Mir144 microRNA 144 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Mir144provided by MGI
Official Full Name: microRNA 144provided by MGI
Primary source: MGI:MGI:2676829
See related: Ensembl:ENSMUSG00000065401 miRBase:MI0000168; AllianceGenome:MGI:2676829
Gene type: ncRNA
RefSeq status: PROVISIONAL
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Mirn144; mir-144; mmu-mir-144
Summary: microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. [provided by RefSeq, Sep 2009]
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Genomic context

Location:: 11; 11 B5

Exon count:: 1

Annotation release	Status	Assembly	Chr	Location
109	current	GRCm39 (GCF_000001635.27)	11	NC_000077.7 (77963831..77963896)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	11	NC_000077.6 (78073005..78073070)

Chromosome 11 - NC_000077.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Blood miR-144-3p: a novel diagnostic and therapeutic tool for depression.
Title: Blood miR-144-3p: a novel diagnostic and therapeutic tool for depression.
Exosomes Derived from BMSCs Ameliorate Intestinal Ischemia-Reperfusion Injury by Regulating miR-144-3p-Mediated Oxidative Stress.
Title: Exosomes Derived from BMSCs Ameliorate Intestinal Ischemia-Reperfusion Injury by Regulating miR-144-3p-Mediated Oxidative Stress.
microRNA-144/451 decreases dendritic cell bioactivity via targeting interferon-regulatory factor 5 to limit DSS-induced colitis.
Title: microRNA-144/451 decreases dendritic cell bioactivity via targeting interferon-regulatory factor 5 to limit DSS-induced colitis.
Extracellular vesicle-derived miR-144 as a novel mechanism for chronic intermittent hypoxia-induced endothelial dysfunction.
Title: Extracellular vesicle-derived miR-144 as a novel mechanism for chronic intermittent hypoxia-induced endothelial dysfunction.
MicroRNA-144-3p Represses the Growth and EMT of Thyroid Cancer via the E2F2/TNIK Axis in Cells and Male BALB/c Nude Mice.
Title: MicroRNA-144-3p Represses the Growth and EMT of Thyroid Cancer via the E2F2/TNIK Axis in Cells and Male BALB/c Nude Mice.
MiR-144-3p induced by SP1 promotes IL-1beta-induced pyroptosis in chondrocytes via PTEN/PINK1/Parkin axis.
Title: MiR-144-3p induced by SP1 promotes IL-1β-induced pyroptosis in chondrocytes via PTEN/PINK1/Parkin axis.
Potency of miR-144-3p in promoting abdominal aortic aneurysm progression in mice correlates with apoptosis of smooth muscle cells.
Title: Potency of miR-144-3p in promoting abdominal aortic aneurysm progression in mice correlates with apoptosis of smooth muscle cells.
LncRNA TUG1 attenuates ischaemia-reperfusion-induced apoptosis of renal tubular epithelial cells by sponging miR-144-3p via targeting Nrf2.
Title: LncRNA TUG1 attenuates ischaemia-reperfusion-induced apoptosis of renal tubular epithelial cells by sponging miR-144-3p via targeting Nrf2.
MiR-144-induced KLF2 inhibition and NF-kappaB/CXCR1 activation promote neutrophil extracellular trap-induced transfusion-related acute lung injury.
Title: MiR-144-induced KLF2 inhibition and NF-kappaB/CXCR1 activation promote neutrophil extracellular trap-induced transfusion-related acute lung injury.
Hepatic miR-144 Drives Fumarase Activity Preventing NRF2 Activation During Obesity.
Title: Hepatic miR-144 Drives Fumarase Activity Preventing NRF2 Activation During Obesity.

Submit: New GeneRIF Correction See all GeneRIFs (48)

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Targeted (3) 1 citation

General gene information

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Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables translation regulator activity	IGI Inferred from Genetic Interaction more info	PubMed

Process	Evidence Code	Pubs
involved_in erythrocyte differentiation	IGI Inferred from Genetic Interaction more info	PubMed
involved_in gene expression	IGI Inferred from Genetic Interaction more info	PubMed
involved_in mRNA catabolic process	IGI Inferred from Genetic Interaction more info	PubMed
involved_in mRNA destabilization	IGI Inferred from Genetic Interaction more info	PubMed
acts_upstream_of_or_within male sex differentiation	IEP Inferred from Expression Pattern more info	PubMed
acts_upstream_of_or_within response to bacterium	IEP Inferred from Expression Pattern more info	PubMed

Component	Evidence Code	Pubs
part_of RISC complex	IDA Inferred from Direct Assay more info	PubMed
part_of RNAi effector complex	IDA Inferred from Direct Assay more info	PubMed
part_of RNAi effector complex	IMP Inferred from Mutant Phenotype more info	PubMed

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.