Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mir-146a wild-type 3ʹ sequence identity is dispensable for proper innate immune function in vivo (miRNA-Seq)

ABSTRACT: Mir-146a wild-type 3ʹ sequence identity is dispensable for proper innate immune function in vivo (miRNA-Seq)

PROVIDER: PRJNA516456 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8473882.fastq.gz	Fastqsanger.gz
	SRR8473883.fastq.gz	Fastqsanger.gz
	SRR8473884.fastq.gz	Fastqsanger.gz
	SRR8473885.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Mir-146a wild-type 3ʹ sequence identity is dispensable for proper innate immune function in vivo

Project description:A long-prevailing model has held that the “seed” region (nucleotides 2-8) of a microRNA is typically sufficient to mediate target recognition and repression. However, numerous recent studies, both within the context of defining miRNA/target pairs by direct physical association and by directly assessing this model in vivo in C. elegans have brought this model into question. To test the importance of miRNA 3' pairing in vivo, in a mammalian system, we engineered a mutant murine mir-146a allele in which the 5' half of the mature microRNA retains the sequence of the wild-type mir-146a but the 3ʹ half has been altered to be anti-complementary to the wild-type miR-146a sequence. Mice homozygous or hemizygous for this mutant allele are phenotypically indistinguishable from wild-type controls and do not recapitulate any of the immunopathology previously described for mir-146a-null mice. Our results strongly support the conclusion that 3ʹ pairing is dispensable in the context of the function of a key mammalian microRNA.

2019-02-09 | PXD011413 | Pride

Mir-146a wild-type 3ʹ sequence identity is dispensable for proper innate immune function in vivo (miRNA-Seq)

2019-02-06 | GSE125473 | GEO

Mir-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo (RNA-Seq)

2019-02-06 | GSE121232 | GEO

Mir-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo

Project description:Mir-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo

| PRJNA516453 | ENA

Mir-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo (RNA-Seq)

Project description:Mir-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo (RNA-Seq)

| PRJNA496417 | ENA

MiR-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo.

Project description:The prevailing model of microRNA function is that the "seed region" (nt 2-8) is sufficient to mediate target recognition and repression. However, numerous recent studies have challenged this model, either by demonstrating extensive 3' pairing between physically defined miRNA-mRNA pairs or by showing in Caenorhabditis elegans that disrupted 3' pairing can result in impaired function in vivo. To test the importance of miRNA 3' pairing in a mammalian system in vivo, we engineered a mutant murine mir-146a allele in which the 5' half of the mature microRNA retains its wild-type sequence, but the 3' half's sequence has been altered to robustly disrupt predicted pairing to this latter region. Mice homozygous or hemizygous for this mutant allele are phenotypically indistinguishable from wild-type controls and do not recapitulate any of the immunopathology previously described for mir-146a-null mice. Our results indicate that 3' pairing is dispensable for the established myeloid function of this key mammalian microRNA.

| S-EPMC6379685 | biostudies-literature

Mir-146a wild-type 3' sequence identity is dispensable for proper innate immune function in vivo

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-06 | GSE125474 | GEO

miR-146a regulates many lncRNAs in RAS induced senescence [Anti-146a]

Project description:miR-146a is a known anti-inflammatory miRNA. Intringuigly, it is overexpressed in RAS-induced senescent cells which is accompanied with a rich pro-inflammatoy secretpry phenotype. We aim to study possible sponges for miR-146a.

2021-05-11 | GSE150325 | GEO

Gene Regulation in Bob1-/- and miR-146a-/- Murine Pre-B Cells

Project description:5d IL-7-supported bone marrow cultures from C57BL/6 mice deficient for either the transcription factor Bob1 or microRNA-146a Micro-RNAs (miRNAs) are required for many processes during hematopoietic development and activation, including B-cell differentiation. The lymphocyte-specific transcription factor Bob1 is critical for the proper development and function of B cells. Bob1-/- mice are immunodeficient and lack germinal centers. Microarray expression analysis of Bob1-deficient B cells shows numerous up-regulated genes, suggesting that Bob1 may affect targets indirectly via the control of miRNAs. Using a gain-of-function/loss-of-function approach in WEHI-231 and primary pro-B and pre-B cells, we identified miR-146a as a direct target of Bob1. Ttranscriptome-wide analysis of miR-146a-/- B cells shows a number of misregulated genes involved in immune regulation, while analysis of Bob1-/- cells shows increased expression of cell cycle-related genes. These results support previous evidence that Bob1 suppresses proliferation, a previously underappreciated role for Bob1 that is in line with the cancer-prone phenotype of mir-146a-/- mice.

2013-09-07 | GSE44986 | GEO

Role of miR-146a in mouse brain development: relevance for developmental brain disorders

Project description:MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression post-transcriptionally. miRs are involved in a wide range of regulation networks, including those involved in brain development. We and other showed an upregulation of miR-146a in autism spectrum disorders, intellectual disability and epilepsy. Taking advantage of a mouse model constitutively inactivated for miR-146a, we investigated its functions during brain development using a combination of imaging, molecular, cell biology techniques and behavioral studies. We demonstrated that loss of miR-146a causes time and region specific expression defects in the mouse brain. Pyramidal and interneurons are the most severely affected cell types with deregulated pathways reflecting different stages of neuronal differentiation and synaptic maturation. We showed that absence of miR-146a impairs the balance between proliferation and differentiation of neural progenitors. We observed no difference in neither brain weight nor total volume but an increased hemispheric asymmetry of hippocampal volume. Lastly, impaired associative memory was also observed. Our results show that miR-146 is important for proper brain development and support the hypothesis that miR-146a deregulation may play a role in developmental brain disorders.

2019-06-01 | GSE114491 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data