Gap19 |
Catalog No.GC17681 |
Gap19 (KQIEIKKFK) blocks HCs but not GJCs and is specific for Cx43.
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Cas No.: 1507930-57-5
Sample solution is provided at 25 µL, 10mM.
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:
[1]. Chen B, Yang L, et,al. Inhibition of Connexin43 hemichannels with Gap19 protects cerebral ischemia/reperfusion injury via the JAK2/STAT3 pathway in mice. Brain Res Bull. 2019 Mar;146:124-135. doi: 10.1016/j.brainresbull.2018.12.009. Epub 2018 Dec 26. PMID: 30593877.
[2]. Wang JP, Yang ZT, et,al. L-carnosine inhibits neuronal cell apoptosis through signal transducer and activator of transcription 3 signaling pathway after acute focal cerebral ischemia. Brain Res. 2013 Apr 24;1507:125-33. doi: 10.1016/j.brainres.2013.02.032. Epub 2013 Feb 27. PMID: 23454231.
[3]. Wang N, De Vuyst E, et,al. Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury. Basic Res Cardiol. 2013 Jan;108(1):309. doi: 10.1007/s00395-012-0309-x. Epub 2012 Nov 8. PMID: 23184389; PMCID: PMC3666173.
[4]. Chen Y, Wang L, et,al. Inhibition of Connexin 43 Hemichannels Alleviates Cerebral Ischemia/Reperfusion Injury via the TLR4 Signaling Pathway. Front Cell Neurosci. 2018 Oct 17;12:372. doi: 10.3389/fncel.2018.00372. PMID: 30386214; PMCID: PMC6199357.
[5]. Abudara V, Bechberger J, et,al. The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes. Front Cell Neurosci. 2014 Oct 21;8:306. doi: 10.3389/fncel.2014.00306. PMID: 25374505; PMCID: PMC4204617.
[6]. Ahmed F, Rahman M, et,al. Role of Connexin 43 in an Inflammatory Model for TMJ Hyperalgesia. Front Pain Res (Lausanne). 2021 Aug 3;2:715871. doi: 10.3389/fpain.2021.715871. PMID: 35295418; PMCID: PMC8915650.
[7]. Lissoni A, Wang N, et,al. Gap19, a Cx43 Hemichannel Inhibitor, Acts as a Gating Modifier That Decreases Main State Opening While Increasing Substate Gating. Int J Mol Sci. 2020 Oct 5;21(19):7340. doi: 10.3390/ijms21197340. PMID: 33027889; PMCID: PMC7583728.
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