| 包装 | 价格(元) |
| 1mg | 询价 |
| 5mg | 询价 |
Cell lines | Astrocyte cell |
Preparation Method | Concentration-dependent inhibition by Gap19 (30 min pre-incubation) of ATP release in cultured cortical astrocytes triggered by glutamate. |
Reaction Conditions | 0-104uM Gap19 for 30 min |
Applications | Gap19 (30 min treatment) inhibited glutamate-triggered ATP release (Figure 2A).Etd+ uptake was inhibited in the presence of Gap19 in a dose-dependent manner, with the peptide applied prior to (30 min) and during Etd+ uptake.Gap19 was without any effect on gap junctional communication in astrocytes which in culture express only Cx43. |
Animal models | Male ICR mice (25-30 g) |
Preparation Method | Animals were randomly divided into different groups as follows: (I) vehicle group (sham); (II) Gap19 treated vehicle group (Gap19 group); (III) I/R group; (IV) Gap26 treated I/R group (I/R + Gap26 group); (V) Gap19 treated I/R group (I/R + Gap19 group).10 µg Gap19/Gap26 in 10 µl ddH2O was injected in lateral ventricle (300 µg/kg body weight, i.c.v.). TAT-Gap19 was administered at a dose of 25 mg/kg body weight (i.p.) in the post-treatment groups. |
Dosage form | 10 µg Gap19 |
Applications | When investigated the role of Gap19 on cerebral ischemia/reperfusion (I/R) injury in a mouse model of middle cerebral artery occlusion (MCAO). Ventricle-injected Gap19 significantly alleviated infarct volume, neuronal cell damage and neurological deficits after ischemia, the neuroprotective effect of Gap19 was significant stronger than Gap26. Post-treatment with TAT-Gap19 still provided neuroprotection when it was administered intraperitoneally at 4 h after reperfusion. |
| 产品描述 | Gap19 (KQIEIKKFK) blocks HCs but not GJCs and is specific for Cx43. Gap19 may resist myocardial ischemic injury[2]. Gap19 has a bimodal effect on Cx43 HC gating, decreasing gating to the fully open state while increasing substate gating, suggesting that Gap19 acts like a gating modifier on Cx43 HC.Gap19 disrupts the CT-CL interaction, thus making hc difficult to open[7]. Gap19, as a nonapeptide derived from the cytoplasmic loop of Cx43, inhibits astroglial Cx43 hemichannels in a dose-dependent manner, without affecting gap junction channels. This peptide, which not only selectively inhibits hemichannels but is also specific for Cx43[5]. When investigated the role of Gap19 on cerebral ischemia/reperfusion (I/R) injury in a mouse model of middle cerebral artery occlusion (MCAO). Ventricle-injected Gap19 significantly alleviated infarct volume, neuronal cell damage and neurological deficits after ischemia, the neuroprotective effect of Gap19 was significant stronger than Gap26. Post-treatment with TAT-Gap19 still provided neuroprotection when it was administered intraperitoneally at 4 h after reperfusion[1]. Gap19 exerted a neuroprotective effect after stroke via inhibition of the TLR4-mediated signaling pathway[4]. Treatment with Gap19 prevented metabolic inhibition-enhanced hemichannel openings, protected cardiomyocytes against volume overload and cell death following ischemia/reperfusion in vitro and modestly decreased the infarct size after myocardial ischemia/reperfusion in mice in vivo[3]. Intra-TG injection of the mimetic peptide GAP19, which inhibits Cx43 hemichannel formation, greatly reduced TMJ-evoked MMemg activity in all CFA-inflamed groups, while activity in sham groups was not affected[6]. References: |
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