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Dynamin inhibitory peptide Sale

(Synonyms: Gln-Val-Pro-Ser-Arg-Pro-Asn-Arg-Ala-Pro ) 目录号 : GP10022

动力蛋白抑制肽竞争性地阻断动力蛋白与两性蛋白的结合,从而防止内吞作用。

Dynamin inhibitory peptide Chemical Structure

Cas No.:251634-21-6

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产品描述

Dynamin Inhibitory Peptide is a peptide (Gln-Val-Pro-Ser-Arg-Pro-Asn-Arg-Ala-Pro) inhibitor of the GTPase dynamin.

Dynamin is a 100-kDa large GTPase that functions to tabulate membranes and liberate nascent vesicles from the Golgi apparatus and plasma membrane. Dynamin also plays a role in many processes including division of organelles,cytokinesis and microbial pathogen resistance.

Dynamin inhibitory peptide competitively blocks binding of dynamin to amphiphysin thus prevents endocytosis when administered intracellularly. Reduces GABAA receptor internalization and increases miniature ISPC amplitude and frequency in neurons expressing GABAA receptors.

References:
1. McNiven, M. A., Cao, H., Pitts, K. R. & Yoon, Y. (2000) Trends Biochem. Sci. 25, 115-120.
2. Hinshaw, J. E. (2000) Annu. Rev. Cell Dev. Biol 16, 483-519.
3. Thoms S, Erdmann R (Oct 2005). "Dynamin-related proteins and Pex11 proteins in peroxisome division and proliferation.". FEBS J 272 (20): 5169-81.
4. Grabs et al (1997) The SH3 domain of amphiphysin binds the proline-rich domain of dynamin at a single site that defines a new SH3 binding consensus sequence. J.Biol.Chem. 272 13419-25.
5. Kittler et al (2000) Constitutive endocytosis of GABAA receptors by an association with the adaptin AP2 complex modulates inhibitory synaptic currents in hippocampal neurons. J.Neurosci. 20 7972-7.
6. Nong et al (2003) Glycine binding primes NMDA receptor internalization. Nature 422 302-7.

Chemical Properties

Cas No. 251634-21-6 SDF
别名 Gln-Val-Pro-Ser-Arg-Pro-Asn-Arg-Ala-Pro
化学名 Dynamin inhibitory peptide
Canonical SMILES CC(C)C(C(=O)N1CCCC1C(=O)NC(CO)C(=O)NC(CCCN=C(N)N)C(=O)N2CCCC2C(=O)NC(CC(=O)N)C(=O)NC(CCCN=C(N)N)C(=O)NC(C)C(=O)N3CCCC3C(=O)O)NC(=O)C(CCC(=O)N)N
分子式 C47H80N18O14 分子量 1121.26
溶解度 ≥ 112.1mg/mL in DMSO 储存条件 Desiccate at -20°C
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1 mM 0.8919 mL 4.4593 mL 8.9185 mL
5 mM 0.1784 mL 0.8919 mL 1.7837 mL
10 mM 0.0892 mL 0.4459 mL 0.8919 mL
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Research Update

Pharmacological Investigation of Fluoro-Gold Entry into Spinal Neurons

The fluorescent tracer Fluoro-Gold has been widely used to label neurons retrogradely. Here we show that Fluoro-Gold can also enter neurons through AMPA receptor endocytosis. We found that a 30 minute application of Fluoro-Gold to the isolated spinal cord labeled neurons under control conditions and in the presence of glutamatergic agonists including NMDA and AMPA. The labeling was abolished or greatly reduced by glutamatergic antagonists and the endocytic inhibitors Dynasore and dynamin inhibitory peptide. Whole cell recordings from spinal neurons exposed to extracellular AMPA revealed large inward currents that spontaneously decayed in the presence of the agonist but were maintained when a dynamin inhibitory peptide was included in the electrode. These findings suggest that Fluoro-Gold enters spinal neurons through AMPA-mediated receptor internalization. Drugs used to induce locomotor-like activity in the spinal cord also increased and decreased Fluoro-Gold labeling in a drug and lamina specific manner, indicating that AMPAR endocytosis is altered in the presence of the locomotor cocktail. Our findings suggest that endocytosis of Fluoro-Gold could potentially complicate the interpretation of experiments in which the tracer is used to label neurons retrogradely. Moreover, they also demonstrate that many drugs, including the locomotor cocktail, can modulate the number and/or the composition of AMPA receptors on spinal neurons and thereby affect network excitability.

Emergence of Endocytosis-Dependent mGlu1 LTD at Nucleus Accumbens Synapses After Withdrawal From Cocaine Self-Administration

Extended-access cocaine self-administration induces a progressive intensification of cue-induced drug craving during withdrawal termed "incubation of cocaine craving". Rats evaluated after >1 month of withdrawal (when incubation of craving is robust) display alterations in excitatory synapses onto medium spiny neurons (MSNs) of the nucleus accumbens (NAc), including elevated levels of Ca2+-permeable AMPA receptors (CP-AMPAR) and a transition from group I metabotropic glutamate receptor (mGluR) mGlu5- to mGlu1-mediated synaptic depression. It is important to further characterize the emergent form of mGlu1-mediated synaptic depression because it has been demonstrated that mGlu1 stimulation, by normalizing CP-AMPAR transmission, reduces cue-induced cocaine craving. In the present study, we conducted whole-cell patch-clamp recordings in NAc core MSNs, comparing rats that underwent >35 days of withdrawal from cocaine self-administration to control rats that had self-administered saline. Bath application of the nonselective group I mGluR agonist dihydroxyphenylglycine (DHPG) produced a transient mGlu5-mediated synaptic depression in saline controls, whereas a persistent mGlu1-mediated synaptic depression emerged in cocaine rats. This form of long-term depression (LTD) was abolished by the inclusion of dynamin inhibitory peptide (DIP) in the recording electrode, indicating that it is mediated by removal of CP-AMPARs through a dynamin-dependent endocytosis mechanism. We further showed that CP-AMPAR endocytosis is normally coupled to the PICK1-mediated insertion of Ca2+-impermeable AMPARs (CI-AMPAR). Interestingly, this coupling is not obligatory because disruption of PICK1-mediated CI-AMPAR insertion with pep2-EVKI spared mGlu1-mediated CP-AMPAR endocytosis. Collectively, these results reveal similarities but also differences from mGlu1-LTD observed in other brain regions, and further our understanding of a form of plasticity that may be targeted to reduce cue-induced craving for cocaine and methamphetamine.

Dopamine D3 receptors regulate GABAA receptor function through a phospho-dependent endocytosis mechanism in nucleus accumbens

The dopamine D3 receptor, which is highly enriched in nucleus accumbens (NAc), has been suggested to play an important role in reinforcement and reward. To understand the potential cellular mechanism underlying D3 receptor functions, we examined the effect of D3 receptor activation on GABAA receptor (GABAAR)-mediated current and inhibitory synaptic transmission in medium spiny neurons of NAc. Application of PD128907 [(4aR,10bR)-3,4a,4,10b-tetrahydro-4-propyl-2H,5H-[1]benzopyrano-[4,3-b]-1,4-oxazin-9-ol hydrochloride], a specific D3 receptor agonist, caused a significant reduction of GABAAR current in acutely dissociated NAc neurons and miniature IPSC amplitude in NAc slices. This effect was blocked by dialysis with a dynamin inhibitory peptide, which prevents the clathrin/activator protein 2 (AP2)-mediated GABAA receptor endocytosis. In addition, the D3 effect on GABAAR current was prevented by agents that manipulate protein kinase A (PKA) activity. Infusion of a peptide derived from GABAAR beta subunits, which contains an atypical binding motif for the clathrin AP2 adaptor complex and the major PKA phosphorylation sites and binds with high affinity to AP2 only when dephosphorylated, diminished the D3 regulation of IPSC amplitude. The phosphorylated equivalent of the peptide was without effect. Moreover, PD128907 increased GABAAR internalization and reduced the surface expression of GABAA receptor beta subunits in NAc slices, which was prevented by dynamin inhibitory peptide or cAMP treatment. Together, our results suggest that D3 receptor activation suppresses the efficacy of inhibitory synaptic transmission in NAc by increasing the phospho-dependent endocytosis of GABAA receptors.

Regulation of N-methyl-D-aspartate receptors by calpain in cortical neurons

The N-methyl-D-aspartate (NMDA) receptor is a cation channel highly permeable to calcium and plays critical roles in governing normal and pathologic functions in neurons. Calcium entry through NMDA receptors (NMDARs) can lead to the activation of the Ca2+-dependent protease, calpain. Here we investigated the involvement of calpain in regulation of NMDAR channel function. After prolonged (5-min) treatment with NMDA or glutamate, the whole-cell NMDAR-mediated current was significantly reduced in both acutely dissociated and cultured cortical pyramidal neurons. The down-regulation of NMDAR current was blocked by bath application of selective calpain inhibitors. Intracellular injection of a specific calpain inhibitory peptide also eliminated the down-regulation of NMDAR current induced by prolonged NMDA treatment. In contrast, dynamin inhibitory peptide had no effect on the depression of NMDAR current, suggesting the lack of involvement of dynamin/clathrin-mediated NMDAR internalization in this process. Immunoblotting analysis showed that the NR2A and NR2B subunits of NMDARs were markedly degraded in cultured cortical neurons treated with glutamate, and the degradation of NR2 subunits was prevented by calpain inhibitors. Taken together, our results suggest that prolonged activation of NMDARs in neurons activates calpain, and activated calpain in turn down-regulates the function of NMDARs, which provides a neuroprotective mechanism against NMDAR overstimulation accompanying ischemia and stroke.