| + |
miR-495 | down-regulates 
|
Proliferation |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268044 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19219026 |
Here we report that the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MLL-ENL | down-regulates quantity by repression 
transcriptional regulation
|
miR-495 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261972 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17996649 |
MiR-223 Expression Is Downregulated in AML1/ETO-Positive Primary Blasts and Cell Lines Here, we show that miR-223 is a direct transcriptional target of AML1/ETO. By recruiting chromatin remodeling enzymes at an AML1-binding site on the pre-miR-223 gene, AML1/ETO induces heterochromatic silencing of miR-223. Ectopic miR-223 expression, RNAi against AML1/ETO, or demethylating treatment enhances miR-223 levels and restores cell differentiation. Here, we identify an additional action for a leukemia fusion protein linking the epigenetic silencing of a microRNA locus to the differentiation block of leukemia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
miR-495 | up-regulates 
|
Cell_death |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255801 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26055960 |
Our results suggest that activating mutation of FLT3 in AML can lead, through the induction of JUN, to an increased expression of miR-155, which then causes down-regulation of SPI1 and CEBPB and consequently may causes block of myeloid differentiation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
miR-495 | up-regulates 
|
Apoptosis |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264545 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26344767 |
To further determine whether MeCP2 regulates the expression of miR-199a, we also re-expressed MeCP2 in MeCP2-KO neurons. As expected, this restored the level of mature-miR-199a expression to that in WT neurons |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Rett syndrome |
| + |
MLL-AF4 | down-regulates quantity by repression
transcriptional regulation
|
miR-495 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256242 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 21730352 |
We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155) through temporally dynamic occupation of binding sites within regulatory chromatin regions adjacent to their genomic coding loci. We conclude that PU.1 bound to open chromatin near 4 of its induced miR loci with 2 types of kinetics: (1) permanent (miR-146a, miR-342, and miR-338) and (2) transient (miR-155) during myeloid differentiation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
MLL-AF9 | down-regulates quantity by repression
transcriptional regulation
|
miR-495 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261971 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24332853 |
We have found that PRMT4 is highly expressed in HSPCs, where it functions as an inhibitor of myeloid differentiation (Figure 7G). In these cells, PRMT4 methylates RUNX1 at R223, promoting the assembly of a DPF2-containing transcriptional co-repressive complex, and repressing transcription at the miR-223 locus. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
miR-495
