Part of the book: Application of Nanotechnology in Drug Delivery
General complexities in versatile animals are not always proportional to their genome size. A notable example is that the salamander genome size is 15-fold larger than that of human, which mostly contains unfolded “junk DNA.” A vast portion of this non-protein-coding unfolded DNA undergoes transcriptional regulation and produces a large number of long noncoding RNAs (lncRNAs). LncRNAs play key roles in gene expression and therapies of different human diseases. Recently, novel lncRNAs and their function on the silencing or activation of a particular gene(s) are regularly being discovered. Another important component of gene regulation is high packing of chromatin, which is composed of mainly repetitive sequences with negligible coding potential. In particular, an epigenetic marker determines the state of the gene associated with it, whether the gene will be expressed or silenced. Here, we elaborately discuss the biogenesis pathway of lncRNAs as well as their mechanism of action and role in gene silencing and regulation, including RNA interference. Moreover, several lncRNAs are the common precursors of small regulatory RNAs. It is thus becoming increasingly clear that lncRNAs can function via numerous paradigms as key regulatory molecules in different organisms.
Part of the book: RNA Interference
Progressing muscle wasting and dramatic neurodegeneration of upper and lower motor neurons are the initial symptoms of amyotrophic lateral sclerosis (ALS) that eventually cause aetiology or death in quick succession. The functional mechanism of ALS is non-cell autonomous but it strongly influences on non-neural cells including microglia, astrocyte muscles and T cell. In ALS, neurodegeneration is triggered by at least four gene mutations that are not related to any classical signalling pathways, molecular mechanism or known cellular ingredients. MicroRNA is endogenous tiny non-coding RNA, which is required for fine-tuning or micromanaging protein expression post-transcriptionally. In this review, we identified numerous microRNAs and their possible targets in ALS-related genes. These microRNAs misprocess ALS-related protein-coding genes via microRNA-gene circuits. This result sheds a strong link between microRNA and ALS genes. The mechanistic insight of multiple microRNAs related to ALS is required to treat neuro-inflammation and neuro-degradation. It is proposed that the micro-regulation of multiple microRNAs is involved in generation of unique neuroprotective agent against ALS. Therefore, a classical and novel microRNA-mediated therapy might unravel an alternative strategy for ALS-related neurodegeneration. This strategy indeed implicates real promises to illustrate a unique impact for ALS cure.
Part of the book: Update on Amyotrophic Lateral Sclerosis