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Fig. 5 | Molecular Brain

Fig. 5

From: ApCPEB4, a non-prion domain containing homolog of ApCPEB, is involved in the initiation of long-term facilitation

Fig. 5

Phosphorylation of ApCPEB4 is required for both the LTF formation. a In vitro phosphorylation assay showed that purified ApCPEB4 was directly phosphorylated by PKA on its 294th threonine residue. b Phosphorylation of purified ApCPEB4 was examined using Aplysia pleural ganglia extracts as an endogenous mixture of kinases. Concurrent treatment of 40 μM KT5720 (KT), a PKA inhibitor, significantly reduced the amount of phosphorylation on ApCPEB4. Neither 20 μM PD98059 (PD), a MEK inhibitor, nor 10 μM chelerythrine (Chele), a PKC inhibitor, affected the phosphorylation of ApCPEB4. c Phosphorylation of ApCPEB4 on its 294th threonine residue was required for the LTF formation. (c, left) Representative traces of EPSP measured at the sensory-to-motor synapses before and 24 h after the 5 pulses of 5-HT. (c, right) Bar graph represents the mean percentage change ± SEM in EPSP amplitude. Overexpression of ApCPEB4(T294A), non-phosphorylatable mutant of ApCPEB4, significantly blocked LTF. *, p < 0.05. two-tailed unpaired t test

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