The Stress-Induced Atf3-Gelsolin Cascade Underlies Dendritic Spine Deficits in Neuronal Models of Tuberous Sclerosis Complex.
Duyu NieZehua ChenDarius Ebrahimi-FakhariAlessia Di NardoKristina JulichVictoria R BradfordYung-Chih ChengClifford J WoolfMyriam HeimanMustafa SahinPublished in: The Journal of neuroscience : the official journal of the Society for Neuroscience (2015)
Tuberous sclerosis complex (TSC) is a genetic disease associated with epilepsy and autism. Dysregulated protein synthesis has been implicated as a cause of this disease. However, cell type-specific translational profiles that are aberrant in this disease are unknown. Here we show that expression of many stress and/or activity-dependent proteins is highly induced while some synaptic proteins are repressed in neurons missing the Tsc2 gene expression. Identification of genes whose translation is abnormal in TSC may provide insights to previously unidentified therapeutic targets.
Keyphrases
- stress induced
- gene expression
- poor prognosis
- autism spectrum disorder
- traumatic brain injury
- transcription factor
- intellectual disability
- oxidative stress
- copy number
- endoplasmic reticulum stress
- diabetic rats
- temporal lobe epilepsy
- high glucose
- blood brain barrier
- drug induced
- subarachnoid hemorrhage
- prefrontal cortex