Browse
Submit Data
Databases
API
Help

Dataset Information

502 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans

ABSTRACT: Comparative proteomic study between C. elegans wild type, mir-58.1 single, mir-80; mir-58.1 double and mir-80; mir-58.1; mir-81-82 quadruple mutants.

OTHER RELATED OMICS DATASETS IN: PRJNA258285PRJNA258215PRJNA258214

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Caenorhabditis Elegans

TISSUE(S): Whole Body

SUBMITTER: Yibo Wu

LAB HEAD: Yibo Wu

PROVIDER: PXD001998 | Pride | 2015-08-06

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mir58_MaxQuant_4conditions.zip	Other
	target_interact.pep.xls	Xls
	uniprot-taxonomy_Caenorhabditis_elegans.fasta	Fasta
	ywu_C1309_109.raw	Raw
	ywu_C1309_110.raw	Raw

Items per page:

1 - 5 of 55

Publications

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans.

Subasic Deni D Brümmer Anneke A Wu Yibo Y Pinto Sérgio Morgado SM Imig Jochen J Keller Martin M Jovanovic Marko M Lightfoot Helen Louise HL Nasso Sara S Goetze Sandra S Brunner Erich E Hall Jonathan J Aebersold Ruedi R Zavolan Mihaela M Hengartner Michael O MO

Genome research 20150731 11

In animals, microRNAs frequently form families with related sequences. The functional relevance of miRNA families and the relative contribution of family members to target repression have remained, however, largely unexplored. Here, we used the Caenorhabditis elegans miR-58 miRNA family, composed primarily of the four highly abundant members miR-58.1, miR-80, miR-81, and miR-82, as a model to investigate the redundancy of miRNA family members and their impact on target expression in an in vivo s ...[more]

PMID: 26232411

Similar Datasets

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [RNA-Seq]

Project description:In animals, microRNAs frequently form families with related sequences. The functional relevance of miRNA families and the relative contribution of family members to target repression have remained, however, largely unexplored. Here, we used the C. elegans miR-58 miRNA family, comprised primarily of four highly abundant members: miR-58.1, miR-80, miR-81 and miR-82, as a model to investigate the redundancy of miRNA family members and their impact on target expression in an in vivo setting. RNA was extracted from different miR-58 family mutants (mir-58.1, mir-80; mir-58.1 and mir-80; mir-58.1; mir-81-82) and wild-type Bristol C. elegans strain at late L4 stage and submitted to transcriptome sequencing with Illumina HiSeq2000. The goal was to compare miR-58 target RNA expression and system-wide perturbations across various samples.

2015-06-05 | E-GEOD-60420 | biostudies-arrayexpress

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [miRNA-Seq]

Project description:In animals, microRNAs frequently form families with related sequences. The functional relevance of miRNA families and the relative contribution of family members to target repression have remained, however, largely unexplored. Here, we used the C. elegans miR-58 miRNA family, comprised primarily of four highly abundant members: miR-58.1, miR-80, miR-81 and miR-82, as a model to investigate the redundancy of miRNA family members and their impact on target expression in an in vivo setting. RNA was extracted from different miR-58 family mutants (mir-58.1, mir-80; mir-58.1 and mir-80; mir-58.1; mir-81-82) and wild-type Bristol C. elegans strain at late L4 stage and submitted to small RNA profiling with Illumina HiSeq2000. The goal was to see whether miR-58 family members can compensate each other's expression.

2015-06-05 | E-GEOD-60419 | biostudies-arrayexpress

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [RNA-Seq]

2015-06-05 | GSE60420 | GEO

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [miRNA-Seq]

2015-06-05 | GSE60419 | GEO

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-06-05 | E-GEOD-60421 | biostudies-arrayexpress

Identification of miR-16/29 targets in adipocytes by LC-MSMS

Project description:Cancer cachexia is a multifactorial metabolic syndrome defined by the rapid loss of skeletal muscle mass and the loss of fat mass. Up 80% of cancer patients at the late stage with cachexia suffer from progressive atrophy of adipose tissue. Unlike studies on skeletal muscle wasting, there is limited research on fat loss in cachexia. It was noted that most patients suffer from fat loss as cancer progress. Fat loss precedes muscle loss, is associated with shorter survival, and is variable to timing and intensity in various cancer populations. Increased lipolysis may be the leading cause of fat loss in cancer cachexia. miRNAs are a class of non-coding RNAs of 19~25 nucleotides that regulate gene silencing by interacting with the 3’ untranslated region (UTR) of target mRNA to cause mRNA degradation and translational repression. miRNAs play multifaceted roles in pancreatic cancer proliferation, survival, metastasis, and chemoresistance. Aberrant expression of miRNA in circulating exosomes may play potential roles in modulating fat loss in cancer cachexia. We identified 2 miRNAs, miR-16 and miR-29, which have 2-fold higher expression existed in at PDAC cells. To explore which genes in adipogenesis and lipolysis were directly affected by miR-16-5p or/and miR-29a-3p, we analyzed the targets which were down-regulated in both miR-16-5p and miR-29a-3p-transfected 3T3-L1 cells by mass analysis.

2024-06-13 | PXD037998 | Pride

Identification of miR-16/29 targets in adipocytes by LC-MSMS

2024-06-13 | PXD037862 | Pride

Project description:Age-related changes in microRNA levels in serum 20 nM biotinylated miRIDIAN miR-1248 mimic (Thermo Scientific) or a negative control, biotinylated miRIDIAN C. elegans miR-67 (here named Con-miR) using Lipofectamine 2000. Forty eight hours post transfection, total RNA was isolated using the mirVana kit (Invitrogen) according to manufacturer’s procedure. Three replicate experiments were performed and a technical repeat was included for each sample. Samples were analyzed using Illumina's Sentrix Human HT-12 ver4 Expression BeadChips (Illumina, San Diego, CA).

2013-10-09 | E-GEOD-51309 | biostudies-arrayexpress

Hsa-miR-31-5p controls a metabolic switch in psoriatic keratinocytes that identifies therapeutic intervention

Project description:Next to genetic alterations, it is being recognized that the cellular environment also acts as a major determinant in onset and progression of disease. In cases where different cell types contribute to the final disease outcome, this imposes environmental challenges as different cell types likely differ in their extracellular dependencies. A number of skin diseases, including psoriasis is characterized by a combination of keratinocyte hyperproliferation and immune cell activation. Activation of immune cells involves increased glucose consumption thereby intrinsicly limiting glucose availability for other cell types. Thus, these type of skin diseases require metabolic adaptations that enable coexistence between hyperproliferative keratinocytes and activated immune cells in a nutrient-limited environment. Hsa-microRNA-31-5p (miR-31) is highly expressed in keratinocytes within the psoriatic skin. Here we show that miR-31 expression in keratinocytes is induced by limited glucose availability and enables increased survival of keratinocytes under limiting glucose conditions, by increasing glutamine metabolism. In addition, miR-31 induced glutamine metabolism results in secretion of specific metabolites (aspartate and glutamate) but also secretion of immuno-modulatory factors. We show that this miR-31-induced secretory phenotype is sufficient to induce Th17 cell differentiation, a hallmark of psoriasis. Inhibition of glutaminase (GLS) using CB-839 impedes miR31-induced metabolic rewiring and secretion of immuno-modulatory factors. Concordantly, pharmacological targeting of GLS alleviated psoriasis pathology in a mouse model of psoriasis. Together our data illustrate an emerging concept of metabolic interaction across cell compartments that characterizes disease development, which can be employed to design effective treatment options for disease, as shown here for psoriasis.

2023-02-06 | PXD029030 | Pride

A miR-494 dependent feedback loop regulates ER stress (ANAN-376 Project)

Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.

2021-09-09 | PXD019992 | Pride