ArticleMolecular neurobiology2017
Increased Src Family Kinase Activity Disrupts Excitatory Synaptic Transmission and Impairs Remote Fear Memory in Forebrain Shp2-Deficient Mice.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- How muscle talks to brain: apelin protein mediates exercise-induced antidepressant effects.Molecular psychiatry · 2026Article
- SHP2 regulates GluA2 tyrosine phosphorylation required for AMPA receptor endocytosis and mGluR-LTD.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Chronic administration of ketamine induces cognitive deterioration by restraining synaptic signaling.Molecular psychiatry · 2021Article
- Src and Memory: A Study of Filial Imprinting and Predispositions in the Domestic Chick.Frontiers in physiology · 2021Article
- The Noonan syndrome-associated D61G variant of the protein tyrosine phosphatase SHP2 prevents synaptic down-scaling.The Journal of biological chemistry · 2020Article
- Connecting the dots between SHP2 and glutamate receptors.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Review
- Excitatory neuron-specific SHP2-ERK signaling network regulates synaptic plasticity and memory.Science signaling · 2019Article
- Kinase and Phosphatase Engagement Is Dissociated Between Memory Formation and Extinction.Frontiers in molecular neuroscience · 2019Article
- Noonan Syndrome-Associated SHP2 Dephosphorylates GluN2B to Regulate NMDA Receptor Function.Cell reports · 2018Article
- Src homology 2 domain-containing phosphotyrosine phosphatase 2 (Shp2) controls surface GluA1 protein in synaptic homeostasis.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Src homolog domain-containing phosphatase 2 (Shp2) signals a variety of cellular and physiological functions including learning and memory. Dysregulation of ERK signaling is known to be responsible for the cognitive deficits associated with gain-of-function mutated Shp2 mimicking Noonan syndrome. However, here, we report that CaMKIIα-cre induced knockout (CaSKO) of Shp2 in hippocampal pyramidal neurons resulted in increased Src activity, upregulated phosphorylation of N-methyl-D-aspartate receptors (NMDARs) at Y1325 of GluN2A and at Y1472 of GluN2B, disrupted the balance of synaptic transmission, and impaired long-term potentiation and remote contextual fear memory. Administration of PP2, a specific Src family kinase inhibitor, reversed the tyrosine phosphorylation of NMDARs, restored basal synaptic transmission, and rescued the contextual fear memory deficit in CaSKO mice without altering the phospho-ERK level. Taken together, our results reveal a novel role of Shp2 in NMDAR-dependent synaptic function and fear memory via the Src signaling pathway rather than the ERK pathway, and suggest a complicated mechanism for Shp2-associated cognitive deficits.
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