RI-STAD-2
RI-STAD-2 is a high-affinity interfering peptide that regulates the subunit RI of protein kinase A (PKA). RI-STAD-2 interferes with the binding of AKAPs and PKA-RI by simulating the interaction between AKAPs' α-helix domain and PKA-RI's dimerization/anchoration (D/D) domain, thereby affecting PKA activity and intracellular localization. RI-STAD-2 can be used to study the role of AKAPs interaction with PKA-RI in pathological processes such as cardiovascular disease and cancer.
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- Formule: C109H181N25O35
- Masse moléculaire:2401.75
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
Chemical Information
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Masse moléculaire 2401.75
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Formule C109H181N25O35
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Sequence
{NH2-PEG3-CH2-CO}-Leu-S5-Gln-Tyr-Ala-S5-Gln-Leu-Ala-Asp-Gln-Ile-Ile-Lys-Glu-Ala-Thr-Glu-Lys
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Sequence Shortening
{NH2-PEG3-CH2-CO}-L-S5-QYA-S5-QLADQIIKEATEK
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)