| Details |
| Disease Name | Alzheimer Disease |
| Nocoding RNA Name | hsa-miR-26b |
| Expression Pattern | up-regulated |
| Species | Homo sapiens |
| Detection Methods | qRT-PCR,Western Blot,Luciferase Reporter Assay etc. |
| Target | Rb1 |
| Tissue | brain |
| Treatment | N/A |
| PubMed ID | 24027266 |
| Year | 2013 |
| Detail Description | Ectopic overexpression of miR-26b in rat primary postmitotic neurons led to the DNA replication and aberrant cell cycle entry (CCE) and, in parallel, increased tau-phosphorylation, which culminated in the apoptotic cell death of neurons. Similar tau hyperphosphorylation and CCE are typical features of neurons in pre-AD brains.Sequence-specific inhibition of miR-26b in culture is neuroprotective against oxidative stress. Retinoblastoma protein (Rb1), a major tumor suppressor, appears as the key direct miR-26b target, which mediates the observed neuronal phenotypes. The downstream signaling involves upregulation of Rb1/E2F cell cycle and pro-apoptotic transcriptional targets, including cyclin E1, and corresponding downregulation of cell cycle inhibitor p27/Kip1.Elevated levels of miR-26b may thus contribute to the AD neuronal pathology. |
NSDNA: The Nervous System Disease NcRNAome Atlas
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