GLPBio

Gap 26

Catalog No.: GP10107Purity:>99.50%Synonyms: Val-Cys-Tyr-Asp-Lys-Ser-Phe-Pro-Ile-Ser-His-Val-Arg
COASDSData Sheet
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.

المنتجات مخصصة للاستخدام البحثي فقط، وليست للاستخدام البشري. نحن لا نبيع للمرضى.

Gap 26
Cas No.: 197250-15-0
5mgIn Stock
$104.00
1
10mgIn Stock
$154.00
1
25mgIn Stock
$216.00
1
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المراجع (Citations)

1 publicationsمنشورات الباحثين الذين استخدموا هذا المنتج

الوصف (Description)

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.

البروتوكول (Protocol)

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:
[1] 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.
[2] 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.

وثائق المنتج (Product Documents)

Purity:>99.50%Appearance:A solid
COASDSData Sheet

الخصائص الكيميائية (Chemical Properties)

رقم CAS
197250-15-0
المرادفات
Val-Cys-Tyr-Asp-Lys-Ser-Phe-Pro-Ile-Ser-His-Val-Arg
الصيغة الجزيئية
C70H107N19O19S
الوزن الجزيئي
1550.79
الذوبانية
≥77.55 mg/mL in DMSO with ultrasonic and warming, <7.75 mg/mL in EtOH, ≥155.1 mg/mL in Water with ultrasonic
التخزين
-20°C, protect from light
إرشادات عامة
اختر مذيبًا مناسبًا وفقًا لبيانات ذوبانية المنتج. بعد التحضير، قسّم المحلول المخزون إلى أجزاء لتجنب دورات التجميد والذوبان المتكررة.
استخدم المحاليل المخزونة خلال 6 أشهر عند حفظها في -80°C، أو خلال شهر واحد عند حفظها في -20°C.
لتحسين الذوبانية، سخّن الأنبوب إلى 37°C وعرّضه للموجات فوق الصوتية لمدة مناسبة.
شروط الشحن
تُشحن عينات التقييم مع عبوات تبريد. وتُشحن الأحجام الأخرى المتاحة في درجة حرارة الغرفة، أو مع عبوات تبريد عند الطلب.

الحاسبات (Calculators)المولارية / التخفيف / الوزن الجزيئي / تحويل الوحدات / تركيبة داخل الجسم الحي / الذوبانية

g/mol

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