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Gap 27 is a peptide derived from connexin 43 that is a selective gap junction blocker. Attenuates ACh-induced arterial relaxation and reduces K+-mediated smooth muscle repolarization in endothelium-intact vessels in vitro.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 1 mg/ml in water|
References are publications that support the biological activity of the product.
Chaytor et al (1998) Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. J.Physiol. 508 561 PMID: 9508817
Ko et al (2000) Biochemical and functional characterization of intercellular adhesion and gap junctions in fibroblasts. Am.J.Physiol.Cell Physiol. 279 C147 PMID: 10898726
Richards et al (2001) Suppression of K+-induced hyperpolarization by phenylephrine in rat mesenteric artery: relevance to studies of endothelium-derived hyperpolarizing factor. Br.J.Pharmacol. 134 1 PMID: 11522590
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Keywords: Gap 27, Gap 27 supplier, Selective, gap, junction, blockers, Connexins, Gap, Channels, modulators, Gap27, 1476, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for Gap 27 include:
Dosch et al (2019) Connexin-43-dependent ATP release mediates macrophage activation during sepsis. Elife 8 PMID: 30735126
Westphalen et al (2014) Sessile alveolar macrophages communicate with alveolar epithelium to modulate immunity. Nature 506 503 PMID: 24463523
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.