pep2-AVKIPeptide inhibitor of GluR2 subunit binding to PICK1 CAS# 1315378-69-8 |
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Quality Control & MSDS
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| Cas No. | 1315378-69-8 | SDF | Download SDF |
| PubChem ID | 90479810 | Appearance | Powder |
| Formula | C60H93N13O17 | M.Wt | 1268.47 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble to 2 mg/ml in water | ||
| Sequence | YNVYGIEAVKI | ||
| Chemical Name | (2S,3S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-amino-3-(4-hydroxyphenyl)propanoyl]amino]-4-oxobutanoyl]amino]-3-methylbutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]acetyl]amino]-3-methylpentanoyl]amino]-4-carboxybutanoyl]amino]propanoyl]amino]-3-methylbutanoyl]amino]hexanoyl]amino]-3-methylpentanoic acid | ||
| SMILES | CCC(C)C(C(=O)NC(CCC(=O)O)C(=O)NC(C)C(=O)NC(C(C)C)C(=O)NC(CCCCN)C(=O)NC(C(C)CC)C(=O)O)NC(=O)CNC(=O)C(CC1=CC=C(C=C1)O)NC(=O)C(C(C)C)NC(=O)C(CC(=O)N)NC(=O)C(CC2=CC=C(C=C2)O)N | ||
| Standard InChIKey | SODUKHPKIVEQLX-OCXIBOJYSA-N | ||
| Standard InChI | InChI=1S/C60H93N13O17/c1-10-32(7)49(59(88)67-41(23-24-46(78)79)54(83)65-34(9)51(80)71-47(30(3)4)57(86)66-40(14-12-13-25-61)55(84)73-50(60(89)90)33(8)11-2)70-45(77)29-64-53(82)42(27-36-17-21-38(75)22-18-36)69-58(87)48(31(5)6)72-56(85)43(28-44(63)76)68-52(81)39(62)26-35-15-19-37(74)20-16-35/h15-22,30-34,39-43,47-50,74-75H,10-14,23-29,61-62H2,1-9H3,(H2,63,76)(H,64,82)(H,65,83)(H,66,86)(H,67,88)(H,68,81)(H,69,87)(H,70,77)(H,71,80)(H,72,85)(H,73,84)(H,78,79)(H,89,90)/t32-,33-,34-,39-,40-,41-,42-,43-,47-,48-,49-,50-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Inhibitor peptide that selectively disrupts binding of the AMPA receptor subunit GluA2 (at the C-terminal PDZ site) to protein interacting with C kinase (PICK1). Does not affect binding of GluA2 to GRIP or ABP and does not increase AMPA current amplitude or affect long term depression (LTD). |
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Trafficking of presynaptic AMPA receptors mediating neurotransmitter release: neuronal selectivity and relationships with sensitivity to cyclothiazide.[Pubmed:16242162]
Neuropharmacology. 2006 Mar;50(3):286-96.
Postsynaptic glutamate AMPA receptors (AMPARs) can recycle between plasma membrane and intracellular pools. In contrast, trafficking of presynaptic AMPARs has not been investigated. AMPAR surface expression involves interactions between the GluR2 carboxy tail and various proteins including glutamate receptor-interacting protein (GRIP), AMPA receptor-binding protein (ABP), protein interacting with C kinase 1 (PICK1), N-ethyl-maleimide-sensitive fusion protein (NSF). Here, peptides known to selectively block the above interactions were entrapped into synaptosomes to study the effects on the AMPA-evoked release of [3H]noradrenaline ([3H]NA) and [3H]acetylcholine ([3H]ACh) from rat hippocampal and cortical synaptosomes, respectively. Internalization of pep2-SVKI to prevent GluR2-GRIP/ABP/PICK1 interactions potentiated the AMPA-evoked release of [3H]NA but left unmodified that of [3H]ACh. Similar potentiation was caused by pep2-AVKI, the blocker of GluR2-PICK1 interaction. Conversely, a decrease in the AMPA-evoked release of [3H]NA, but not of [3H]ACh, was caused by pep2m, a selective blocker of the GluR2-NSF interaction. In the presence of pep2-SVKI the presynaptic AMPARs on noradrenergic terminals lost sensitivity to cyclothiazide. AMPARs releasing [3H]ACh, but not those releasing [3H]NA, were sensitive to spermine, suggesting that they are GluR2-lacking AMPARs. To conclude: (i) release-regulating presynaptic AMPARs constitutively cycle in isolated nerve terminals; (ii) the process exhibits neuronal selectivity; (iii) AMPAR trafficking and desensitization may be interrelated.
NSF ATPase and alpha-/beta-SNAPs disassemble the AMPA receptor-PICK1 complex.[Pubmed:11931741]
Neuron. 2002 Mar 28;34(1):53-67.
AMPA receptor (AMPAR) trafficking is crucial for synaptic plasticity that may be important for learning and memory. NSF and PICK1 bind the AMPAR GluR2 subunit and are involved in trafficking of AMPARs. Here, we show that GluR2, PICK1, NSF, and alpha-/beta-SNAPs form a complex in the presence of ATPgammaS. Similar to SNARE complex disassembly, NSF ATPase activity disrupts PICK1-GluR2 interactions in this complex. Alpha- and beta-SNAP have differential effects on this reaction. SNAP overexpression in hippocampal neurons leads to corresponding changes in AMPAR trafficking by acting on GluR2-PICK1 complexes. This demonstrates that the previously reported synaptic stabilization of AMPARs by NSF involves disruption of GluR2-PICK1 interactions. Furthermore, we are reporting a non-SNARE substrate for NSF disassembly activity.
Interaction of the AMPA receptor subunit GluR2/3 with PDZ domains regulates hippocampal long-term depression.[Pubmed:11573007]
Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11725-30.
The interaction of PDZ domain-containing proteins with the C termini of alpha-amino-3-hydroxy-5-methylisoxazolepropionate (AMPA) receptors has been suggested to be important in the regulation of receptor targeting to excitatory synapses. Recent studies have shown that the rapid internalization of AMPA receptors at synapses may mediate, at least in part, the expression of long-term depression (LTD). We have previously shown that phosphorylation of Ser-880 on the AMPA receptor GluR2 subunit differentially regulated the interaction of GluR2 with the PDZ domain-containing proteins GRIP1 and PICK1. Here, we show that induction of LTD in hippocampal slices increases phosphorylation of Ser-880 within the GluR2 C-terminal PDZ ligand, suggesting that the modulation of GluR2 interaction with GRIP1 and PICK1 may regulate AMPA receptor internalization during LTD. Moreover, postsynaptic intracellular perfusion of GluR2 C-terminal peptides that disrupt GluR2 interaction with PICK1 inhibit the expression of hippocampal LTD. These results suggest that the interaction of GluR2 with PICK1 may play a regulatory role in the expression of LTD in the hippocampus.
PDZ proteins interacting with C-terminal GluR2/3 are involved in a PKC-dependent regulation of AMPA receptors at hippocampal synapses.[Pubmed:11163273]
Neuron. 2000 Dec;28(3):873-86.
We investigated the role of PDZ proteins (GRIP, ABP, and PICK1) interacting with the C-terminal GluR2 by infusing a ct-GluR2 peptide ("pep2-SVKI") into CA1 pyramidal neurons in hippocampal slices using whole-cell recordings. Pep2-SVKI, but not a control or PICK1 selective peptide, caused AMPAR-mediated EPSC amplitude to increase in approximately one-third of control neurons and in most neurons following the prior induction of LTD. Pep2-SVKI also blocked LTD; however, this occurred in all neurons. A PKC inhibitor prevented these effects of pep2-SVKI on synaptic transmission and LTD. We propose a model in which the maintenance of LTD involves the binding of AMPARs to PDZ proteins to prevent their reinsertion. We also present evidence that PKC regulates AMPAR reinsertion during dedepression.
AMPA receptor-PDZ interactions in facilitation of spinal sensory synapses.[Pubmed:10526335]
Nat Neurosci. 1999 Nov;2(11):972-7.
Silent synapses form between some primary sensory afferents and dorsal horn neurons in the spinal cord. Molecular mechanisms for activation or conversion of silent synapses to conducting synapses are unknown. Serotonin can trigger activation of silent synapses in dorsal horn neurons by recruiting AMPA receptors. AMPA-receptor subunits GluR2 and GluR3 interact via their cytoplasmic C termini with PDZ-domain-containing proteins such as GRIP (glutamate receptor interacting protein), but the functional significance of these interactions is unclear. Here we demonstrate that protein interactions involving the GluR2/3 C terminus are important for serotonin-induced activation of silent synapses in the spinal cord. Furthermore, PKC is a necessary and sufficient trigger for this activation. These results implicate AMPA receptor-PDZ interactions in mechanisms underlying sensory synaptic potentiation and provide insights into the pathogenesis of chronic pain.
