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miR-92 is part of a large precursor sequence that forms a stem loop once transcribed into RNA. This long precursor sequence is a component of the mir-17-92 cluster which contains 5 additional mir precursor sequences: mir-17, mir-18a, mir-19a, mir-20a and mir19b-1. [4]
miRNA biogenesis in plants differs from animal biogenesis mainly in the steps of nuclear processing and export. Instead of being cleaved by two different enzymes, once inside and once outside the nucleus, both cleavages of the plant miRNA are performed by a Dicer homolog, called Dicer-like1 (DL1). DL1 is expressed only in the nucleus of plant ...
MicroRNAs function to regulate the expression levels of other genes by several mechanisms. miR-451 regulates the drug-transporter protein P-glycoprotein , potentially promoting resistance to the chemotherapy drug Paclitaxel .
A miRNA can be derived from each arm of the pre-miRNA hairpin. Historically, the least common of these two miRNA products was denoted by the addition of * to the miRNA name, however the modern convention is to denote mature miRNA products as 5p or 3p. [11] Both mir-10 and mir-10* have been detected in Drosophila.
These two proteins homeostatically control miRNA biogenesis by an auto-feedback loop. [16] A 2nt 3' overhang is generated by Drosha in the nucleus recognized by Dicer in the cytoplasm, which couples the upstream and downstream processing events. Pre-miRNA is then further processed by the RNase Dicer into mature miRNAs in the cell cytoplasm.
StarBase; Content; Description: microRNA-mRNA interaction maps from Argonaute CLIP-Seq and Degradome-Seq data.: Contact; Research center: Sun Yat-sen University: Laboratory: Key Laboratory of Gene Engineering of the Ministry of Education
p53-deficient human gastric cancer cells, restoration of functional miR-34 inhibits cell growth and induces chemosensitization and apoptosis, indicating that miR-34 may restore p53 function. Restoration of miR-34 inhibits tumorsphere formation and growth, which is reported to be correlated to the self-renewal of cancer stem cells.
The paralogous miRNA gene clusters that give rise to miR-17 family microRNAs (miR-17~92, miR-106a~363, and miR-106b~25) have been implicated in a wide variety of malignancies and are sometimes referred to as oncomirs. [4] The oncogenic potential of these non-protein encoding genes was first identified in mouse viral tumorigenesis screens.