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Gene Review

Ppp3cb  -  protein phosphatase 3, catalytic subunit,...

Mus musculus

Synonyms: 1110063J16Rik, CAM-PRP catalytic subunit, Calmodulin-dependent calcineurin A subunit beta isoform, Calnb, CnAbeta, ...
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High impact information on Ppp3cb

  • A mechanism for the compromised immune response is suggested by the observation that CnA beta(-/-) T cells are defective in stimulation-induced NFATc1, NFATc2, and NFATc3 activation [1].
  • Total peripheral T cell numbers were significantly reduced in CnA beta(-/-) mice and were defective in proliferative capacity and IL-2 production in response to PMA/ionomycin and T cell receptor cross-linking [1].
  • These results establish a critical role for CnA beta signaling in regulating T cell development and activation in vivo [1].
  • Three separate genes encode the catalytic subunit of calcineurin in mammalian cells, CnAalpha, CnAbeta, and CnAgamma [2].
  • To unequivocally establish the importance of calcineurin signaling as a mediator of the immune response, we deleted the gene encoding the predominant calcineurin isoform expressed in lymphocytes, calcineurin A beta (CnA beta) [1].

Biological context of Ppp3cb

  • In summary, absence of CnA-alpha but not CnA-beta leads to a defect in normal maturation of the NZ and glomeruli, alterations in the cell cycle, and impaired kidney function [3].

Anatomical context of Ppp3cb

  • A similar regression in scgd-dependent disease manifestation was also observed in calcineurin Abeta (CnAbeta) gene-targeted mice in both skeletal muscle and heart [4].
  • Characterization of a human regulatory subunit of protein phosphatase 3 gene (PPP3RL) expressed specifically in testis [5].

Associations of Ppp3cb with chemical compounds


Other interactions of Ppp3cb

  • Total calcineurin expression and activity was significantly reduced in whole kidney homogenates from both CnA-alpha -/- and CnA-beta -/- mice [3].
  • In contrast, mice fed (n-3)-PUFA exhibited significant increases in MKP1 and CnAbeta expression [6].


  1. Defective T cell development and function in calcineurin A beta -deficient mice. Bueno, O.F., Brandt, E.B., Rothenberg, M.E., Molkentin, J.D. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  2. Impaired cardiac hypertrophic response in Calcineurin Abeta -deficient mice. Bueno, O.F., Wilkins, B.J., Tymitz, K.M., Glascock, B.J., Kimball, T.F., Lorenz, J.N., Molkentin, J.D. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  3. Calcineurin A-alpha but not A-beta is required for normal kidney development and function. Gooch, J.L., Toro, J.J., Guler, R.L., Barnes, J.L. Am. J. Pathol. (2004) [Pubmed]
  4. Genetic disruption of calcineurin improves skeletal muscle pathology and cardiac disease in a mouse model of limb-girdle muscular dystrophy. Parsons, S.A., Millay, D.P., Sargent, M.A., Naya, F.J., McNally, E.M., Sweeney, H.L., Molkentin, J.D. J. Biol. Chem. (2007) [Pubmed]
  5. Characterization of a human regulatory subunit of protein phosphatase 3 gene (PPP3RL) expressed specifically in testis. Liu, L., Zhang, J., Yuan, J., Dang, Y., Yang, C., Chen, X., Xu, J., Yu, L. Mol. Biol. Rep. (2005) [Pubmed]
  6. Truncated deoxynivalenol-induced splenic immediate early gene response in mice consuming (n-3) polyunsaturated fatty acids. Kinser, S., Li, M., Jia, Q., Pestka, J.J. J. Nutr. Biochem. (2005) [Pubmed]
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