Articles tagged with Alternative Splicing
Scientists used a transgenic system to monitor developmental regulated alternative mRNA splicing in live C. elegans worms, revealing conserved molecular mechanisms across metazoan evolution. The study enables experimental analysis of regulation mechanisms underlying alternative splicing patterns.
A University of Toronto-led study found that alternative splicing is more highly regulated in nervous system tissues, allowing for specific functions in memory and learning. This new understanding of gene regulation has significant implications for human diseases such as cancers.
Dr. Douglas Black and colleagues reveal that a switch in PTB expression induces changes in alternative splicing patterns during neuronal development, adding a new layer of genetic regulation. This reprogramming enables the creation of unique genetic code in post-mitotic neurons.
Researchers discovered that microRNA miR-133 targets the alternative splicing factor nPTB during early myogenesis, promoting muscle cell differentiation. This regulation affects a larger temporal program of muscle cell gene expression by altering mRNA splicing.
A new RNA map provides the first comprehensive understanding of how alternative splicing works throughout the genome. The results reveal that specific locations of short RNA snippets affect the regulation of alternative splicing in the brain, with implications for learning, memory, neurological diseases, and cancer biology.
A new study has shed light on the process of alternative splicing, which allows one gene to produce multiple proteins. Researchers discovered that tandem repeats between exons are highly correlated with the process, enabling them to predict genes that can re-arrange and potentially leading to disease.
Hormones like estrogen and progesterone regulate protein production in cells by recruiting coactivators that enhance RNA production and alter splicing. This controlled process results in different proteins being made, leading to diverse protein diversity.
The study identifies a protein called ASF/SF2 as a regulator of calcium enzyme responsible for heart contraction and tissue growth. The researchers found differences in male versus female mice, with males experiencing greater disease and dying earlier.