Accession ID: MIRT001935 [miRNA, hsa-miR-106a ::
APP, target gene]
| pre-miRNA ID | hsa-mir-106a LinkOut: [miRBase ] |
|---|---|
| Description | Homo sapiens miR-106a stem-loop |
| Comment | This miRNA was not cloned in reference . |
| 2nd Structure of pre-miRNA |  |
| Mature miRNA | hsa-miR-106a-3p |
|---|---|
| Mature Sequence | 50| CUGCAAUGUAAGCACUUCUUAC |71 |
| Evidence | Experimental |
| Experiments | Cloned |
| Putative hsa-miR-106a-3p Targets | LinkOut: [ TargetScanS 5.1 | MicroCosm | microRNA.org | miRecords | miRDB | miRo | miRNAMap 2.0 ] |
| Mature miRNA | hsa-miR-106a-5p |
| Mature Sequence | 13| AAAAGUGCUUACAGUGCAGGUAG |35 |
| Evidence | Experimental |
| Experiments | Cloned |
| Putative hsa-miR-106a-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) |
|
| miRNA:Target | hsa-miR-106a :: APP [ Functional MTI ] |
|---|---|
| Validation Method | Luciferase reporter assay , Western blot , qRT-PCR |
| Conditions | HEK293 |
| Location of target site | 3'UTR |
| Tools used in this research | Literature survey |
| Original Description (Extracted from the article) | ... Utilizing human cell lines, we demonstrate that miRNAs hsa-mir-106a and hsa-mir-520c bind to their predicted target sequences in the APP 3UTR and negatively regulate reporter gene expression. Over-expression of these miRNAs, but not control miRNAs,results in translational repression of APP mRNA and significantly reduces APP protein levels. ... - Patel, N. Hoang, D. Miller, N. Ansaloni, S. et al., 2008, Mol Neurodegener. |
| Article |
- Patel, N.
Hoang, D.
Miller, N.
Ansaloni, S. et al. - Mol Neurodegener, 2008
ABSTRACT: A number of studies have shown that increased APP levels, resulting from either a genomic locus duplication or alteration in APP regulatory sequences, can lead to development of early-onset dementias, including Alzheimer's disease (AD). Therefore, understanding how APP levels are regulated could provide valuable insight into the genetic basis of AD and illuminate novel therapeutic avenues for AD. Here we test the hypothesis that APP protein levels can be regulated by miRNAs, evolutionarily conserved small noncoding RNA molecules that play an important role in regulating gene expression. Utilizing human cell lines, we demonstrate that miRNAs hsa-mir-106a and hsa-mir-520c bind to their predicted target sequences in the APP 3'UTR and negatively regulate reporter gene expression. Over-expression of these miRNAs, but not control miRNAs, results in translational repression of APP mRNA and significantly reduces APP protein levels. These results are the first to demonstrate that levels of human APP can be regulated by miRNAs.
LinkOut: [PMID: 18684319]
|
| miRNA:Target | hsa-miR-106a :: APP [ Non-Functional MTI ] |
|---|---|
| Validation Method | Luciferase reporter assay |
| Conditions | HeLa |
| Location of target site | 3'UTR |
| Tools used in this research | miRanda, miRBase Target Database, PicTar, TargetScan |
| Original Description (Extracted from the article) | ... We found that miR-20a, miR-17-5p, and miRNA106b affected significantly luciferase expression (Fig. 1B). In contrast, a scrambled miRNA sequence, as well as the other candidate miRNAs (miR-15a, miR-130a, let-7d and let-7a) showed no effect in this assay. Curiously, miR-106a, which is closely related to miR-106b, had in this assay an inconsistent effect. ... - 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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