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Gene Review

Ppp6c  -  protein phosphatase 6, catalytic subunit

Rattus norvegicus

Synonyms: PP-V, PP6C, Ppv, Protein phosphatase V, Serine/threonine-protein phosphatase 6 catalytic subunit
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High impact information on Ppp6c

  • BMP4 exposure also directly inhibited the proliferation and induced the apoptosis of PP6 cells, but not PP1 cells [1].
  • The impairment in PP6 cell proliferation was directly associated with the osteogenic differentiation of these cells [1].
  • Microvascular permeability was quantitated by determining the filtration coefficient (Kf), and pulmonary arterial (Ppa), venous (Ppv), and capillary (Ppc) pressures were measured to calculate vascular resistance (Rt) [2].
  • After baseline measurements, imidazole (TxA2 synthase inhibitor) or SQ-29,548 (TxA2-receptor antagonist) was added to the perfusate; then Kf, Ppa, Ppv, and Ppc were again measured [2].
  • Thus isoproterenol significantly attenuated vascular pressure-induced Kfc increases at moderate Ppv, possibly because of an endothelial effect, but it did not affect red cell extravasation at higher vascular pressures [3].

Biological context of Ppp6c

  • Residual blood volumes calculated from tissue hemoglobin contents were significantly increased by 53-66% in the high Ppv groups, compared with low vascular pressure controls, but there was no significant difference between High Ppv and Iso groups [3].

Anatomical context of Ppp6c

  • The antigen (ovalbumin; 0.1 mg) was injected into the reservoir 10 min after pretreatment with l-NAME (100 mmol/L) or d-NAME (100 mmol/L) and changes in portal vein pressure (Ppv), hepatic vein pressure (Phv) and perfusate flow were monitored [4].

Associations of Ppp6c with chemical compounds

  • The PGI2 changes paralleled the increase in portal flow (Qpv), pressure (Ppv), PSS and the decrease in Rspl [5].
  • Norepinephrine infusion into the portal vein (1-5 caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv [6].
  • RESULTS: After baseline measurements, the nonselective inhibitor (N(omega)-nitro-L-arginine methyl ester), the selective nNOS inhibitor 1-(2-trifluoromethylphenyl) imidazole (TRIM), TxA(2) synthase inhibitor imidazole or TxA(2)-receptor antagonist SQ-29,548 was added to the perfusate prior to measurements of Ppa, Ppv, and Ppc [7].

Analytical, diagnostic and therapeutic context of Ppp6c

  • Reported hemodynamic changes after partial hepatectomy (PH) include elevations in portal blood flow and pressure (Ppv) [5].


  1. Converse relationship between in vitro osteogenic differentiation and in vivo bone healing elicited by different populations of muscle-derived cells genetically engineered to express BMP4. Peng, H., Usas, A., Gearhart, B., Olshanski, A., Shen, H.C., Huard, J. J. Bone Miner. Res. (2004) [Pubmed]
  2. Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion. Turnage, R.H., LaNoue, J.L., Kadesky, K.M., Meng, Y., Myers, S.I. J. Appl. Physiol. (1997) [Pubmed]
  3. Isoproterenol attenuates high vascular pressure-induced permeability increases in isolated rat lungs. Parker, J.C., Ivey, C.L. J. Appl. Physiol. (1997) [Pubmed]
  4. N-NITRO-l-ARGININE METHYL ESTER POTENTIATES ANAPHYLACTIC VENOCONSTRICTION IN RAT PERFUSED LIVERS. Shibamoto, T., Ishibashi, T., Shimo, T., Cui, S., Takano, H., Tsuchida, H., Nishio, M., Kurata, Y. Clin. Exp. Pharmacol. Physiol. (2006) [Pubmed]
  5. Hormonal and splanchnic hemodynamic alterations following hepatic resection. Wu, Y., Campbell, K.A., Sitzmann, J.V. J. Surg. Res. (1993) [Pubmed]
  6. Hepatic venular pressures of rats, dogs, and rabbits. Bohlen, H.G., Maass-Moreno, R., Rothe, C.F. Am. J. Physiol. (1991) [Pubmed]
  7. Nitric oxide and thromboxane A2 modulate pulmonary pressure after ischemia and intestinal reperfusion. Słupski, M., Szadujkis-Szadurska, K., Szadujkis-Szadurski, R., Szadujkis-Szadurski, L., Włodarczyk, Z., Andruszkiewicz, J., Sinjab, A.T. Transplant. Proc. (2006) [Pubmed]
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