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Snapshot of translation in mammalian cells that are depleted of polyamines or replete with polyamines

ABSTRACT: Snapshot of translation in mammalian cells that are depleted of polyamines or replete with polyamines

PROVIDER: PRJNA437287 | ENA |

REPOSITORIES: ENA

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Snapshot of translation in mammalian cells that are depleted of polyamines or replete with polyamines

Project description:Snapshot of translation in mammalian cells that are depleted of polyamines or replete with polyamines. Hek293T cells treated with DFMO or Spermidine.

2018-10-11 | GSE111517 | GEO

Transcriptonal response of mammalian cells lacking FLVCR1 to choline depleted or replete media conditions

Project description:Integrative genetic analysis identified FLVCR1 as a choline transporter in mammalian cells. We profilied the transcriptional response of HeLa cells with and without FLVCR1 to choline depeleted or replete conditions.

2023-08-08 | GSE228126 | GEO

Gene expression profiling from glutamine-depleted and -replete H460 cells.

Project description:Gene expression profiling from glutamine-depleted and -replete H460 cells.

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Expression data from human pancreatic cancer cell lines and mouse orthotopic tumors generated using human PDAC cell lines replete and depleted for RBFOX2

Project description:RBFOX2 is an RNA binding protein that directs alternative splicing. In this study, we characterized RBFOX2-mediated alternative splicing in pancreatic cancer (PDAC) In this dataset, we assayed gene-level and exon-level expression differences in pancreatic cancer cell lines replete and depleted for RBFOX2 expression and in 8 pairs of orthotopic pancreas tumors and related liver metastases generated from human 4039 or Panc1 cell lines replete or depleted for RBFOX2.

2023-11-07 | GSE211435 | GEO

Gene expression profiling from glutamine-depleted and -replete H460 cells.

Project description:We performed RNA-seq to compare immune modulators in glutamine-deprived versus glutamine-replete cancer cells.

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Malawi pneumococcal genomic snapshot

Project description:Malawi pneumococcal genomic snapshot

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SnapShot-Seq: a method for extracting genome-wide, in vivo mRNA dynamics from a single total RNA sample

Project description:mRNA synthesis, processing, and destruction involve a complex series of molecular steps that are incompletely understood.Â Because the RNA intermediates in each of these steps have finite lifetimes, extensive mechanistic and dynamical information is encoded in total cellular RNA. Here we report the development of SnapShot-Seq, a set of computational methods that allow the determination of in vivo rates of pre-mRNA synthesis, splicing, intron degradation, and mRNA decay from a single RNA-Seq snapshot of total cellular RNA. SnapShot-Seq can detect in vivo changes in the rates of specific steps of splicing, and it provides genome-wide estimates of pre-mRNA synthesis rates comparable to those obtained via labeling of newly synthesized RNA. We used SnapShot-Seq to investigate the origins of the intrinsic bimodality of metazoan gene expression levels, and our results suggest that this bimodality is partly due to spillover of transcriptional activation from highly expressed genes to their poorly expressed neighbors. SnapShot-Seq dramatically expands the information obtainable from a standard RNA-Seq experiment. These data are total RNA-Seq data, from RNA sequencing of rRNA-depleted total cellular RNA -- except the LCL 4SU data, which derive from 4SU-labeled RNA. Please see the associated paper for more details.

2014-02-04 | E-GEOD-48889 | biostudies-arrayexpress

COMPARE Global Sewage Snapshot - EMC

Project description:COMPARE global sewage snapshot virome sequencing part

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METTL17 is an Fe-S cluster checkpoint for mitochondrial translation

Project description:Friedreich’s ataxia (FA) is the most common monogenic mitochondrial disease. FA is caused by a depletion of the mitochondrial protein frataxin (FXN), an iron-sulfur (Fe-S) cluster biogenesis factor. To better understand the cellular consequences of FA, we performed quantitative proteome profiling of human cells depleted for FXN. Nearly every known Fe-S cluster-containing protein was depleted in the absence of FXN, indicating that as a rule, cluster binding confers stability to Fe-S proteins. Proteomic and genetic interaction mapping identified impaired mitochondrial translation downstream of FXN loss, and specifically highlighted the methyltransferase-like protein METTL17 as a candidate effector. Using comparative sequence analysis, mutagenesis, biochemistry and cryogenic electron microscopy we show that METTL17 binds to the mitoribosomal small subunit during late assembly and harbors a previously unrecognized [Fe4S4]2+ cluster required for its stability on the mitoribosome. Notably, METTL17 overexpression rescued the mitochondrial translation and bioenergetic defects, but not the cellular growth, of FXN depleted cells. Our data suggest that METTL17 serves as an Fe-S cluster checkpoint: promoting the translation and assembly of Fe-S cluster rich OXPHOS proteins only when Fe-S cluster levels are replete.

2023-12-27 | PXD045443 | Pride

Acute PresentatiOn of CoLorectaL Cancer: an internatiOnal Snapshot

Project description:APOLLO (Acute PresentatiOn of CoLorectaL Cancer: an internatiOnal snapshot) is an international, multi-centre, prospective observational study which will address this need and aims to describe the operative and non-operative management of emergency presentations of colon and rectal cancer in an international cohort.

| 1654 | ecrin-mdr-crc

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