Pep2m, myristoylated

Pep2m, myristoylated (Myr-Pep2m) is a cell-permeable peptide. Pep2m, myristoylated 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].

Signaling Pathways >> Epigenetics >> PKC

Research Areas >> Neurological Disease

Signaling Pathways >> TGF-beta/Smad >> PKC

NSF/GluR2 interactions[1]

Pep2m, myristoylated (10 μM) blocks PKMζ-mediated AMPA receptor (AMPAR) potentiation[1]. Pep2m, myristoylated 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 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 (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] Dosage: 10 µg (in 20 µL) Administration: Intrathecal injection Result: Resulted in an increase in PWTs, in both male and female rats at various time points tested.

[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.