The small RNA molecules of about 19-22 nucleotides in length, aptly called microRNAs, perform the task of gene regulation in the cell. Interestingly, till the early nineties very little was known about them but eventually, the microRNAs have become forefront in the area of research. The huge number of microRNAs plus each one of them targeting a vast number of related as well as unrelated genes makes them very interesting molecules to study. To add to the mystery of miRNAs is the fact that the same miRNA can have antagonizing role in two different cell types i.e. in one cell type; the miRNA promotes proliferation whereas in another cell type the same miRNA inhibits proliferation. Another remarkable aspect of the microRNAs is that many of them exist in clusters. In humans alone, out of 721 microRNAs known, 247 of them occur in 64 clusters at an inter-miRNA distance of less than 5000bp. The reason for this clustering of miRNAs is not fully understood but since the miRNA clusters are evolutionary conserved, their significance cannot be ruled out. The objective of this review is to summarize the recent progress on the functional characterization of miR-23a~27a~24-2 cluster in humans in relation to various health and diseased conditions and to highlight the cooperative effects of the miRNAs of this cluster.
Background: The periodic dielectric multilayers sustaining Bloch surface waves have been proposed as a platform for the sensing applications and the two dimensional integrated optics. In this paper, we present the experimental and theoretical investigation of propagation properties of Bloch surface waves, for example propagation length and refractive index of the surface mode, at the interface of a dielectric multilayer platform. We use thin layers (~λ/25) of titanium dioxide as an additional layer of high index material. Methods: We exploit multi-heterodyne scanning near-field optical microscopy and total internal reflection configuration as a near-field and far-field characterization tools. Results: The longest propagation length is achieved when the multilayer is designed to have the dispersion curve positioned close to the middle of the photonics band gap. We measure a Bloch surface wave mode of propagation length 3.24 mm and of an effective refractive index contrast 0.15. Conclusions: The experimental results are in conformity with theoretical results. This study paves a way to realize efficient and compact two dimensional components and systems.
Previously, we had reported that overexpression of miR-23a~27a~24-2 cluster induces caspase-dependent and -independent apoptosis via JNK in human embryonic kidney (HEK293T) cells. Herein, we describe the molecular mechanism(s) responsible for miR-23a~27a~24-2 cluster induced apoptosis. Gene expression profiling was used to characterize the transcriptional response to miR-23a~27a~24-2 cluster overexpression in HEK293T cells. The microarray analysis gave 1,025 differentially expressed genes and analysis of the gene expression data with Ingenuity Pathway Analysis (IPA) software revealed p53 signaling, oxidative stress response and mitochondrial dysfunction among the top processes being affected. This data substantiates our previous study where we had reported increase of ROS and the release of proapoptotic factors such as cytochrome c (cyt c) and apoptosis-inducing factor (AIF) from the mitochondria to cytosol. Additionally, components of ER stress-mediated apoptosis pathway i.e., C/EBP homologous protein (CHOP/DDIT3/GADD153) and TRIB3, an Akt inhibitor were found to be significantly enriched. Also, the enhanced expression of ATF3 and ATF4 was observed at RNA as well as protein level in miR-23a~27a~24-2 cluster overexpressed HEK293T cells. Induction of BIM appeared to be specific, because ER stress caused only a minor change in the expression of the related BH3-only proteins BID or PUMA. The fact that miR-23a~27a~24-2 cluster triggered endoplasmic reticulum stress (ER stress) was further established by the increase in cytosolic calcium levels after overexpression of this cluster in HEK293T cells. These findings were also supported by PANTHER analysis wherein biological process categories of apoptosis and stress response were enriched. Taken together, this work underlines the role of ER stress in miR-23a~27a~24-2 cluster mediated apoptosis in HEK293T cells. Since the detailed knowledge of this cluster induced apoptosis has now been elucidated, the in vivo study of this cluster would help evaluate the prospect of its use as a therapeutic in diseases known to occur because of deregulation of apoptosis.
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