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PPP1R1A  -  protein phosphatase 1, regulatory...

Canis lupus familiaris

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Disease relevance of PPP1R1A


High impact information on PPP1R1A

  • Thus, phosphorylation of inhibitor-1 at threonine 75 represents a new mechanism of cardiac contractility regulation, partially through the alteration of sarcoplasmic reticulum calcium transport activity [2].
  • Adenoviral-mediated expression of the constitutively phosphorylated threonine 75 inhibitor-1 in isolated myocytes was associated with specific stimulation of type-1 protein phosphatase activity and marked inhibition of the sarcoplasmic calcium pump affinity for calcium, resulting in depressed contractility [2].
  • Inhibitor-1 represents a nodal integrator of two major second messenger pathways, adenosine 3',5'-cyclic monophosphate (cAMP) and calcium, which mediate its phosphorylation at threonine 35 and serine 67, respectively [2].
  • Plasminogen activator inhibitor-1 activity decreased during rt-PA infusion and thereafter increased in all dogs, but less so in dogs given lys-plasminogen (p < 0.05 vs. those given saline solution before rt-PA) [3].
  • We studied PP1 activity and protein and mRNA expression of the catalytic subunit of PP1 (PP1C) and protein levels of PP1-specific inhibitors [inhibitor 1 (Inh-1) and inhibitor 2 (Inh-2)] in the left ventricular (LV) myocardium of 6 dogs with heart failure (HF; LV ejection fraction, 23 +/- 2%) and 6 normal dogs [4].

Biological context of PPP1R1A

  • The catalytic subunits derived from protein phosphatases-2Ao, 2A1 and 2A2 possessed identical substrate specificities, preferentially dephosphorylated the alpha-subunit of phosphorylase kinase, were unaffected by inhibitor-1 and inhibitor-2 and were inhibited by similar concentrations of ATP [5].
  • The objective of this study was to test the hypothesis if thrombolysis induced by recombinant tissue-type plasminogen activator, (rt-PA) could be facilitated by inhibiting carboxypeptidase U (CPU, active Thrombin Activatable Fibrinolysis Inhibitor, TAFIa) activity [6].

Anatomical context of PPP1R1A


Associations of PPP1R1A with chemical compounds

  • The enzyme dephosphorylated and inactivated phosphorylase kinase and inhibitor 1, and dephosphorylated and activated glycogen synthase and acetyl-CoA carboxylase [9].
  • OxyHb and blood CSF, in contrast, failed to produce consistent or marked changes in p21Ras precipitation. p21Ras inhibitors FTPase inhibitor 1 and manumycin abolished hemolysate-induced enhancement of p21Ras immunoprecipitation [10].
  • MDCK cells cryopreserved in CryoStor CS 5 supplemented with an apoptotic inhibitor (Caspase I Inhibitor V), hereafter termed CryoStor CS 5N, resulted in a 24-h postthaw survival and recovery rate exceeding that of any other cryoprotective solution tested (85%) [11].
  • Experiments were performed to examine whether the protein phosphatase inhibitor cantharidin inhibits the negative inotropic effect induced by endothelin-1 and carbachol in isolated canine ventricular trabeculae [12].

Other interactions of PPP1R1A

  • Elucidation of the Effects of the CYP1A2 Deficiency Polymorphism in the Metabolism of 4-Cyclohexyl-1-ethyl-7-methylpyrido[2,3-d]pyrimidine-2-(1H)-one (YM-64227), a Phosphodiesterase Type 4 Inhibitor, and Its Metabolites in Dogs [13].

Analytical, diagnostic and therapeutic context of PPP1R1A

  • Since the enzyme isolated from the glycogen complex by DEAE-cellulose chromatography could be inhibited by inhibitor-1 as well as the modulator protein, it was assumed that an unknown mechanism or factor present in the glycogen fraction was responsible for this reduced sensitivity of the protein phosphatase [14].
  • In Vitro and In Vivo Metabolism of a Gamma-Secretase Inhibitor BMS-299897 and Generation of Active Metabolites in Milligram Quantities with a Microbial Bioreactor [15].


  1. Evaluation of PAI-039 [{1-benzyl-5-[4-(trifluoromethoxy)phenyl]-1H-indol-3-yl}(oxo)acetic acid], a novel plasminogen activator inhibitor-1 inhibitor, in a canine model of coronary artery thrombosis. Hennan, J.K., Elokdah, H., Leal, M., Ji, A., Friedrichs, G.S., Morgan, G.A., Swillo, R.E., Antrilli, T.M., Hreha, A., Crandall, D.L. J. Pharmacol. Exp. Ther. (2005) [Pubmed]
  2. Identification of a novel phosphorylation site in protein phosphatase inhibitor-1 as a negative regulator of cardiac function. Rodriguez, P., Mitton, B., Waggoner, J.R., Kranias, E.G. J. Biol. Chem. (2006) [Pubmed]
  3. Recombinant lys-plasminogen, but not glu-plasminogen, improves recombinant tissue-type plasminogen activator-induced coronary thrombolysis in dogs. Mehta, J.L., Chen, L., Nichols, W.W., Johannesen, M., Bregengård, C., Hedner, U., Saldeen, T.G. J. Am. Coll. Cardiol. (1995) [Pubmed]
  4. Cardiac SR-coupled PP1 activity and expression are increased and inhibitor 1 protein expression is decreased in failing hearts. Gupta, R.C., Mishra, S., Rastogi, S., Imai, M., Habib, O., Sabbah, H.N. Am. J. Physiol. Heart Circ. Physiol. (2003) [Pubmed]
  5. The protein phosphatases involved in cellular regulation. 2. Glycogen metabolism. Ingebritsen, T.S., Foulkes, J.G., Cohen, P. Eur. J. Biochem. (1983) [Pubmed]
  6. Inhibition of carboxypeptidase U (TAFIa) activity improves rt-PA induced thrombolysis in a dog model of coronary artery thrombosis. Björkman, J.A., Abrahamsson, T.I., Nerme, V.K., Mattsson, C.J. Thromb. Res. (2005) [Pubmed]
  7. Okadaic acid, a specific protein phosphatase inhibitor, induces maturation and MPF formation in Xenopus laevis oocytes. Goris, J., Hermann, J., Hendrix, P., Ozon, R., Merlevede, W. FEBS Lett. (1989) [Pubmed]
  8. Okadaic acid inhibits activation of K-Cl cotransport in red blood cells containing hemoglobins S and C. Orringer, E.P., Brockenbrough, J.S., Whitney, J.A., Glosson, P.S., Parker, J.C. Am. J. Physiol. (1991) [Pubmed]
  9. The MgATP-dependent protein phosphatase and protein phosphatase 1 have identical substrate specificities. Stewart, A.A., Hemmings, B.A., Cohen, P., Goris, J., Merlevede, W. Eur. J. Biochem. (1981) [Pubmed]
  10. Hemolysate activates P21RAS in rabbit basilar artery. Patlolla, A., Zubkov, A., Parent, A., Zhang, J. Life Sci. (2000) [Pubmed]
  11. Cell viability improves following inhibition of cryopreservation-induced apoptosis. Baust, J.M., Van Buskirk, n.u.l.l., Baust, J.G. In Vitro Cell. Dev. Biol. Anim. (2000) [Pubmed]
  12. Inhibitory action of the phosphatase inhibitor cantharidin on the endothelin-1-induced and the carbachol-induced negative inotropic effect in the canine ventricular myocardium. Chu, L., Norota, I., Ishii, K., Endoh, M. J. Cardiovasc. Pharmacol. (2003) [Pubmed]
  13. Elucidation of the Effects of the CYP1A2 Deficiency Polymorphism in the Metabolism of 4-Cyclohexyl-1-ethyl-7-methylpyrido[2,3-d]pyrimidine-2-(1H)-one (YM-64227), a Phosphodiesterase Type 4 Inhibitor, and Its Metabolites in Dogs. Tenmizu, D., Noguchi, K., Kamimura, H. Drug Metab. Dispos. (2006) [Pubmed]
  14. Regulation of protein phosphatase activity by the deinhibitor protein. Goris, J., Waelkens, E., Camps, T., Merlevede, W. Adv. Enzyme Regul. (1984) [Pubmed]
  15. In Vitro and In Vivo Metabolism of a Gamma-Secretase Inhibitor BMS-299897 and Generation of Active Metabolites in Milligram Quantities with a Microbial Bioreactor. Zhang, D., Hanson, R., Roongta, V., Dischino, D.D., Gao, Q., Sloan, C.P., Polson, C., Keavy, D., Zheng, M., Mitroka, J., Yeola, S. Curr. Drug Metab. (2006) [Pubmed]
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