Gap 26

$209.00
331-10044-1
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Molecule Information

CAS Number
197250-15-0
Molecular Weight
1550.79
Formula
C70H107N19O19S
Purity
99.56%

Solubility

77.55 mg/mL in DMSO with ultrasonic and warming, <7.75 mg/mL in EtOH, 155.1 mg/mL in H2O with ultrasonic

Physical Appearance

A solid

Storage

Desiccate at -20°C

Biological Activity

Description Gap26 (Val-Cys-Tyr-Asp-Lys-Ser-Phe-Pro-Ile-Ser-His-Val-Arg) is a connexin mimetic peptide, corresponding to residues 63-75 of connexin 43, which is a gap junction blocker.
Targets            
IC50            

Protocol

Cell experiment: [1]

Cell lines

ECV304 cells

Preparation method

The solubility of this peptide in sterile water is >10 mM. Stock solution should be splited and stored at -80°C for several months.

Reaction Conditions

0.25mg/ml, 30min

Applications

Preventing the InsP3-triggered calcium increase by ester loading the cells with the calcium chelator BAPTA reduced the InsP3-triggered ATP release back to the control level. Incubation of the cells with gap 26 completely abolished the InsP3-triggered ATP response and reduced the ATP release to below the control level, indicating that the basal ATP release is also affected.

Animal experiment: [2]

Animal models

Female Sprague-Dawley rats

Dosage form

300 µM, 45 min

Applications

The rats were prepared with closed cranial windows 24 h before the study. A 10-mm-diameter craniotomy was performed over the skull midline. The dura was removed carefully to keep the sagittal sinus intact. An 11-mm-diameter glass window outfitted with three ports was glued to the skull using cyanoacrylate. The skin overlying the window was sutured, and the animals were permitted to recover. On the day of study, three stainless steel screws were inserted into the skull, along the periphery of the cranial window, for electroencephalogram (EEG) recording. Cannulae were then connected to the three ports. The rats were subjected to one of two neuronal activation paradigms: SNS or bicuculline-induced seizure. Following the initial measurement of pial arteriolar diameter changes during SNS or during bicuculline exposure, baseline conditions were reestablished. After 20 min, a suffusion of gap-26 was initiated. Forty-five minutes later, the neural activation was repeated. Exposure to the Cx40/Cx37 inhibitory peptide, gap-26 (300 µM), was without effect on bicuculline- or SNS-induced pial arteriolar dilations.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Braet K, Vandamme W, Martin P E M, et al. Photoliberating inositol-1, 4, 5-trisphosphate triggers ATP release that is blocked by the connexin mimetic peptide gap 26. Cell calcium, 2003, 33(1): 37-48.

[2] Xu H L, Mao L, Ye S, et al. Astrocytes are a key conduit for upstream signaling of vasodilation during cerebral cortical neuronal activation in vivo. American Journal of Physiology-Heart and Circulatory Physiology, 2008, 294(2): H622-H632.

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Usage

This product is furnished for LABORATORY RESEARCH USE ONLY.
Not for diagnostic or therapeutic use.