Alternative splicing of transcript mediates the response of circadian clocks to temperature changes.

Circadian clocks respond to temperature changes over the calendar year, allowing organisms to adjust their daily biological rhythms to optimize health and fitness. In , seasonal adaptations are regulated by temperature-sensitive alternative splicing (AS) of () and () genes that encode key transcriptional repressors of clock gene expression. Although () gene encodes the critical activator of circadian gene expression, AS of its transcripts and its potential role in temperature regulation of clock function have not been explored.

Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability.

Disruption of SYNGAP1 directly causes a genetically identifiable neurodevelopmental disorder (NDD) called SYNGAP1-related intellectual disability (SRID). Without functional SynGAP1 protein, individuals are developmentally delayed and have prominent features of intellectual disability (ID), motor impairments, and epilepsy. Over the past two decades, there have been numerous discoveries indicating the critical role of Syngap1.

Alternative splicing of transcript mediates the response of circadian clocks to temperature changes.

Circadian clocks respond to temperature changes over the calendar year, allowing organisms to adjust their daily biological rhythms to optimize health and fitness. In , seasonal adaptations and temperature compensation are regulated by temperature-sensitive alternative splicing (AS) of () and () genes that encode key transcriptional repressors of clock gene expression. Although () gene encodes the critical activator of clock gene expression, AS of its transcripts and its potential role in temperature regulation of clock function have not been explored.

Hyperexcitability and translational phenotypes in a preclinical mouse model of Related Intellectual Disability.

Disruption of directly causes a genetically identifiable neurodevelopmental disorder (NDD) called SYNGAP1-related intellectual disability (SRID). Without functional SynGAP1 protein, individuals are developmentally delayed and have prominent features of intellectual disability, motor impairments, and epilepsy. Over the past two decades, there have been numerous discoveries indicting the critical role of Syngap1.

Hyperexcitability and translational phenotypes in a preclinical model of mutations.

is a critical gene for neuronal development, synaptic structure, and function. Although rare, the disruption of directly causes a genetically identifiable neurodevelopmental disorder (NDD) called SYNGAP1-related intellectual disability. Without functional SynGAP1 protein, patients present with intellectual disability, motor impairments, and epilepsy.