PKA inhibitor fragment (6-22) amide - CAS 121932-06-7
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
PKA inhibitor fragment (6-22) amide is a synthetic peptide inhibitor of cAMP-dependent protein kinase (PKA) (Ki = 2.5 nM) derived from the heat-stable PKA inhibitor protein PKI. It is the shortest synthetic PKI peptide that retains high potency for PKA inhibition.
PKI (6-22) amide; Protein Kinase A Inhibitor Fragment 6-22 amide
Store in a cool and dry place (or refer to the Certificate of Analysis).
Canonical SMILES:
1.Inhibition of the cAMP pathway decreases early long-term potentiation at CA1 hippocampal synapses.
Otmakhova NA;Otmakhov N;Mortenson LH;Lisman JE J Neurosci. 2000 Jun 15;20(12):4446-51.
Long-term potentiation (LTP) has several different phases, and there is general agreement that the late phase of LTP requires the activation of adenylyl cyclase (AC) and cAMP-dependent protein kinase (PKA). In contrast, several studies indicate that the early LTP is not affected by interfering with the cAMP pathway. We have further tested the role of the cAMP pathway in early LTP using several types of inhibitors. Bath application of the PKA inhibitor H89 suppressed the early LTP induced by a single tetanus. Similarly, the LTP induced by a pairing protocol was decreased by postsynaptic intracellular perfusion of the peptide PKA inhibitor PKI(6-22) amide. The decrease of LTP produced by these inhibitors was evident immediately after induction. These results indicate that PKA is important in early LTP, that its locus of action is postsynaptic, and that it does not act merely by enhancing the depolarization required for LTP induction. The failure of some other inhibitors of the cAMP pathway to affect the early phase of LTP might be attributable to the saturation of some step in the cAMP pathway during a tetanus. In agreement with this hypothesis we found that application of the AC inhibitor SQ 22536 by itself did not affect the early phase of LTP, but did produce a reduction if the cAMP pathway was already attenuated by the PKA inhibitor H89.
2.ACTH inhibits bTREK-1 K+ channels through multiple cAMP-dependent signaling pathways.
Liu H;Enyeart JA;Enyeart JJ J Gen Physiol. 2008 Aug;132(2):279-94. doi: 10.1085/jgp.200810003.
Bovine adrenal zona fasciculata (AZF) cells express bTREK-1 K(+) channels that set the resting membrane potential and function pivotally in the physiology of cortisol secretion. Inhibition of these K(+) channels by adrenocorticotropic hormone (ACTH) or cAMP is coupled to depolarization and Ca(2+) entry. The mechanism of ACTH and cAMP-mediated inhibition of bTREK-1 was explored in whole cell patch clamp recordings from AZF cells. Inhibition of bTREK-1 by ACTH and forskolin was not affected by the addition of both H-89 and PKI (6-22) amide to the pipette solution at concentrations that completely blocked activation of cAMP-dependent protein kinase (PKA) in these cells. The ACTH derivative, O-nitrophenyl, sulfenyl-adrenocorticotropin (NPS-ACTH), at concentrations that produced little or no activation of PKA, inhibited bTREK-1 by a Ca(2+)-independent mechanism. Northern blot analysis showed that bovine AZF cells robustly express mRNA for Epac2, a guanine nucleotide exchange protein activated by cAMP. The selective Epac activator, 8-pCPT-2'-O-Me-cAMP, applied intracellularly through the patch pipette, inhibited bTREK-1 (IC(50) = 0.63 microM) at concentrations that did not activate PKA. Inhibition by this agent was unaffected by PKA inhibitors, including RpcAMPS, but was eliminated in the absence of hydrolyzable ATP.
3.Modulation of the cardiac sodium current by inhalational anesthetics in the absence and presence of beta-stimulation.
Weigt HU;Kwok WM;Rehmert GC;Bosnjak ZJ Anesthesiology. 1998 Jan;88(1):114-24.
BACKGROUND: ;Cardiac dysrhythmias during inhalational anesthesia in association with catecholamines are well known, and halothane is more "sensitizing" than isoflurane. However, the underlying mechanisms of action of volatile anesthetics with or without catecholamines on cardiac Na channels are poorly understood. In this study, the authors investigated the effects of halothane and isoflurane in the absence and presence of beta-stimulation (isoproterenol) on the cardiac Na+ current (INa) in ventricular myocytes enzymatically isolated from adult guinea pig hearts.;METHODS: ;A standard whole-cell patch-clamp technique was used. The INa was elicited by depolarizing test pulses from a holding potential of -80 mV in reduced Na+ solution (10 mM).;RESULTS: ;Isoproterenol alone depressed peak INa significantly by 14.6 +/- 1.7% (means +/- SEM). Halothane (1.2 mM) and isoflurane (1.0 mM) also depressed peak INa significantly by 42.1 +/- 3.4% and 21.3 +/- 1.9%, respectively. In the presence of halothane, the effect of isoproterenol (1 microM) was potentiated, further decreasing peak INa by 34.7 +/- 4.1%. The halothane effect was less, although significant, in the presence of a G-protein inhibitor (GDPbetaS) or a specific protein kinase A inhibitor [PKI-(6-22)-amide], reducing peak INa by 24.
Molecular Weight Calculator Molarity Calculator Solution Dilution Calculator

Related PKA Products

CAS 1135306-29-4 6-Bnz-cAMP sodium salt

6-Bnz-cAMP sodium salt
(CAS: 1135306-29-4)

6-Bnz-cAMP sodium salt is a cell-permeable cAMP analogue that selectively activates cAMP-dependent PKA but not Epac signaling pathways. It inhibits the prolifer...

CAS 121932-06-7 PKA inhibitor fragment (6-22) amide

PKA inhibitor fragment (6-22) amide
(CAS: 121932-06-7)

PKA inhibitor fragment (6-22) amide is a synthetic peptide inhibitor of cAMP-dependent protein kinase (PKA) (Ki = 2.5 nM) derived from the heat-stable PKA inhib...

CAS 99534-03-9 PKI (5-24)

PKI (5-24)
(CAS: 99534-03-9)

PKI (5-24) is a competitive, non-reversible peptide inhibitor of PKA (cAMP-dependent protein kinase) (Ki = 2.3 nM). Its sequence is derived from the heat-stable...

CAS 116700-36-8 H-9 dihydrochloride

H-9 dihydrochloride
(CAS: 116700-36-8)

H-9 dihydrochloride is a protein kinase inhibitor. It inhibits PKA (Ki = 1.9 μM), PKG (Ki = 0.9 μM), CaMK II (Ki = 60 μM), PKC (Ki = 18 μM), casein kinase I (Ki...

CAS 201422-03-9 PKI 14-22 amide, myristoylated

PKI 14-22 amide, myristoylated
(CAS: 201422-03-9)

PKI 14-22 amide, myristoylated is a cell-permeable version of protein kinase inhibitor PKI (14-22) amide. N-terminus is myristoylated to increase cell membrane ...

CAS 65189-71-1 Kemptide

(CAS: 65189-71-1)

Kemptide, a synthetic heptapeptide, acts as a specific substrate for cAMP-dependent protein kinase (PKA) and is shown to be a basic serine-containing heptapepti...

CAS 130964-39-5 H-89 dihydrochloride

H-89 dihydrochloride
(CAS: 130964-39-5)

H-89 is a potent and selective inhibitor of cyclic AMP-dependent protein kinase (protein kinase A) with IC50 of 48 nM, and exhibits weak inhibition on PKG, PKC,...

CAS 1813527-81-9 CCG215022

(CAS: 1813527-81-9)

CCG215022 is a G protein-coupled receptor kinases (GRKs) inhibitor (IC50s= 0.15±0.07 μM, 0.38±0.06 μM and 3.9±1 μM for GRK2, GRK5 and GRK1, respectively), with ...

CAS 108068-98-0 KT 5720

KT 5720
(CAS: 108068-98-0)

KT 5720, an anti-bacterial agent synthesized by the fungus Nocardiopsis sp, specificly blocks PKA signaling through competitive inhibition of ATP with a Ki valu...

CAS 108930-17-2 H-7 dihydrochloride

H-7 dihydrochloride
(CAS: 108930-17-2)

H-7 dihydrochloride is a protein kinase inhibitor (IC50 = 6.0, 5.8, 3.0 and 97.0 μM for inhibition of PKC, PKG, PKA and myosin light chain kinase, respectively)...

Chemical Structure

CAS 121932-06-7 PKA inhibitor fragment (6-22) amide

Quick Inquiry

Verification code

Featured Items