Cytoplasmic mRNA and Heavy polysome-associated mRNAs from U251 Cells treated with Control or eIF3e siRNAs
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PROVIDER: PRJNA662223 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of Cytoplasmic mRNA and Heavy polysome-associated mRNAs extracted from U251 Cells treated with control siRNA or siRNA targeting eIF3e . Goal was to determine the effect of eIF3e knockdown on translation of specific mRNAs.
2020-09-09 | GSE157608 | GEO
Project description:Int6/yin6 encodes the eIF3e subunits of the eukaryotic translation initiation factor 3 complex (eIF3). To assess the impact of eIF3e on the global transcriptome, RNA seq of total mRNA was performed. Total RNA was prepared from wildtype S. pombe (h- ura4-D18 leu1-32) and cells deleted for eif3e (int6, yin6, SPBC646.09c; h- int6::kanMX6 ura4-D18 leu1-32). Following rRNA depletion and library construction, samples were sequenced on the SOLID4 platform. Two replicates were analyzed and statistical analysis was performed to identify significant differences in mRNA levels.
2016-07-29 | E-GEOD-80349 | biostudies-arrayexpress
Project description:Int6/yin6 encodes the eIF3e subunits of the eukaryotic translation initiation factor 3 complex (eIF3). To assess the impact of eIF3e on the global transcriptome, RNA seq of total mRNA was performed.
2016-07-29 | GSE80349 | GEO
Project description:Exposure to hypoxia is linked to increased cellular plasticity and enhanced metastasis; effects which are primarily attributed to the transcriptional activation of large gene programs downstream of hypoxia inducible factors (HIFs). However, translational effects in hypoxia, that likely precede transcriptional effects, have remained largely unexplored. Using ribosome-profiling, we uncovered a selective translational response in acute hypoxia that is eIF3d/eIF3e-dependent and controls downstream hypoxic responses including HIF1a accumulation and cellular invasion. We further demonstrated that eIF3e copy number and eIF3e- and eIF3d-expression signatures are associated with worsened outcomes for breast cancer patients. Finally, we identified a class of novel small molecules that target eIF3e specifically, reducing the translational response to hypoxia and to ER stress, another stressor that is dependent on eIF3d/eIF3e-mediated translation. Our data uncover critical functions for eIF3d/eIF3e in the hypoxic response and identify a potential means to inhibit stress-induced translation, and potentially plasticity and metastasis, mediated by eIF3e.
2025-11-06 | GSE307666 | GEO
Project description:we performed microarray expression profiling to analyze the differentially expressed genes between U251-shCtrl and U251-shCPVL cells.
2024-11-01 | GSE188414 | GEO
Project description:BACKGROUND: As an iron-dependent form of regulated cell death caused by lipid peroxidation, ferroptosis has been implicated in ischemic injury, but the underlying mechanisms in acute myocardial infarction (AMI) remain poorly defined. Acetaldehyde dehydrogenase 2 (ALDH2) catalyzes detoxification of lipid aldehydes derived from lipid peroxidation and acetaldehydes from alcohol consumption. The Glu504Lys polymorphism of ALDH2 (rs671, ALDH2*2), affecting around 40% of East Asians, is associated with increased risk of MI. This study aims to investigate the role of ALDH2*2 and ferroptosis in AMI. METHODS: A Chinese cohort of 177 acute heart failure patients with ALDH2 wild type and ALDH2*2 was enrolled. The MI mouse model of left anterior descending (LAD) coronary artery ligation was conducted on wild-type, ALDH2*2, and mice with cardiomyocyte-specific knockdown of eukaryotic translation initiation factor 3 subunit E (eIF3E) by adeno-associated virus. The lipid peroxidation products were measured by mass spectrometry-based lipidomics and metabolomics in human plasma, mouse serum samples, mouse heart tissues, and primary cardiac myocytes. RESULTS: Human ALDH2*2 carriers exhibit more severe heart failure post-AMI with features of ferroptosis in plasma through lipidomic analysis, characterized by increased bioactive lipids and decreased antioxidants, such as Coenzyme Q10 (CoQ10) and tetrahydrobiopterin (BH4). Similar features were observed in MI mouse models of ALDH2*2, whereas ferroptosis inhibition by Fer-1 significantly improved heart functions and reversed ferroptosis markers. Importantly, ALDH2*2 significantly decreased ALDH2 protein levels, while ferroptosis-related markers, including Transferrin receptor (TFRC) and Acyl-CoA synthetase long-chain family member 4 (ACSL4), were notably upregulated in the infarct heart tissues. Mechanistically, ALDH2 physically interacts with the eIF3 complex via the eIF3E factor, which prevents the eIF3E-eIF4G1-mRNA assembly. The ALDH2*2 variant causes ALDH2 deficiency, disrupting its interaction with the eIF3 complex through releasing the bound eIF3E to assemble an eIF3E-eIF4G1-mRNA ternary complex, thereby driving selective translation of mRNAs (e.g., TFRC, ACSL4, and UAP1) containing the GAGGACR (R: represents A/G) motif to promote ferroptosis. Consistently, cardiomyocyte-specific eIF3E knockdown restored ALDH2*2 cardiac function by attenuating ferroptosis in MI. CONCLUSIONS: ALDH2*2 aggravates acute heart failure post-MI through promoting the selective translation of mRNAs containing the GAGGACR motif, thereby driving cardiomyocytes ferroptosis. Targeting ferroptosis represents a potential therapeutic option for mitigating MI injury, especially for ALDH2*2 carriers. Key Words: ALDH2, myocardial infarction, eIF3E, ferroptosis, protein translation
2026-03-11 | GSE305516 | GEO
Project description:To investigate the function of COL8A1 in GSCs progression, we established U251-COL8A1 cell lines with COL8A1 overexpressed. Then we performed gene expression profiling analysis using data obtained from RNA-seq of 2 cells (U251NC and U251-COL8A1)
2024-07-01 | GSE246528 | GEO
Project description:Expression data from U251-shCtrl and U251-shCPVL cells
| PRJNA778755 | ENA
Project description:U251 cells were treated with Vinblastine or Taxol and phosphotyrosine signaling was measured.
2018-11-30 | PXD008939 | Pride
Project description:The objective of the study was to examine the gene expression changes in glioma cell line U87 and U251 with LAMP2A knockdown. There were 15 samples in total- U87-1, U87-2, U87-3, U87-1812-1, U87-1812-2, U87-1812-3, U251-1, U251-2, U251-3, U251-1812-1, U251-1812-2, U251-1812-3, U251-1813-1, U251-1813-2, and U251-1813-3. U87-1 to U87-3 and U251--1 to U251-3 were used as the control groups (CON). U87-1812-1 to U871812-3, U251-1812-1 to U251-1812-3, and U251-1813-1 to U251-1813-3 were used as the experimental groups (shLAMP2A-1 and shLAMP2A-2). The total RNA of each sample was extracted from the stable transfected glioma cells by using TRIzol reagent. Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform. There were two types of libraries: the circRNA, mRNA, and lncRNA were all constructed by removing rRNA (one library, three types of RNA were analyzed together), and the insert fragment was about 300bp; the small RNA was constructed and analyzed separately, mainly microRNA of about 22bp. Results: among 60612 cleaned mRNAs, 781 were differentially expressed in U87-1812 group compared with U87 group, 146 were differentially expressed in U251-1812 group compared with U251 group, 43 were differentially expressed in U251-1813 group compared with U251 group (padj ≤ 0.05 and expression change ≥2 fold). The differential expressed genes distributed in all chromosomes. Functional annotation with GO and KEGG enrichment revealed the top functional groups including inflammation, DNA replication, cell adhesion, TNF, IL17, and axon guidance signaling pathways.
2024-07-15 | GSE270618 | GEO