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PKA inhibitor fragment (6-22) amide
Biological Activity for PKA inhibitor fragment (6-22) amide
PKA inhibitor fragment (6-22) amide is a potent inhibitor of cAMP-dependent protein kinase (PKA) (Ki = 2.5 nM); derived from the active portion of the heat-stable PKA inhibitor protein PKI.
Technical Data for PKA inhibitor fragment (6-22) amide
(Modifications: Ile-17 = C-terminal amide)
|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 PKA inhibitor fragment (6-22) amide
|Solubility||Soluble to 1 mg/ml in water|
Product Datasheets for PKA inhibitor fragment (6-22) amide
References for PKA inhibitor fragment (6-22) amide
References are publications that support the biological activity of the product.
Glass et al (1989) Primary structural determinants essential for potent inhibition of cAMP-dependent protein kinase by inhibitory peptides corresponding to the active portion of the heat-stable inhibitor protein. J.Biol.Chem. 264 8802 PMID: 2722799
Glass et al (1989) Protein kinase inhibitor-(6-22)-amide peptide analogs with standard and nonstandard amino acid substitutions for phenylalanine 10. J.Biol.Chem. 264 14579 PMID: 2760075
Otmakhova et al (2000) Inhibition of the cAMP pathway decreases early long-term potentiation at CA1 hippocampal synapses. J.Neurosci. 20 4446 PMID: 10844013
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Keywords: PKA Inhibitor Fragment (6-22) amide, PKA Inhibitor Fragment (6-22) amide supplier, Potent, protein, kinases, A, inhibitors, inhibits, PKA, Protein, kinase, inhibitor-(6-22)-amide, PKI-(6-22)-amide, Kinase, 1904, Tocris Bioscience
7 Citations for PKA inhibitor fragment (6-22) amide
Citations are publications that use Tocris products. Selected citations for PKA inhibitor fragment (6-22) amide include:
Tumati et al (2009) Sustained mor. treatment augments capsaicin-evoked calcitonin gene-related peptide release from primary sensory neurons in a protein kinase A- and Raf-1-dependent manner. J Neurosci 330 810 PMID: 19491327
O'Neill & Sylantyev (2018) Selective modulation of tonically active GABAA receptor functional subgroups by G-proteins and protein kinase C. Exp Biol Med (Maywood) 243 1046 PMID: 30205722
Cui et al (2016) Endocannabinoid dynamics gate spike-timing dependent depression and potentiation. Elife 5 e13185 PMID: 26920222
Caiati et al (2013) PrPC controls via protein kinase A the direction of synaptic plasticity in the immature hippocampus. J Neurosci 33 2973 PMID: 23407955
Pleil et al (2015) NPY signaling inhibits extended amygdala CRF neurons to suppress binge alcohol drinking. Nat Neurosci 18 545 PMID: 25751534
Hopf et al (2005) Atypical protein kinase C is a novel mediator of DA-enhanced firing in nucleus accumbens neurons. FASEB J 25 985 PMID: 15673680
Costa et al (2018) Activation of Serotonin 5-HT7 Receptors Modulates Hippocampal Synaptic Plasticity by Stimulation of Adenylate Cyclases and Rescues Learning and Behavior in a Mouse Model of Fragile X Syndrome. Front Mol Neurosci 11 353 PMID: 30333723
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Reviews for PKA inhibitor fragment (6-22) amide
Average Rating: 5 (Based on 1 Review.)
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PKA inhibitor fragment (PKI) was used to compare effects of PKA and G-protein signalling on root mean square noise (RMS) produced by GABA-A receptors in electrophysiological recording. We found that after block of PKA with PKI GABA-A receptor antagonists SR 95531 and Picrotoxin generate stronger impact on RMS noise than after block of G-protein signalling with pertussis toxin.
Literature in this Area
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