Gap 26 (Synonyms: Val-Cys-Tyr-Asp-Lys-Ser-Phe-Pro-Ile-Ser-His-Val-Arg ) |
| Katalog-Nr.GP10107 |
Gap 26, as a connexin mimetic peptide, which has the SHVR amino acid regions contributing crucially to the docking of connexons to generate gap junctions.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 197250-15-0
Sample solution is provided at 25 µL, 10mM.
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Gap 26, as a connexin mimetic peptide, which has the SHVR amino acid regions contributing crucially to the docking of connexons to generate gap junctions[1]. Gap 26 can inhibit the release of ATP induced by an increase in calcium[2]. Gap 26 inhibited electrical coupling in cell pairs mediated by gap junctions[3].
Gap 26 (25μM; 24h) attenuated the apoptosis of tubular epithelial cells[4]. Gap 26 (150μM; 24h) decreased ROS production, inhibited ASK1-JNK/p38 signaling, and decreased apoptosis in the alveolar type II epithelial cells of rats (RLE-6TN)[5].
Gap 26 (1μg/kg/day; i.p. ; 3 times a week for 8 weeks) alleviated the chronotropic hyporesponsiveness and the severity of liver damage and had an antioxidant effect on the heart in cirrhotic cardiomyopathy rats model[6]. Gap 26 (25μg/kg; i.p. ; 4 day) further deteriorated the destruction of synapses and decreased the spine density of hippocampal in middle cerebral artery occlusion (MCAO) rats model[7].
References:
[1] BOITANO S, EVANS W H. Connexin mimetic peptides reversibly inhibit Ca(2+) signaling through gap junctions in airway cells [J]. American journal of physiology Lung cellular and molecular physiology, 2000, 279(4): L623-30.
[2] BRAET K, VANDAMME W, MARTIN P E, et al. Photoliberating inositol-1,4,5-trisphosphate triggers ATP release that is blocked by the connexin mimetic peptide gap 26 [J]. Cell calcium, 2003, 33(1): 37-48.
[3] DESPLANTEZ T, VERMA V, LEYBAERT L, et al. Gap26, a connexin mimetic peptide, inhibits currents carried by connexin43 hemichannels and gap junction channels [J]. Pharmacol Res, 2012, 65(5): 546-52.
[4] TANG L, YU J, ZHUGE S, et al. Oxidative stress and Cx43-mediated apoptosis are involved in PFOS-induced nephrotoxicity [J]. Toxicology, 2022, 478(153283.
[5] QING C, XINYI Z, XUEFEI Y, et al. The Specific Connexin 43-Inhibiting Peptide Gap26 Improved Alveolar Development of Neonatal Rats With Hyperoxia Exposure [J]. Front Pharmacol, 2021, 12(587267.
[6] MOHAMMED D, TAVANGAR S M, KHODADOOSTAN A, et al. Effects of Gap 26, a Connexin 43 Inhibitor, on Cirrhotic Cardiomyopathy in Rats [J]. Cureus, 2024, 16(4): e59053.
[7] YANG K, ZHOU Y, ZHOU L, et al. Synaptic Plasticity After Focal Cerebral Ischemia Was Attenuated by Gap26 but Enhanced by GAP-134 [J]. Front Neurol, 2020, 11(888.
| Cell experiment [1]: | |
Cell lines | Normal rat kidney epithelial (NRK52E) cell |
Preparation Method | NRK52E cells were cultured in Dulbecco’s Modified Eagle’s Medium supplemented with 10% fetal bovine serum. NRK52E cells were exposed to Gap 26 for 24h. |
Reaction Conditions | 25μM; 24h |
Applications | Gap 26 (25μM; 24h) attenuated the apoptosis of tubular epithelial cells. |
| Animal experiment [2]: | |
Animal models | Male CD1 mice |
Preparation Method | Rats were anesthetized with 10% chloral hydrate. Subsequently, a mid-line incision was made in the neck of rats. The right common carotid artery (CCA), external carotid artery (ECA), and internal carotid artery (ICA) were isolated. The ECA was cut approximately 4mm above the common carotid artery bifurcation. A 4.0-s nylon monofilament suture was inserted into ICA through the stump until resistance. In this way, the blood flow to the middle cerebral artery (MCA) was blocked. 2h later, the filament was taken out for reperfusion, and the incision was ligated. Gap 26 was dissolved in saline and given intraperitoneally at the dose of 25μg/kg once a day. To avoid the influence in the acute phase, we chose to apply Gap 26 from day 3 after ischemia, when the infarction volume stabilized and the repair period began. At 7 day after MCAO, rats were sacrificed, and brains were removed as soon as possible. Rapid Golgi Stain Kit was applied for tissue preparation and staining procedures. The whole Golgi-Cox staining procedures were conducted in strict accordance with instructions. Using a freezing microtome, each block was then cut coronally into 100-μm-thick serial sections starting at +1.00 to 5.00mm from the bregma. The sections were mounted onto slides and observed under a laser scanning confocal microscope. |
Dosage form | 25μg/kg; 4 day; i.p. |
Applications | Gap 26 further deteriorated the destruction of synapses and decreased the spine density of hippocampal in middle cerebral artery occlusion (MCAO) rats model. |
References: | |
| Cas No. | 197250-15-0 | SDF | |
| Überlieferungen | Val-Cys-Tyr-Asp-Lys-Ser-Phe-Pro-Ile-Ser-His-Val-Arg | ||
| Formula | C70H107N19O19S | M.Wt | 1550.79 |
| Löslichkeit | ≥77.55 mg/mL in DMSO with ultrasonic and warming, <7.75 mg/mL in EtOH, ≥155.1 mg/mL in Water with ultrasonic | Storage | -20°C, protect from light |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.6448 mL | 3.2242 mL | 6.4483 mL |
| 5 mM | 0.129 mL | 0.6448 mL | 1.2897 mL |
| 10 mM | 0.0645 mL | 0.3224 mL | 0.6448 mL |
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- Purity: >99.50%
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