a(GO:synapse)
to p(HGNC:MAPT)
To date, the physiological function of dendritic tau has not been well characterized. It may be involved in the regulation of synaptic plasticity, as pharmacological synaptic activation induces translocation of endogenous tau from the dendritic shaft to excitatory postsynaptic compartments in cultured mouse neurons and in acute hippocampal slices
act(a(GO:synapse)) increases tloc(p(HGNC:MAPT), fromLoc(GO:"dendritic shaft"), toLoc(GO:"excitatory synapse"))
13c3e000f9
Hyperphosphorylation, mutations and overexpression of tau can drive the mislocalization of tau into postsynaptic spines, resulting in synaptic dysfunction
act(a(GO:synapse)) negativeCorrelation p(HGNC:MAPT)
4ac63394c7
tloc(p(HGNC:MAPT), fromLoc(GO:axon), toLoc(MESH:"Dendritic Spines")) decreases act(a(GO:synapse))
72663a4b2f
p(HGNC:MAPT) negativeCorrelation act(a(GO:synapse))
6fb5e96124
Tau oligomers from TauRDΔK and TauFLΔK mice reduced the density of the synapses by w50%, whereas tau from wild-type mice had no effect on the density (Fig. 7G).
p(HGNC:MAPT) causesNoChange a(GO:synapse)
f43933aed8
First, hyperphosphorylation of tau might induce tau missorting from axons to the somatodendritic compartment, which can cause synaptic dysfunction
tloc(p(HGNC:MAPT), fromLoc(GO:axon), toLoc(GO:"somatodendritic compartment")) decreases act(a(GO:synapse))
ce658de44c
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.