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Graf Isolan
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Untersuchte Arbeit:
Seite: 24, Zeilen: 1-12
Quelle: Blitzer et al 2005
Seite(n): 115, Zeilen: Legende zu Figure 2
1.6.3. The interaction of three major postsynaptic signaling pathways in LTP

Ca2+/calmodulin protein kinase II (CaMKII), mitogen-activated protein kinase (MAPK), and adenosine 3′,5′-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) are all required for the induction of LTP (Frey et al., 1993;English and Sweatt, 1997;Bortolotto and Collingridge, 1998). The influx of Ca2+ through N-methyl-D-aspartate-type receptors (NMDA-R) or voltage-dependent Ca2+ channels (VDCC) can engage signaling cascades that activate these kinases. MAPK and CaMKII can promote the phosphorylation of each other, and MAPK is required for an increase in CaMKII levels produced by LTP-inducing stimulation (Giovannini et al., 2001). PKA activity promotes CaMKII phosphorylation by indirectly inhibiting the protein phosphatase PP1, which would otherwise limit the degree or persistence of CaMKII activation by dephosphorylating the kinase (Atkins et al., 2005).


15. Atkins CM, Davare MA, Oh MC, Derkach V, Soderling TR (2005) Bidirectional regulation of cytoplasmic polyadenylation element-binding protein phosphorylation by Ca2+/calmodulin-dependent protein kinase II and protein phosphatase 1 during hippocampal long-term potentiation. J Neurosci 25: 5604-5610.

26. Bortolotto ZA, Collingridge GL (1998) Involvement of calcium/calmodulin-dependent protein kinases in the setting of a molecular switch involved in hippocampal LTP. Neuropharmacology 37: 535-544.

47. English JD, Sweatt JD (1997) A requirement for the mitogen-activated protein kinase cascade in hippocampal long term potentiation. J Biol Chem 272: 19103-19106.

54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664.

64. Giovannini MG, Blitzer RD, Wong T, Asoma K, Tsokas P, Morrison JH, Iyengar R, Landau EM (2001) Mitogen-activated protein kinase regulates early phosphorylation and delayed expression of Ca2+/calmodulin-dependent protein kinase II in long-term potentiation. J Neurosci 21: 7053-7062.

Figure 2. The interaction of three major postsynaptic signaling pathways in LTP. Ca2+/calmodulin protein kinase II (CaMKII), mitogen-activated protein kinase (MAPK), and adenosine 3’,5’-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) are all required for the induction of LTP. The influx of Ca2+ through N-methyl-D-aspartate-type receptors (NMDA-R) or voltage-dependent Ca2+ channels (VDCC) can engage signaling cascades that activate these kinases, and PKA can additionally be activated by β-adrenergic receptors (β-AR) and other G protein-coupled receptors. MAPK and CaMKII can promote the phosphorylation of each other, and MAPK is required for an increase in CaMKII levels produced by LTP-inducing stimulation. PKA activity promotes CaMKII phosphorylation by indirectly inhibiting the protein phosphatase PP1, which would otherwise limit the degree or persistence of CaMKII activation by dephosphorylating the kinase.
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