Pep2m,myristoylatedTFA(Myr-Pep2mTFA)是一种细胞通透性肽。Pep2m,myristoylatedTFA能破坏蛋白激酶ζ(PKMζ)下游靶点NSF/GluR2相互作用。PKMζ具有自主活性的PKC同工酶。
Pep2m, myristoylated TFA (Myr-Pep2m TFA) is a cell-permeable peptide. Pep2m, myristoylated TFA can disrupt the protein kinase ζ (PKMζ) downstream targets, N-ethylmaleimide-sensitive factor/glutamate receptor subunit 2 (NSF/GluR2) interactions. PKMζ is an autonomously active isozyme of protein kinase C (PKC)[1][2].
Pep2m, myristoylated TFA (10 μM) blocks PKMζ-mediated AMPA receptor (AMPAR) potentiation[1].Pep2m, myristoylated TFA does not block the increase of PKMζ in the hippocampal slices during long-term potentiation (LTP) maintenance, indicating that blocking NSF/GluR2 interactions do not prevent the induction of PKMζ synthesis[1].Pep2m, myristoylated TFA blocks NSF/GluR2-mediated AMPAR trafficking, and reverses persistent potentiation at both the strongly stimulates synapses and the weakly stimulats synapses that underwent synaptic tagging and capture[1].
Pep2m, myristoylated TFA (10 µg) results in an increase in paw withdrawal thresholds (PWTs) on nociceptive responses in the formalin test[2]. Animal Model: Female and male Long-Evans hooded rats (8 weeks)[2]
[1]. Yudong Yao, et al. PKMζ Maintains Late Long-Term Potentiation by N-Ethylmaleimide-Sensitive Factor/GluR2-Dependent Trafficking of Postsynaptic AMPA Receptors. J Neurosci. 2008 Jul 30; 28(31): 7820-7827. [2]. Nicole C George, et al. Sex differences in the contributions of spinal atypical PKCs and downstream targets to the maintenance of nociceptive sensitization. Mol Pain. 2019; 15: 1744806919840582.
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