Biology:mir-219 microRNA precursor family

From HandWiki
mir-219 microRNA precursor family
RF00251.jpg
Predicted secondary structure and sequence conservation of mir-219
Identifiers
Symbolmir-219
RfamRF00251
miRBaseMI0000296
miRBase familyMIPF0000044
Other data
RNA typeGene; miRNA
Domain(s)Eukaryota
GO0035195 0035068
SO0001244
PDB structuresPDBe

In molecular biology, the microRNA miR-219 was predicted in vertebrates by conservation between human, mouse and pufferfish and cloned in pufferfish.[1] It was later predicted and confirmed experimentally in Drosophila.[2] Homologs of miR-219 have since been predicted or experimentally confirmed in a wide range of species, including the platyhelminth Schmidtea mediterranea, several arthropod species and a wide range of vertebrates (MIPF0000044). The hairpin precursors (represented here) are predicted based on base pairing and cross-species conservation; their extents are not known. In this case, the mature sequence is excised from the 5' arm of the hairpin.

miR-219 has also been linked with NMDA receptor signalling in humans by targeting CaMKIIγ (a kind of protein kinase dependent to calcium and calmodulin) expression. And it has been suggested that deregulation of this miRNA can lead to the expression of mental disorders such as schizophrenia.[3] Recent findings show that miR-219 is linked with Tau toxicity, suggesting that miR-219 is involved in neurodegenerative disease, such as Alzheimer's disease, Parkinson's disease etc.[4]

References

  1. ↑ "Vertebrate microRNA genes". Science 299 (5612): 1540. March 2003. doi:10.1126/science.1080372. PMID 12624257. 
  2. ↑ "Computational identification of Drosophila microRNA genes". Genome Biology 4 (7): R42. 2003. doi:10.1186/gb-2003-4-7-r42. PMID 12844358. 
  3. ↑ "MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction". Proceedings of the National Academy of Sciences of the United States of America 106 (9): 3507–12. March 2009. doi:10.1073/pnas.0805854106. PMID 19196972. 
  4. ↑ "Dysregulation of microRNA-219 promotes neurodegeneration through post-transcriptional regulation of tau". The Journal of Clinical Investigation 125 (2): 681–6. February 2015. doi:10.1172/JCI78421. PMID 25574843. 

External links



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