0000000000680703
AUTHOR
Irene Reyes-resina
Preventing Jacob-induced transcriptional inactivation of CREB protects synapses from β-amyloid in Alzheimer’s Disease
Abstract Disruption of transcriptional activity of cAMP–responsive element-binding protein (CREB), a master regulator of cell survival and plasticity-related gene expression, is a hallmark of Alzheimer’s disease (AD). CREB shut-off results in early synaptic dysfunction, contributes to AD pathology and eventually neuronal cell death and is elicited by amyloid-β (Aβ)-induced activation of extrasynaptic N-methyl-D-aspartate-receptors (NMDAR). In previous work we found that the protein messenger Jacob encodes and transduces the synaptic or extrasynaptic origin of NMDAR signals to the nucleus. In response to cell survival and plasticity-related synaptic NMDAR stimulation macromolecular transport…
Detection, Analysis, and Quantification of GPCR Homo- and Heteroreceptor Complexes in Specific Neuronal Cell Populations Using the In Situ Proximity Ligation Assay
GPCR’s receptosome operates via coordinated changes between the receptor expression, their modifications and interactions between each other. Perturbation in specific heteroreceptor complexes and/or their balance/equilibrium with other heteroreceptor complexes and corresponding homoreceptor complexes is considered to have a role in pathogenic mechanisms. Such mechanisms lead to mental and neurological diseases, including drug addiction, depression, Parkinson’s disease, and schizophrenia. To understand the associations of GPCRs and to unravel the global picture of their receptor–receptor interactions in the brain, different experimental detection techniques for receptor–receptor interactions…