Accession ID: MIRT003382 [miRNA, hsa-miR-20a ::
APP, target gene]
| pre-miRNA ID | hsa-mir-20a LinkOut: [miRBase ] |
|---|---|
| Synonyms | MIR20, MIRN20, MIRN20A, hsa-mir-20, hsa-mir-20a, miR-20, miRNA20A, MIR20A |
| Description | Homo sapiens miR-20a stem-loop |
| 2nd Structure of pre-miRNA |  |
| Mature miRNA | hsa-miR-20a-3p |
|---|---|
| Mature Sequence | 44| ACUGCAUUAUGAGCACUUAAAG |65 |
| Evidence | Experimental |
| Experiments | Cloned |
| Putative hsa-miR-20a-3p Targets | LinkOut: [ TargetScanS 5.1 | MicroCosm | microRNA.org | miRecords | miRDB | miRo | miRNAMap 2.0 ] |
| Mature miRNA | hsa-miR-20a-5p |
| Mature Sequence | 8| UAAAGUGCUUAUAGUGCAGGUAG |30 |
| Evidence | Experimental |
| Experiments | Cloned |
| Putative hsa-miR-20a-5p Targets | LinkOut: [ TargetScanS 5.1 | MicroCosm | microRNA.org | miRecords | miRDB | miRo | miRNAMap 2.0 ] |
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| Gene Symbol | APP LinkOut: [ Entrez Gene | BioGPS | Wikipedia | iHop ] | ||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Synonyms | AAA, ABETA, ABPP, AD1, APPI, CTFgamma, CVAP, PN2 | ||||||||||||||||||||
| Description | amyloid beta (A4) precursor protein | ||||||||||||||||||||
| Transcript | NM_000484 LinkOut: [ RefSeq ] | ||||||||||||||||||||
| Other Transcripts | NM_001136129, NM_001136130, NM_201413, NM_201414 | ||||||||||||||||||||
| Expression | LinkOut: [ BioGPS ] | ||||||||||||||||||||
| KEGG Pathway |
hsa05010 Alzheimer's disease - Homo sapiens (human) |
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| Putative miRNA Targets on APP | LinkOut: [ TargetScan 5.1 | MicroCosm | miRNAMap 2.0 ] | ||||||||||||||||||||
| 3'UTR of APP (miRNA target sites are highlighted) |
>APP|NM_000484|3'UTR 1 TAGACCCCCGCCACAGCAGCCTCTGAAGTTGGACAGCAAAACCATTGCTTCACTACCCATCGGTGTCCATTTATAGAATA 81 ATGTGGGAAGAAACAAACCCGTTTTATGATTTACTCATTATCGCCTTTTGACAGCTGTGCTGTAACACAAGTAGATGCCT 161 GAACTTGAATTAATCCACACATCAGTAATGTATTCTATCTCTCTTTACATTTTGGTCTCTATACTACATTATTAATGGGT 241 TTTGTGTACTGTAAAGAATTTAGCTGTATCAAACTAGTGCATGAATAGATTCTCTCCTGATTATTTATCACATAGCCCCT 321 TAGCCAGTTGTATATTATTCTTGTGGTTTGTGACCCAATTAAGTCCTACTTTACATATGCTTTAAGAATCGATGGGGGAT 401 GCTTCATGTGAACGTGGGAGTTCAGCTGCTTCTCTTGCCTAAGTATTCCTTTCCTGATCACTATGCATTTTAAAGTTAAA 481 CATTTTTAAGTATTTCAGATGCTTTAGAGAGATTTTTTTTCCATGACTGCATTTTACTGTACAGATTGCTGCTTCTGCTA 561 TATTTGTGATATAGGAATTAAGAGGATACACACGTTTGTTTCTTCGTGCCTGTTTTATGTGCACACATTAGGCATTGAGA 641 CTTCAAGCTTTTCTTTTTTTGTCCACGTATCTTTGGGTCTTTGATAAAGAAAAGAATCCCTGTTCATTGTAAGCACTTTT 721 ACGGGGCGGGTGGGGAGGGGTGCTCTGCTGGTCTTCAATTACCAAGAATTCTCCAAAACAATTTTCTGCAGGATGATTGT 801 ACAGAATCATTGCTTATGACATGATCGCTTTCTACACTGTATTACATAAATAAATTAAATAAAATAACCCCGGGCAAGAC 881 TTTTCTTTGAAGGATGACTACAGACATTAAATAATCGAAGTAATTTTGGGTGGGGAGAAGAGGCAGATTCAATTTTCTTT 961 AACCAGTCTGAAGTTTCATTTATGATACAAAAGAAGATGAAAATGGAAGTGGCAATATAAGGGGATGAGGAAGGCATGCC 1041 TGGACAAACCCTTCTTTTAAGATGTGTCTTCAATTTGTATAAAATGGTGTTTTCATGTAAATAAATACATTCTTGGAGGA 1121 GCAAAAAAAAAAAAAAAA Target sites Provided by authors Predicted by miRanda |
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| miRNA-target interactions (Predicted by miRanda) |
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| miRNA:Target | hsa-miR-20a :: APP [ Functional MTI ] |
|---|---|
| Validation Method | Luciferase reporter assay , Western blot |
| Conditions | HeLa, NEURO-2A, SK-N-SH |
| Location of target site | 3'UTR |
| Original Description (Extracted from the article) | ... We found that miR-20a, miR-17-5p, and miRNA106b affected significantly luciferase expression (Fig. 1B).//We transfected complementary anti-miR oligonucleotides and these caused a sig- nificant increase in luciferase expression (Fig. 1F). Thus we identify three miRNAs that bind directly and specifically to the 3′UTR of APP. ... - Hebert, S. S. Horre, K. Nicolai, L. et al., 2009, Neurobiol Dis. |
| Article |
- Hebert, S. S.
Horre, K.
Nicolai, L. et al. - Neurobiol Dis, 2009
Gene dosage effects of Amyloid precursor protein (APP) can cause familial AD. Recent evidence suggest that microRNA (miRNA) pathways, implicated in gene transcriptional control, could be involved in the development of sporadic Alzheimer's disease (AD). We therefore investigated whether miRNAs could participate in the regulation of APP gene expression. We show that miRNAs belonging to the miR-20a family (that is, miR-20a, miR-17-5p and miR-106b) could regulate APP expression in vitro and at the endogenous level in neuronal cell lines. A tight correlation between these miRNAs and APP was found during brain development and in differentiating neurons. We thus identify miRNAs as novel endogenous regulators of APP expression, suggesting that variations in miRNA expression could contribute to changes in APP expression in the brain during development and disease. This possibility is further corroborated by the observation that a statistically significant decrease in miR-106b expression was found in sporadic AD patients.
LinkOut: [PMID: 19110058]
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| miRNA:Target | hsa-miR-20a :: APP [ Functional MTI ] | ||||||
|---|---|---|---|---|---|---|---|
| Validation Method | GFP reporter assay , qRT-PCR , Western blot | ||||||
| Conditions | OVCAR-3 | ||||||
| Location of target site | 3'UTR | ||||||
| Original Description (Extracted from the article) | ... miR-20a targets directly at the APP 3' UTR//From these results, we concluded that miR-20a could negatively regulate APP expression through directly binding to the special sequence of APP mRNA 3' UTR.//The EGFP reporter analysis showed that with wild-type 3' UTR inserting, the EGFP value was significantly lower than mutants when they were all treated with irrespective sequences[Fig. 2(D)], demonstrating the effects of endogenous miR-20a on APP. ... - Fan, X. Liu, Y. Jiang, J. Ma, Z. Wu, H. et al., 2010, Acta Biochim Biophys Sin (Shanghai). |
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| miRNA-target interactions (Provided by authors) |
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| Article |
- Fan, X.
Liu, Y.
Jiang, J.
Ma, Z.
Wu, H. et al. - Acta Biochim Biophys Sin (Shanghai), 2010
MicroRNAs (miRNAs) are emerging as a class of small regulated RNAs, and the alterations of miRNAs are implicated in the initiation and progression of human cancers. Our study shows that inhibition of miR-20a in OVCAR3 ovarian cancer cell line could suppress, whereas overexpression of miR-20a could enhance cell long-term proliferation and invasion. We also confirmed amyloid precursor protein (APP) as a direct target gene of miR- 20a. Furthermore, suppression of APP expression could also promote ovarian cancer cell proliferation and invasion, which is consistent with the results of miR-20a overexpression. Therefore, we concluded that the regulation of APP is an important mechanism for miR-20a to promote proliferation and invasion in ovarian cancer cells.
LinkOut: [PMID: 20458444]
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