370655
PKG Iα Inhibitor, Cell-Permeable
The PKG Iα Inhibitor, Cell-Permeable controls the biological activity of PKG Iα. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
别名:
PKG Iα Inhibitor, Cell-Permeable, DT-3, RQIKIWFQNRRMKWKKLRKKKKKH, PKG Inhibitor VIII
assay
≥95% (HPLC)
form
lyophilized
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, desiccated (hygroscopic)
solubility
DMSO: 10 mg/mL
shipped in
ambient
storage temp.
−20°C
Quality Level
General description
A highly potent, reversible, and substrate competitive membrane-permeable peptide that selectively inhibits protein kinase G Iα (PKG Iα) (Ki = 25 nM). Inhibitor peptide is fused to the Drosophila Antennapedia homeo domain peptide to allow membrane permeability. Shown to efficiently cross the membrane of arterial smooth muscle cells and inhibit nitric oxide-induced (NO-induced) vasodilation (EC50 = 47 µM). Inhibits protein kinase A (PKA) activity only at much higher concentrations (Ki = 493 µM). The carrier peptide is also available under Cat. no. 287895.
Biochem/physiol Actions
Cell permeable: yes
Primary Target
PKG1α
PKG1α
Product competes with ATP.
Reversible: yes
Target Ki: 25 nM against protein kinase G Iα
Packaging
Packaged under inert gas
Physical form
Supplied as a trifluoroacetate salt.
Preparation Note
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 2 months at -20°C.
Other Notes
Dostmann, W. R.G., et al. 2000. Proc. Natl. Acad. Sci. USA 97, 14772.
H-Arg-Gln-Ile-Lys-Ile-Trp-Phe-Gln-Asn-Arg-Arg-Met-Lys-Trp-Lys-Lys-Leu-Arg-Lys-Lys-Lys-Lys-Lys-His-OH
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Standard Handling (A)
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Malgorzata Szaroszyk et al.
Nature communications, 13(1), 149-149 (2022-01-12)
Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持