Journal
TRENDS IN CELL BIOLOGY
Volume 21, Issue 10, Pages 594-603Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2011.07.003
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Funding
- Deutsche Forschungsgemeinschaft DFG [SFB497/B8, BO1718/3-1, BO1718/4-1]
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Intact synaptic homeostasis is a fundamental prerequisite for a healthy brain. Thus, it is not surprising that altered synaptic morphology and function are involved in the molecular pathogenesis of so-called synaptopathies including autism, schizophrenia (SCZ) and Alzheimer's disease (AD). Intriguingly, various recent studies revealed a crucial role of postsynaptic ProSAP/Shank scaffold proteins in all of the aforementioned disorders. Considering these findings, we follow the hypothesis that ProSAP/Shank proteins are key regulators of synaptic development and plasticity with clear-cut isoform-specific roles. We thus propose a model where ProSAP/Shank proteins are in the center of a postsynaptic signaling pathway that is disrupted in several neuropsychiatric disorders.
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