PKA inhibitor fragment (6-22) amide
Purity: ≥95%
Biological Activity
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
(Modifications: Ile-17 = C-terminal amide)
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.
Background References
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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.
Glass et al.
J.Biol.Chem., 1989;264:8802 -
Protein kinase inhibitor-(6-22)-amide peptide analogs with standard and nonstandard amino acid substitutions for phenylalanine 10.
Glass et al.
J.Biol.Chem., 1989;264:14579 -
Inhibition of the cAMP pathway decreases early long-term potentiation at CA1 hippocampal synapses.
Otmakhova et al.
J.Neurosci., 2000;20:4446
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Citations for PKA inhibitor fragment (6-22) amide
The citations listed below are publications that use Tocris products. Selected citations for PKA inhibitor fragment (6-22) amide include:
7 Citations: Showing 1 - 7
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Selective modulation of tonically active GABAA receptor functional subgroups by G-proteins and protein kinase C.
Authors: O'Neill & Sylantyev
Exp Biol Med (Maywood) 2018;243:1046
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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.
Authors: Costa Et al.
Front Mol Neurosci 2018;11:353
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Endocannabinoid dynamics gate spike-timing dependent depression and potentiation.
Authors: Cui Et al.
Elife 2016;5:e13185
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NPY signaling inhibits extended amygdala CRF neurons to suppress binge alcohol drinking.
Authors: Pleil Et al.
Nat Neurosci 2015;18:545
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PrPC controls via protein kinase A the direction of synaptic plasticity in the immature hippocampus.
Authors: Caiati Et al.
J Neurosci 2013;33:2973
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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.
Authors: Tumati Et al.
J Neurosci 2009;330:810
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Atypical protein kinase C is a novel mediator of DA-enhanced firing in nucleus accumbens neurons.
Authors: Hopf Et al.
FASEB J 2005;25:985
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