pep2-EVKI

Product Name:pep2-EVKI

Synonyms:AKOS024456694

CAS No:1315378-67-6

Purity:95%

Molar Mass:1326.5

Chemical Formula:C62H95N13O19

Storage:Store at -20 degrees Celsius

Sequence:YNVYGIEEVKI

Application:pep2-EVKI is a specialized peptide designed to interfere with specific protein-protein interactions within kinase-mediated signaling pathways. This peptide is critical for studying the regulation of phosphorylation events and their downstream effects on cellular processes such as growth, differentiation, and apoptosis. pep2-EVKI mimics a key regulatory sequence, making it a powerful tool for exploring therapeutic strategies aimed at modulating aberrant kinase activity. Its high purity and stability ensure reliable and reproducible results, making pep2-EVKI an essential component in advanced research focused on cellular signaling and targeted drug development.

Current Research:

pep2-EVKI (sequence: YNVYGIEEVKI) is a synthetic peptide inhibitor that selectively disrupts the interaction between the AMPA receptor subunit GluA2 and the protein interacting with C kinase 1 (PICK1) at the C-terminal PDZ-binding domain. This selective inhibition does not affect GluA2's binding to other PDZ domain-containing proteins such as glutamate receptor-interacting protein (GRIP) or AMPA receptor-binding protein (ABP).
The GluA2-PICK1 interaction plays a pivotal role in the trafficking and synaptic localization of AMPA receptors, which are critical for synaptic plasticity mechanisms like long-term potentiation (LTP) and long-term depression (LTD). By specifically inhibiting this interaction, pep2-EVKI serves as a valuable tool for dissecting the molecular underpinnings of synaptic transmission and plasticity. Notably, application of pep2-EVKI has been shown to block the maintenance of both LTP and LTD, underscoring PICK1's essential role in these processes.
In the context of neurological research, pep2-EVKI has been instrumental in elucidating the contributions of AMPA receptor dynamics to various physiological and pathological states. For instance, studies utilizing pep2-EVKI have demonstrated that disrupting GluA2-PICK1 interactions can modulate synaptic strength without altering basal AMPA receptor-mediated synaptic transmission. This specificity highlights the therapeutic potential of targeting such protein-protein interactions in conditions characterized by aberrant synaptic plasticity, including certain neurodegenerative diseases and psychiatric disorders.
Moreover, the structural and functional insights gained from studies employing pep2-EVKI have informed the development of novel therapeutic strategies aimed at modulating synaptic plasticity. By providing a means to selectively interfere with specific protein interactions involved in AMPA receptor regulation, pep2-EVKI contributes to a deeper understanding of synaptic function and offers a framework for the design of targeted interventions in neurological disorders.
In summary, pep2-EVKI is a potent and selective inhibitor of the GluA2-PICK1 interaction, serving as a critical tool in neuroscience research to unravel the complex mechanisms governing synaptic plasticity and to explore potential therapeutic avenues for neurological diseases.

Reference:

Lu, H. F., Wu, P. F., Yang, Y. J., Xiao, W., Fan, J., Liu, J., ... & Chen, J. G. (2014). Interactions between N-ethylmaleimide-sensitive factor and GluR2 in the nucleus accumbens contribute to the expression of locomotor sensitization to cocaine. Journal of Neuroscience, 34(10), 3493-3508.