Gap19

目录号: GC17681纯度: >98%

Gap19 (KQIEIKKFK) 阻断 HC 但不阻断 GJC，并且特定于 Cx43。

Cas No.: 1507930-57-5

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1mg	¥1,050.00	现货	1
5mg	¥3,150.00	现货	1

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187(9):2288-2304 (2024)
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183(7):1867-1883 (2020)
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产品描述 Description

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.

Gap19 (KQIEIKKFK) 阻断 HC 但不阻断 GJC，并且特定于 Cx43。 Gap19可能抵抗心肌缺血损伤^[2]。 Gap19 对 Cx43 HC 门控具有双峰效应，减少完全打开状态的门控，同时增加亚状态门控，表明 Gap19 就像 Cx43 HC 上的门控修饰符。Gap19 破坏 CT-CL 相互作用，从而使 hc 难以打开^[7].

Gap19 作为一种来源于 Cx43 细胞质环的九肽，以剂量依赖性方式抑制星形胶质细胞 Cx43 半通道，而不影响间隙连接通道。该肽不仅选择性抑制半通道，而且对 Cx43^[5] 具有特异性。

研究 Gap19 在脑缺血/再灌注 (I/R) 损伤中的作用时在大脑中动脉闭塞 (MCAO) 的小鼠模型中。脑室注射Gap19可显着减轻缺血后的梗死体积、神经元细胞损伤和神经功能缺损，Gap19的神经保护作用明显强于Gap26。再灌注后 4 小时腹膜内给药时，TAT-Gap19 后处理仍提供神经保护作用^[1]。 Gap19 通过抑制 TLR4 介导的信号通路在卒中后发挥神经保护作用^[4]。 Gap19 治疗可防止代谢抑制增强的半通道开放，保护心肌细胞免受体外缺血/再灌注后的体积超载和细胞死亡，并适度减少小鼠体内心肌缺血/再灌注后的梗塞面积^[3] . TG 内注射抑制 Cx43 半通道形成的模拟肽 GAP19，大大降低了所有 CFA 炎症组中 TMJ 诱发的 MMemg 活性，而假手术组的活性未受影响^[6]。< /p>

实验参考方法 Experimental Reference Method

Cell experiment [1]:
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 experiment [2]:
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.
References: [1]. 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. [2].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.

产品文档 Product Documents

Purity:>98%

COA SDS Data Sheet

化学性质Chemical Properties

CAS 号

1507930-57-5

SMILES

CC[C@]([C@@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](N)([H])CCCCN)([H])CCC(O)=N)([H])[C@@](CC)([H])C)([H])CCC(O)=O)([H])/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](C(O)=O)([H])CCCCN)([H])CC1=CC=CC=C1)([H])CCCCN)([H])CCCCN)([H])C

分子式

C₅₅H₉₆N₁₄O₁₃

分子量

1161.45 g/mol

溶解性

≥ 58.0725mg/mL in Water

保存条件

Store at -20°C

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