress
Project description:To explore whether Mst4 limits YAP signaling and suppresses GC development in vivo, RNA sequencing was performed to analyze the genome-wide RNA change in gastric tumors from MST4 KO mice and those from WT mice induced by chemical MNNG.
2020-04-02 | GSE142644 | GEO
Project description:Natural Killer (NK) cell development and effector function requires context-dependent signalling via numerous receptors including the IL-15 receptor. The modulation of receptor signalling can be regulated by the post-translational modifications affecting receptor turnover and trafficking. Core fucosylation is one such modification known to impact receptor expression and is uniquely mediated by fucosyltransferase 8 (FUT8). To investigate core fucosylation in NK cell biology, we generated mice lacking FUT8 in NK cells (Fut8fl/flNcr1cre/+). Loss of core fucose resulted in pronounced NK lymphopenia in Fut8fl/flNcr1cre/+ mice associated with a reduction in IL-15 receptor expression and loss of in vivo proliferation. Inhibition of intrinsic apoptosis pathways could not overcome compromised IL-15 receptor signalling to rescue FUT8-null NK cell development delineating the contribution of proliferation to NK cell homeostasis. Surprisingly, loss of core fucose enhanced NK cell expansion following viral infection and this was associated with upregulation of IL-2Rα following pro-inflammatory cytokine exposure and enhanced IL-2-mediated proliferation. Lastly, loss of FUT8 activity impaired TGFBR2 expression and immunosuppressive effects of TGF-β on NK cells. Taken together, we have identified fucosyltransferase 8 as a key modulator of NK cell development and function by regulating IL-15 receptor responsiveness.
2024-01-01 | GSE243190 | GEO