Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.11 (AMPK)
 12,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sequential alterations in the binding of [3H]cyclic AMP (cAMP) as an indicator of cAMP-dependent protein kinase (cAMP-DPK) binding activity following transient cerebral ischaemia were studied in the gerbil brain using receptor autoradiography. Transient ischaemia was induced for 10 min. [3H]cAMP binding in the stratum oriens and pyramidale of the hippocampal CA1 sector significantly decreased in the early post-ischaemic stage and showed severe reduction 7 days and 1 month after recirculation. By contrast, [3H]cAMP binding showed no significant alterations in the stratum radiatum of the hippocampal CA1 sector and the stratum pyramidale of the hippocampal CA3 sector up to 48 h after ischaemia. However, the binding in these areas significantly decreased 7 days and 1 month after ischaemia. The stratum lacunosum-moleculare of the hippocampal CA1 sector and dentate gyrus showed no significant changes in [3H]cAMP binding throughout the recirculation period. However, in the dorsolateral part of the striatum, where severe neuronal damage was seen morphologically, [3H]cAMP binding was significantly reduced only one month after ischaemia. These results indicate that marked alteration of intracellular signal transduction precedes neuronal damage in the hippocampal CA1 sector, but not in the striatum. Furthermore, our autoradiographic data suggest that post-ischaemic alteration in [3H]cAMP binding between the hippocampal CA1 sector and striatum may be produced by different mechanisms.
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PMID:Sequential changes of [3H]cyclic AMP binding in the gerbil brain following transient cerebral ischaemia. 810 69

Phosphorylation of the GluR1 subunit of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor has been implicated in the regulation of the receptor channel. We investigated the effects of transient global ischemia in rats on phosphorylation of the GluR1 subunit in the hippocampal CA1 and CA3/dentate gyrus. Transient ischemia induced an increase in the phosphorylation of GluR1 at Ser831 in the CA1 at 1 h of reperfusion. In contrast, the phosphorylation of Ser845 in neither region was affected by the ischemia. The amounts of calcium/calmodulin-dependent kinase (CaMKII) and its activated form, but not cAMP-dependent protein kinase subunits, were increased in a crude membrane fraction after ischemia. The results suggest that an activated CaMKII may phosphorylate Ser831 of GluR1 and a consequent phosphorylation of GluR1 may be related to pathogenic events occurring in the vulnerable subfield of the hippocampus after transient global ischemia.
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PMID:Transient global ischemia enhances phosphorylation of the GluR1 subunit of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor in the hippocampal CA1 region in rats. 1267 37