Disease relevance of MIRN410

• Aberrantly expressed miRNA or their targets will provide mechanistic insight and therapeutic targets for cholangiocarcinoma [1].
• We show that the microRNA miR-155 can be processed from sequences present in BIC RNA, a spliced and polyadenylated but non-protein-coding RNA that accumulates in lymphoma cells [2].
• Activation of an oncogenic microRNA cistron by provirus integration [3].
• We found that microRNA Mir-17-5p has extensive complementarity to the mRNA of AIB1 (named for "amplified in breast cancer 1") [4].
• In this study, we report for the first time reduced expression of the let-7 microRNA in human lung cancers [5].

Psychiatry related information on MIRN410

• First in vivo evidence of microRNA-induced fragile X mental retardation syndrome [6].

High impact information on MIRN410

• A new study shows that a microRNA is involved in this process by modulating a component of the Hedgehog signal transduction pathway [7].
• The analysis suggests that some microRNAs may have as many as a few thousand targets, and that between 74% and 92% of the gene transcripts in four model genomes are likely under microRNA control through their untranslated and amino acid coding regions [8].
• Rna22 does not rely upon cross-species conservation, is resilient to noise, and, unlike previous methods, it first finds putative microRNA binding sites in the sequence of interest, then identifies the targeting microRNA [8].
• Human RISC couples microRNA biogenesis and posttranscriptional gene silencing [9].
• Involvement of microRNA in AU-rich element-mediated mRNA instability [10].

Biological context of MIRN410

• We present rna22, a method for identifying microRNA binding sites and their corresponding heteroduplexes [8].
• Recent advances have led to a more detailed understanding of RNA interference and its role in microRNA biogenesis and function [11].
• MicroRNAs have recently emerged as key posttranscriptional regulators of eukaryotic gene expression, yet our understanding of how microRNA expression is itself controlled has remained rudimentary [12].
• Here, we show that miR-181, a microRNA that is strongly upregulated during differentiation, participates in establishing the muscle phenotype [13].
• Alterations in miRNA expression can contribute to tumor growth by modulating the functional expression of critical genes involved in tumor cell proliferation or survival [1].

Anatomical context of MIRN410

• We show here that the repression of nPTB expression during myoblast differentiation results from its targeting by the muscle-restricted microRNA miR-133 [14].
• Involvement of human micro-RNA in growth and response to chemotherapy in human cholangiocarcinoma cell lines [1].
• Discovered just over a decade ago, microRNA (miRNA) is now recognized as one of the major regulatory gene families in eukaryotic cells [15].
• This review focuses on Drosophila FMRP as (i) a negative regulator of translation via noncoding RNA, including microRNA and adaptor BC1 RNA-mediated silencing mechanisms; (ii) a negative regulator of microtubule cytoskeleton stability; and (iii) a negative regulator of neuronal architectural complexity [16].
• Finally, we compared the microRNA expression of megakaryoblastic leukemic cell lines with that of in vitro differentiated megakaryocytes and CD34(+) progenitors [17].

Associations of MIRN410 with chemical compounds

• Other studies reveal how the microRNA pathway and signaling are related to FMRP function through the metabotropic glutamate receptor [18].
• We describe the development of a lentiviral vector platform, pSLIK (single lentivector for inducible knockdown), which permits tetracycline-regulated expression of microRNA-like short hairpin RNAs from a single viral infection of any naïve cell system [19].
• The microRNA (miR29b) molecule tested is targeted to the mRNA for the dihydrolipoamide branched chain acyltransferase component of BCKD and prevents translation when bound [20].
• In addition, ABA signaling is further modulated by mRNA maturation and stability, microRNA (miRNA) levels, nuclear speckling, and protein degradation [21].
• Nonisotopic detection of microRNA using digoxigenin labeled RNA probes [22].

Physical interactions of MIRN410

• The Drosha-DGCR8 complex in primary microRNA processing [23].

Enzymatic interactions of MIRN410

• The bidentate RNase III Dicer cleaves microRNA precursors to generate the 21-23 nt long mature RNAs [24].

Regulatory relationships of MIRN410

• PURPOSE: The aim of this study was to investigate the role of p53 in regulating micro-RNA (miRNA) expression due to its function as a transcription factor [25].

Other interactions of MIRN410

• RNase III proteins play key roles in microRNA (miRNA) biogenesis [23].
• Coordinate Suppression of ERBB2 and ERBB3 by Enforced Expression of Micro-RNA miR-125a or miR-125b [26].
• A role for the P-body component GW182 in microRNA function [27].
• Processing of the microRNA let-7 precursor by Dicer produced an apparently mature let-7 RNA [28].
• MyoD directly activates the expression of a muscle-specific microRNA (miRNA), miR-206, which targets sequences in the Fstl1 and Utrn RNA, and these sequences are sufficient to suppress gene expression in the presence of miR-206 [29].

Analytical, diagnostic and therapeutic context of MIRN410

• CONCLUSIONS: Alterations in miRNA expression contribute to tumor growth and response to chemotherapy [1].
• Expression of selected miRNA and their precursors was evaluated by Northern blots and real-time polymerase chain reaction, respectively [1].
• To quantify microRNA expression, we employed a highly sensitive technique that uses stem-loop primers for reverse transcription followed by real-time PCR [30].
• The genetic dissection of hot spots for chromosomal abnormalities in the age of the sequenced human genome resulted in the discovery that microRNA (miRNA) genes, encoding for a class of small noncoding RNAs, frequently resides in such genomic regions [31].
• Global sequence analysis revealed that over 46% of the 326 miRNA putative promoters contain potential p53-binding sites, suggesting that some of these miRNAs were potentially regulated directly by wt-p53 [25].

References