p(HGNC:MARK4) negativeCorrelation p(RGD:Gria1)

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PubMed:22156579

Overexpression of MARK4 led to tau hyperphosphorylation, reduced expression of synaptic markers, and loss of dendritic spines and synapses, phenotypes also observed after Aβ treatment. Importantly, expression of a non-phosphorylatable form of tau with the PAR-1/MARK site mutated blocked the synaptic toxicity induced by MARK4 overexpression or Aβ treatment. To probe the involvement of endogenous MARK kinases in mediating the synaptic toxicity of Aβ, we employed a peptide inhibitor capable of effectively and specifically inhibiting the activities of all PAR-1/MARK family members. This inhibitor abrogated the toxic effects of Aβ oligomers on dendritic spines and synapses as assayed at the morphological and electrophysiological levels.

Related Edges 8

• a(GO:"dendritic spine") negativeCorrelation p(HGNC:MARK4)
• a(GO:synapse) negativeCorrelation p(HGNC:MARK4)
• p(HGNC:MARK4) increases a(HBP:"Tau epitope, 12E8")
• p(HGNC:MARK4) negativeCorrelation act(p(RGD:Dlg4))
• p(HGNC:MARK4) negativeCorrelation a(GO:"dendritic spine")
• p(HGNC:MARK4) negativeCorrelation a(GO:synapse)
• act(p(RGD:Dlg4)) negativeCorrelation p(HGNC:MARK4)
• p(RGD:Gria1) negativeCorrelation p(HGNC:MARK4)

Uberon

hippocampal formation

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