The proteasome inhibitor MG132 adjusts the transcriptome in Brassica napus roots
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA525819 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The goal of this study was to determine how proteasome inhibition alters the transcriptome in Brassica napus roots. Specifically, we wished to see if proteasome inhibition resulted in transcriptome signatures of oxidative stress, protein catabolism, or nitrogen assimilation
2021-12-03 | GSE127923 | GEO
Project description:The objective of the study was to investigate the effect of proteasome inhibition on glucocorticoid and estrogen receptor regulated gene expression. Experiment Overall Design: MCF-7 cells were treated with proteasome inhibitor (MG132), dexamethasone, 17b-estradiol or MG132 plus dexamethasone or MG132 plus 7b-estardiol. Control cells were not treated. RNA was collected from 2 biological experiments.
2008-06-20 | E-GEOD-8383 | biostudies-arrayexpress
Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of 3 different RNA Pol II CTD modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find the non-phosphorylated form of RNA Pol II CTD accumulates at TSS of all expressed genes in proteasome inhibited cells, particularly after 24H of MG132 treatment. Proteasome inhibition enhances Ser5-P and Ser2-P binding at TSS of genes induced by MG132. We note that proteasome inhibition establishes unique Ser2-P 5’ to 3’ gene profiles at induced compared to repressed genes. Overall proteasome inhibition enhances RNA Pol II processivity and expression of gene networks relevant to breast cancer. The study provides a comprehensive resource of RNA Pol II binding in proteasome inhibited cells.
2020-01-07 | GSE142010 | GEO
Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of histone modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find that MG132 treatment results in the spreading of the H3-trimethyl lysine 4 mark into gene bodies of a subset of induced genes in MCF-7 cells. The spreading of the H3K4me3 is concomitant with hyperacetylation (H3K27ac, K122ac and K9/14ac) of the corresponding gene TSS. H3 Lysine 36 trimethylation mark is enriched at genes that are induced by MG132. Finally, we show that proteasome inhibition establishes a chromatin state that enhances antiproliferative, while dampening cell proliferative gene expression programs relevant to breast cancer. The study provides a comprehensive resource of histone modifications in proteasome inhibited cells.
2020-01-07 | GSE142009 | GEO
Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules). RIF-1 and TR cells were heat shock treated or MG132 treated and harvested after various times of recovery. mRNA expressions were compared to untreated samples. Biological replication was done.
2011-11-09 | E-GEOD-24197 | biostudies-arrayexpress
Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules).
2011-11-09 | GSE24197 | GEO
Project description:The proteasome is a central player in several cellular aspects, such as homeostasis, cell cycle progression, and even transcription. Recent work has shown that proteasome inhibition promotes pervasive epigenetic changes in the human genome. However, the impact of proteasome inhibitors on ncRNAs is poorly understood. We treated control (asynchronous) or G2-synchronized HCT-116 human colon cancer cells with the proteasome inhibitors MG132 and bortezomib and performed total RNA-seq. We also included cells treated simultaneously with MG132 and the RNA-pol II inhibitor α-amanitin to determine the transcriptional changes mediated by such RNA polymerase. We report that MG132 and bortezomib impact similar regions of the genome. A remarkable transcriptional activation was observed in centromeres and pericentromers, especially in α-satellite repeats. RNAs emanating from these regions are known to participate in chromosome segregation. Our results suggest that the proteasome can regulate mitotic progression, not only by participating in protein turnover, but also by regulating ncRNAs.
2021-12-14 | GSE165325 | GEO
Project description:To assess the impact of the proteasome inhibitor MG132 on nascent transcription inMDA-MB-453 cells, csRNA-seq was conducted to compare transcript abundances between treated and DMSO control cells. Analysis of transcripts following MG132 treatment showed that APOBEC3A is one of the most differentially expressed genes. Comparison to other APOBEC family genes, revealed APOBEC3A is unique in its transcriptional upregulation by MG132. Analysis of transcription factor binding sites enriched in the promoter regions of genes changed greater than 2-fold in expression highlighted potential transcription factors driving increased APOBEC3A transcription.
2023-12-05 | GSE248016 | GEO
Project description:The 26S proteasome regulates degradation of many cellular proteins to maintain cellular homeostasis. Disruption of proteasome activity followed by dysregulation of tumor suppressors and oncogenes is rampant in many cancers, hence chemical inhibitors of the proteasome have utility as cancer therapeutics, although the underlying mechanisms of their effects in the clinic is poorly understood. We have employed whole genome microarray expression profiling as a discovery platform to identify genes and potential signaling pathways that are affected MCF7 breast cancer cells are treated with MG132 a chemical inhibitor of the proteasome. Total RNA was collected from MCF7 breast cancer cells treated with DMSO (vehicle control) and 1 uM MG132 for 4 or 24H . We identified time dependent changes in the expression of genes enriched in p53 and estrogen receptor pathways, two signatures relevant to breast cancer biology.
2020-01-07 | GSE141858 | GEO
Project description:J774 cells were treated with MG132, epoxomicin and ONX-0912 for 4 hours, and gene expression was evaluated In order to evaluate the molecular mechanism of inflammatory responses in PRAAS(Proteasome-Associated Autoinflammatory Syndromes ), we established Psmb8-KI mouse that harbors the same mutation in human patients. Psmb8-KI mice showed higher susceptibility to imiquimod-induced skin inflammation (IMS). DNA microarray analysis showed that treatment of J774 cells with proteasome inhibitors increased the expression of the Cxcl9 and Cxcl10 genes, and the skins where imiquimod was painted also expressed both genes at higher levels in Psmb8-KI than control mice. Deficiency in Cxcr3, the gene encoding the receptor of CXCL9 and CXCL10, in wild-type mice did not change IMS susceptibility, while deficiency in Cxcr3 in Psmb8-KI mice ameliorated IMS.
2022-04-01 | GSE189308 | GEO