MIR145
microRNA 145 | MIR-145, hsa-mir-145, MIRN145

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]

Biological processes 49 terms
RISC complex (GO:0016442)actin cytoskeleton organization (GO:0030036)angiotensin-activated signaling pathway (GO:0038166)aorta smooth muscle tissue morphogenesis (GO:0060414)ectodermal cell differentiation (GO:0010668)establishment or maintenance of cell type involved in phenotypic switching (GO:0044663)extracellular exosome (GO:0070062)mRNA 3'-UTR binding (GO:0003730)mRNA base-pairing post-transcriptional repressor activity (GO:1903231)mRNA base-pairing post-transcriptional repressor activity (GO:1903231)mesodermal cell differentiation (GO:0048333)miRNA-mediated gene silencing by inhibition of translation (GO:0035278)miRNA-mediated gene silencing by mRNA destabilization (GO:0035279)miRNA-mediated gene silencing by mRNA destabilization (GO:0035279)miRNA-mediated post-transcriptional gene silencing (GO:0035195)miRNA-mediated post-transcriptional gene silencing (GO:0035195)myofibroblast differentiation (GO:0036446)negative regulation of SMAD protein signal transduction (GO:0060392)negative regulation of angiogenesis (GO:0016525)negative regulation of cardiac muscle cell apoptotic process (GO:0010667)negative regulation of cardiac muscle cell apoptotic process (GO:0010667)negative regulation of cardiac muscle hypertrophy (GO:0010614)negative regulation of cell migration (GO:0030336)negative regulation of cell migration (GO:0030336)negative regulation of cellular response to transforming growth factor beta stimulus (GO:1903845)negative regulation of cholesterol efflux (GO:0090370)negative regulation of epithelial to mesenchymal transition (GO:0010719)negative regulation of extracellular matrix assembly (GO:1901202)negative regulation of extracellular matrix assembly (GO:1901202)negative regulation of inflammatory response (GO:0050728)negative regulation of interleukin-16 production (GO:0032699)negative regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction (GO:0051898)negative regulation of smooth muscle cell proliferation (GO:0048662)negative regulation of somatic stem cell division (GO:1904676)negative regulation of somatic stem cell population maintenance (GO:1904673)negative regulation of transforming growth factor beta receptor signaling pathway (GO:0030512)negative regulation of vascular associated smooth muscle cell dedifferentiation (GO:1905175)positive regulation of canonical Wnt signaling pathway (GO:0090263)positive regulation of cardiac vascular smooth muscle cell differentiation (GO:2000724)positive regulation of cellular response to hypoxia (GO:1900039)positive regulation of fibroblast migration (GO:0010763)positive regulation of interleukin-10 production (GO:0032733)positive regulation of macrophage activation (GO:0043032)positive regulation of macrophage differentiation (GO:0045651)regulation of ERK1 and ERK2 cascade (GO:0070372)regulation of collagen biosynthetic process (GO:0032965)regulation of phenotypic switching (GO:1900239)regulation of smooth muscle contraction (GO:0006940)vascular associated smooth muscle cell differentiation (GO:0035886)
Expression (TPM)
MIR145 — as a Regulated Gene

TFs regulating MIR145 0 TFs

Transcription factors with Perturb-seq knockdown data for MIR145. The Binding column indicates whether any binding evidence exists for this TF–gene pair (ChIP-seq or motif footprint peaks). The Mean coef is the average Perturb-seq regression coefficient across active gRNAs (positive = MIR145 upregulated upon KD; negative = downregulated). The Outlier column indicates whether this gene is in the top or bottom 5% of all TF knockdown effects.

Data: Effect:
TF Mean coef Binding Outlier TF→Gene link

Elements linked to MIR145

Open chromatin peaks (ATAC-seq) in the genomic neighbourhood of MIR145, linked by TSS proximity or chromatin conformation (Multiome / HiCAR). Each element overlaps at least one TF ChIP-seq binding site — the TFs column shows how many distinct TFs bind that element.

Accessibility Element Dist. to TSS Link type TFs
chr5:149,424,439–149,424,708 5.9 kb Proximal (<10kb) 88
chr5:149,428,792–149,428,979 1.7 kb Proximal (<10kb) 98
chr5:149,430,329–149,430,680 at TSS At TSS 443
chr5:149,434,518–149,434,726 3.9 kb Proximal (<10kb) 204
chr5:149,439,985–149,440,233 9.3 kb Proximal (<10kb) 369

Genome Browser

Genomic view of the MIR145 locus showing ATAC-seq accessibility and RNA-seq expression across the ESC → DE time course, together with TF binding peaks and element-to-TSS loop connections.

chr5:149,414,439 – 149,450,233
Proximal 1 kb Distal 10 kb Multiome HiCAR ATAC-seq RNA-seq