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Tat-Gap 19 is a peptide inhibitor of connexin43 (Cx43) hemichannels.1 It is composed of the HIV-1 Tat protein transduction domain linked to a nine-amino acid peptide corresponding to residues 128-136 of Cx43. Tat-Gap 19 (10 µM) inhibits glutamate-induced ATP release, a marker of Cx43 hemichannel activity, in primary rat hepatocytes.2 It reduces infarct volume in a mouse model of cerebral ischemia-reperfusion injury induced by middle cerebral artery occlusion (MCAO) when administered at a dose of 25 mg/kg.1 Intraperitoneal infusion of Tat-Gap 19 (1 mg/kg per day) reduces fibrotic lesion area and the area of hepatic stellate cells, precursors of myofibroblasts, expressing α-smooth muscle actin (α-SMA) in a mouse model of thioacetamide-induced liver injury.2 It increases superoxide dismutase (SOD) activity in hepatic cells isolated from the same mice.
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1. Inhibition of Connexin43 hemichannels with Gap19 protects cerebral ischemia/reperfusion injury via the JAK2/STAT3 pathway in mice. Brain Res. Bull. 146, 124-135 (2019).
2. TAT-