CNTNAP2 Protein Is Degraded by the Ubiquitin-Proteasome System and the Macroautophagy-Lysosome Pathway.

Contactin-associated protein-like 2 (CNTNAP2) gene, located on chromosome 7q35, is one of the largest genes in the human genome. CNTNAP2 protein is a type-I transmembrane protein specifically expressed in the nervous system, with versatile roles in the axonal organization, synaptic functions, neuronal migration, and functional connectivity. CNTNAP2 has been widely investigated as a risk gene for autism spectrum disorder (ASD), and recent studies also implicated CNTNAP2 in Alzheimer's disease (AD).

The synapse as a treatment avenue for Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder with devastating symptoms, including memory impairments and cognitive deficits. Hallmarks of AD pathology are amyloid-beta (Aβ) deposition forming neuritic plaques and neurofibrillary tangles (NFTs). For many years, AD drug development has mainly focused on directly targeting the Aβ aggregation or the formation of tau tangles, but this disease has no cure so far.

Transcriptional activation of USP16 gene expression by NFκB signaling.

Ubiquitin Specific Peptidase 16 (USP16) has been reported to contribute to somatic stem-cell defects in Down syndrome. However, how this gene being regulated is largely unknown. To study the mechanism underlying USP16 gene expression, USP16 gene promoter was cloned and analyzed by luciferase assay.

Autism-related behaviors in the cyclooxygenase-2-deficient mouse model.

Prostaglandin E2 (PGE2) is an endogenous lipid molecule involved in normal brain development. Cyclooxygenase-2 (COX2) is the main regulator of PGE2 synthesis. Emerging clinical and molecular research provides compelling evidence that abnormal COX2/PGE2 signaling is associated with autism spectrum disorder (ASD).