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Regulation of proteome by the proteasome upon ER stress

ABSTRACT: HeLa cells were with Tunicamycin or Thapsigargin for 8 hours in the presence or absence of MG132 or untreated. Cells were lysed by addition of HEPES 50 mM pH7.9 with 5% SDS. Proteins were precipitated with methanol/chloroforme and the proteins were resolubilized in 8 M Urea and digested with trypsin. The peptides were analyzed on a Thermofisher scientific Q Exactive HFX.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Bertrand Fabre

PROVIDER: MSV000083736 | MassIVE | Tue Apr 30 04:36:00 BST 2019

REPOSITORIES: MassIVE

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Publications

Identification of proteins regulated by the proteasome following induction of endoplasmic reticulum stress.

Fabre Bertrand B Livneh Ido I Ziv Tamar T Ciechanover Aaron A

Biochemical and biophysical research communications 20190718 2

The endoplasmic reticulum (ER) is a major site for protein synthesis, folding and transport, lipid and steroid synthesis, regulating redox potential, as well as calcium storage. It therefore relies on delicate homeostasis, and perturbation of the ER function and induction of ER stress can lead to apoptosis. One cause of disruption of the ER homeostasis is the accumulation of misfolded proteins. To prevent this perturbation, the Endoplasmic Reticulum-Associated Degradation (ERAD) quality control ...[more]

PMID: 31327494

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Proteomics analysis of HeLa cells starved with or without MG132

Project description:HeLa cells were amino acid starved for 8 hours in the presence or absence of MG132 or untreated. Cells were lysed by addition of HEPES 50 mM pH7.9 with 5% SDS. Proteins were precipitated with methanol/chloroforme and the proteins were resolubilized in 8 M Urea and digested with trypsin. The peptides were analyzed on a Thermofisher scientific Q Exactive HFX.

2019-03-30 | MSV000083644 | MassIVE

Systemic Comparison of Heat Shock Response Induced by Heat Shock and a Proteasome Inhibitor in Mouse Fibrosarcoma Cells and Their Thermotolerant Counterparts

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

Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [rna_polii_chIP-seq]

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

Alteration of mRNA expression in breast cancer cells upon chemical inhibition of the 26S proteasome

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

Impact of proteasome inhibition on nascent transcription of APOBEC3 cytidine deaminases

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

Transcription profiling of human MCF-7 cells treated with proteasome inhibitor MG132 and either dexamethasone or 17b-estradiol

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

Systemic Comparison of Heat Shock Response Induced by Heat Shock and a Proteasome Inhibitor in Mouse Fibrosarcoma Cells and Their Thermotolerant Counterparts

2011-11-09 | GSE24197 | GEO

Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

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

Primary male adult tail fibroblast cell-state specific response to proteasome inhibition

Project description:polyA RNA sequencing data generated from primary tail male adult fibroblasts in 4 cells states: proliferating, senescent, quiescent or immortalized and across two conditions: DMSO or MG132 treated were analyzed by RNA sequencing.

2022-09-20 | GSE176107 | GEO

Analysis of transcriptional changes associated to proteasome inhibition in HCT-116 human colorectal cancer cells

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

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