ZIP

Product Name:ZIP

CAS No:863987-12-6

Purity:95%

Molar Mass:1928.4

Chemical Formula:C90H154N30O17

Storage:Store at -20 degrees Celsius

Sequence:SIYRRGARRWRKL

Target:PKM??

Application:

ZIP (?? inhibitory peptide) is a synthetic peptide that serves as a selective inhibitor of protein kinase M zeta (PKM??), an isoform of protein kinase C (PKC). PKM?? is involved in maintaining long-term potentiation (LTP), a critical process for synaptic plasticity and memory storage in the brain. ZIP is widely used in neuroscience research to study memory erasure, synaptic plasticity, and the role of PKM?? in learning and memory. By inhibiting PKM??, ZIP can reverse LTP and has been shown to disrupt previously formed memories in animal models, making it a crucial tool for understanding memory maintenance and neurological conditions related to memory dysfunction.

Current Research:

Zeta inhibitory peptide (ZIP), with the CAS number 863987-12-6, is a synthetic, cell-permeable peptide that functions as a selective inhibitor of protein kinase M?? (PKM??), an atypical isoform of protein kinase C (PKC). PKM?? is implicated in the maintenance of long-term potentiation (LTP), a cellular mechanism underlying learning and memory. ZIP has been instrumental in elucidating the role of PKM?? in synaptic plasticity and memory processes.
The peptide sequence of ZIP is Myr-Ser-Ile-Tyr-Arg-Arg-Gly-Ala-Arg-Arg-Trp-Arg-Lys-Leu-OH, where "Myr" denotes an N-terminal myristoylation, enhancing its membrane permeability. By mimicking the pseudosubstrate region of PKM??, ZIP effectively inhibits its kinase activity.
In vitro studies have demonstrated that ZIP can reverse late-phase LTP in hippocampal slices, with an IC?? ranging from 1 to 2.5 ??M. In vivo, central administration of ZIP has been shown to disrupt established spatial memory, indicating its potential to interfere with memory maintenance. These findings have positioned ZIP as a critical tool in neuroscience research, particularly in studies investigating the molecular underpinnings of memory storage and persistence.
However, the specificity of ZIP has been a subject of debate. Some studies suggest that its effects may not be exclusively mediated through PKM?? inhibition, as ZIP has been observed to influence other signaling pathways, including those involving ionotropic glutamate receptors. This has led to discussions regarding the interpretation of experimental outcomes where ZIP is utilized, emphasizing the necessity for cautious analysis of its effects.
In summary, ZIP serves as a potent inhibitor of PKM??, offering valuable insights into the molecular mechanisms of synaptic plasticity and memory. Nonetheless, its broader impact on various signaling pathways necessitates careful consideration in experimental designs and data interpretation.

Reference:

Kambe, T., Hashimoto, A., & Fujimoto, S. (2014). Current understanding of ZIP and ZnT zinc transporters in human health and diseases. Cellular and molecular life sciences, 71, 3281-3295.