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protein kinase modulator

stimulates phosphorylation of histones by mammalian cGPK & inhibits phosphorylation by cAPK; stimulates & inhibits protein kinase; see also records for PKIbeta and PKIgamma
Also Known As:
PKA inhibitor; cAMP-dependent protein kinase protein modulator; cGK Ibeta; cGKIbeta; cGMP-dependent protein kinase protein modulator; cyclic AMP-dependent protein kinase inhibitor; megamodulin; protein kinase inhibitor type I; protein kinase stimulatory modulator
Networked: 51 relevant articles (1 outcomes, 3 trials/studies) for this Bio-Agent, Comments

Relationship Network

Bio-Agent Context: Research Results

Experts

1. Neugebauer, Volker: 2 articles (10/2009 - 04/2008)
2. Lin, Hsun-Hsun: 1 article (11/2009)
3. Lai, Chih-Chia: 1 article (11/2009)
4. Chiu, Hong-Yi: 1 article (11/2009)
5. Zhang, Pei-Hua: 1 article (10/2009)
6. Yan, Xi-Sheng: 1 article (10/2009)
7. Ma, Ji-Hua: 1 article (10/2009)
8. Ji, Guangchen: 1 article (10/2009)
9. Tanabe, Mitsuo: 1 article (06/2009)
10. Takasu, Keiko: 1 article (06/2009)

Related Diseases

1. Infection
2. Anoxia (Hypoxia)
3. Seizures (Seizure)
4. Amnesia (Dissociative Amnesia)
5. Ischemia
01/01/2002 - "The ischemia-induced increase in Ser(16)phosphorylation was significantly diminished in hearts from catecholamine-depleted animals and/or after beta-blockade and abolished in the presence of the PKA-inhibitor, H-89. "
04/01/2005 - "We hypothesized that the ischemia-induced activation of cAMP-dependent protein kinase A (PKA), could beneficially be inhibited by a PKA-inhibitor N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline-sulfonamide (H-89). "
06/01/2005 - "Moreover, PKA inhibitor H89 abolished IHA hypoxia-induced increase in Ser(16) phosphorylation, Ca(2+)-pump ATPase activity, and the recovery of cardiac performance after ischemia. "
10/01/2004 - "The effects of IPC on calpain, alpha-fodrin, and LDH release were blunted by the application of the PKA inhibitor H89 or alprenolol during IPC, while transient stimulation of PKA with CPT-cAMP or isoproterenol before ischemia attenuated calpain activation, alpha-fodrin degradation, and markedly reduced LDH release (P<0.001). "
06/01/2005 - "METHODS: After 6-hydroxydopamine (6-OHDA) pretreatment and a 20-min stabilization period, hearts were perfused at constant pressure for 20 min then subjected to 40 min of global ischemia and 30 min of reperfusion (I/R, Ctrl); exposed to 0.01 microM XA for 5 min with or without 10 microM atenolol (ATE), a specific antagonist of beta1-AR, followed by a 15-min XA-free perfusion before I/R (PC, ATE-PC, respectively); treated during 20 min with either phosphoinositide (PI) 3-kinase inhibitors, LY-294002 (LY, 15 microM), or wortmaninn (WO, 0.1 microM); protein kinase C (PKC) inhibitor, GF-109203X (GF, 4 nM); or protein kinase A (PKA) inhibitor, H89 (H89, 1 microM), with an infusion starting 3 min before XA (LY-PC, WO-PC, GF-PC, and H89-PC, respectively). "
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Related Drugs and Biologics

1. Cyclic AMP-Dependent Protein Kinases (cAMP-Dependent Protein Kinase)
2. H 89 (h89)
3. Staphylococcal Protein A (A, Protein)
4. Phosphotransferases (Kinase)
5. Calcium-Calmodulin-Dependent Protein Kinase Type 2
6. Picrotoxin
7. bisindolylmaleimide
8. KT 5823
9. KN 93
10. KN 62

Related Therapies and Procedures

1. Radiotherapy

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