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Chemical Compound Review

Kainate     (2S,3S,4S)-3-(carboxymethyl)- 4-prop-1-en-2...

Synonyms: Helminal, Digenin, Kainsaeure, Digensaeure, UPCMLD-DP146, ...
 
 
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Disease relevance of Digenic acid

 

Psychiatry related information on Digenic acid

 

High impact information on Digenic acid

  • Our results provide evidence that JNP is dispensable for mouse development, and identify c-Jun as the essential substrate of JNK signalling during kainate-induced neuronal apoptosis [1].
  • GLP-1R-deficient mice also have enhanced seizure severity and neuronal injury after kainate administration, with an intermediate phenotype in heterozygotes and phenotypic correction after Glp1r gene transfer in hippocampal somatic cells [9].
  • Systemic administration of [Ser(2)]exendin(1-9) in wild-type animals prevents kainate-induced apoptosis of hippocampal neurons [9].
  • There are three classes of ionotropic glutamate receptor, namely NMDA (N-methyl-D-aspartate), AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid) and kainate receptors; critical roles in synaptic plasticity have been identified for two of these [10].
  • Recent work on the physiological function of kainate receptors has focused on the hippocampus, where repetitive activation of the mossy-fibre pathway generates a slow, kainate-receptor-mediated excitatory postsynaptic current (EPSC) [11].
 

Chemical compound and disease context of Digenic acid

 

Biological context of Digenic acid

 

Anatomical context of Digenic acid

 

Associations of Digenic acid with other chemical compounds

 

Gene context of Digenic acid

  • Some of the subtypes are also coupled to inward rectifying K(+) channels (SSTR2, 3, 4, 5), to voltage-dependent Ca(2+) channels (SSTR1, 2), a Na(+)/H(+) exchanger (SSTR1), AMPA/kainate glutamate channels (SSTR1, 2), phospholipase C (SSTR2, 5), and phospholipase A(2) (SSTR4) [28].
  • The coexpression of GluR-K2 with either GluR-K3 or GluR-K1 results in the formation of channels whose current-voltage relationships differ from those of the individual subunits alone and more closely approximate the properties of kainate receptors in neurons [29].
  • SAP90 binds and clusters kainate receptors causing incomplete desensitization [30].
  • Transcripts of the GluR7 gene are evident in brain areas that bind [3H]kainate and are susceptible to kainate-induced neurotoxicity [31].
  • Rapid and differential regulation of AMPA and kainate receptors at hippocampal mossy fibre synapses by PICK1 and GRIP [32].
 

Analytical, diagnostic and therapeutic context of Digenic acid

References

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  30. SAP90 binds and clusters kainate receptors causing incomplete desensitization. Garcia, E.P., Mehta, S., Blair, L.A., Wells, D.G., Shang, J., Fukushima, T., Fallon, J.R., Garner, C.C., Marshall, J. Neuron (1998) [Pubmed]
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