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Biological Activity for STAD 2
STAD 2 is an AKAP disruptor. Selectively binds PKA-RII subunit with high affinity (Kd = 6.2 nM) and blocks its interaction with AKAP. Cell permeable. Selectively permeable to malaria-infected red blood cells and displays antimalarial activity through a PKA-independent mechanism.
Technical Data for STAD 2
(Modifications: Lys-1 = NH2-PEG3-CH2-CO-Lys, X = (S)-2-(4-pentenyl)alanine, X-10 and X-14 stapled together with a double bond)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for STAD 2
|Solubility||Soluble to 1 mg/ml in 50% acetonitrile / water|
References for STAD 2
References are publications that support the biological activity of the product.
Bendzunas et al (2018) Investigating PKA-RII specificity using analogs of the PKA:AKAP peptide inhibitor STAD-2. Bioorg.Med.Chem. 26 1174 PMID: 29449124
Flaherty et al (2015) The stapled AKAP disruptor peptide STAD-2 displays antimalarial activity through a PKA-independent mechanism. PLoS One 10 e0129239 PMID: 26010880
Wang et al (2014) Isoform-selective disruption of AKAP-localized PKA using hydrocarbon stapled peptides. ACS Chem.Biol. 9 635 PMID: 24422448
If you know of a relevant reference for STAD 2, please let us know.
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Keywords: STAD 2, STAD 2 supplier, STAD2, stapled, peptide, selective, AKAP, disruptors, disrupts, a-kinase, anchoring, proteins, RII, antimalarial, PKA, protein, kinase, A, A-kinase-anchoring, protiens, Antimalarials, Stapled, Peptides, 6566, Tocris Bioscience
Citations for STAD 2
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Literature in this Area
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.