Gems are the sites of the maturation of spliceosomes, which are learn more composed of uridylate-rich (U) snRNAs (small nuclear RNAs) and protein complex, small nuclear ribonuclearprotein (snRNP). Spliceosomes regulate the splicing of pre-mRNA and are classified into the major or minor classes, according to the consensus sequence

of acceptor and donor sites of pre-mRNA splicing. Although the major class of spliceosomes regulates most pre-mRNA splicing, minor spliceosomes also play an important role in regulating the splicing or global speed of pre-mRNA processing. A mouse model of spinal muscular atrophy, in which the number of Gems is decreased, shows fewer subsets U snRNAs. Interestingly, in the central nervous system, U snRNAs belonging to the minor spliceosomes are markedly reduced. In ALS, the U12 snRNA is decreased only in the tissue affected by ALS and not in other tissues. Although the molecular mechanisms underlying the decreased U12 snRNA resulting in cell dysfunction and cell death in motor neuron diseases remain unclear, these findings

suggest that the disturbance of nuclear bodies and minor splicing may underlie the common molecular pathogenesis of motor neuron diseases. Motor neuron system selectivity is a major mystery of motor neuron diseases. Although research has shown that the pathology is not restricted to motor neurons but also extends into other PI3K Inhibitor Library research buy neurons as well as glial cells, the selective vulnerability of motor neurons is a characteristic feature of amyotrophic lateral sclerosis (ALS). However, the molecular mechanism underlying the vulnerability of the motor neuron system has not been fully explained. To clarify this issue, researchers must clarify what distinguishes the motor neuron. Researchers have identified several molecular markers and physiological characters that distinguish motor neurons from others.[1] However, the morphology and location of the cell have been used as the most significant signature for identifying motor neurons in tissues. The

cells of the CNS are diverse and complex, and they are mostly defined by their shape, size PTK6 and location in the tissues. The complexity of the cells reflects the complexity of the cells’ RNAs. The diversity of RNAs results in part from the methylation of DNA, but studies have shown that other mechanisms also control cell-specific RNA diversity. A higher structure of the nucleus, chromatin, and nuclear bodies, is another mechanism that regulates the cell-specific RNA diversity. Recent findings have revealed that chromatin has a unique structure and location in the nucleus in each type of cell. The chromatin structure is strongly associated with the diversity of RNA.[2] Moreover, the other intranuclear structures also play an important role in maintaining cell function and cell survival. Thus, the intracellular location or character of nuclear bodies may also differ in each cell type.