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Gene Review

Prkca  -  protein kinase C, alpha

Mus musculus

Synonyms: AI875142, PKC-A, PKC-alpha, Pkca, Protein kinase C alpha type
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Disease relevance of Prkca

  • When administered intraperitoneally in mice, the same oligodeoxynucleotide caused a dose-dependent, oligodeoxynucleotide sequence-dependent reduction of PKC-alpha mRNA in liver, with an IC50 value of 30-50 mg/kg of body weight [1].
  • Characterization of conventional protein kinase C (PKC) isotype expression during F9 teratocarcinoma differentiation. Overexpression of PKC alpha alters the expression of some differentiation-dependent genes [2].
  • These data demonstrate an irreversible decrease in and alteration of the subcellular distribution of PKC-alpha and beta 2 in DMBA-initiated/TPA-promoted papillomas [3].
  • However, TPA-induced epidermal hyperplasia in T7-PKC epsilon mice was significantly increased (52%) compared with T7-PKC alpha, T7-PKC delta and wild-type mice [4].
  • Cell type-specific expression of the genes for the protein kinase C family: down regulation of mRNAs for PKC alpha and nPKC epsilon upon in vitro differentiation of a mouse neuroblastoma cell line neuro 2a [5].

Psychiatry related information on Prkca


High impact information on Prkca


Chemical compound and disease context of Prkca


Biological context of Prkca


Anatomical context of Prkca

  • In animals in which lymphocytes were irradiated ex vivo, the expression of the Prkca isozyme was found to be maximum at 3 Gy, while in vivo irradiation did not increase the expression beyond that of 1 Gy [16].
  • In mouse C127 mammary epithelial cells, the reduction in PKC-alpha mRNA expression was both dose and time dependent [1].
  • To this end, we have stably overexpressed a dominant-negative (DN) version of PKC-alpha (DN PKC-alpha) in the murine macrophage cell line RAW 264 [17].
  • We have found that three isoforms of protein kinase C (PKC alpha, -beta, and -gamma) were expressed in undifferentiated stem cells [2].
  • The loss of the basement membrane proteoglycan perlecan and the podocyte protein nephrin in the diabetic state was not prevented in the PKC-beta(-/-) mice as previously demonstrated in the nonalbuminuric diabetic PKC-alpha(-/-) mice [18].

Associations of Prkca with chemical compounds


Regulatory relationships of Prkca

  • In contrast, LPS-induced DNA-binding and transcriptional activities of NF-IL6 were inhibited in DN PKC-alpha-overexpressing RAW 264.7 cells and correlated with an impairment of NF-IL6 nuclear translocation [20].
  • T7-PKC alpha transgenic mice (line 115) express 8-fold more PKC alpha protein than wild-type mice [4].
  • These results suggest that PKC-alpha may play a role in regulating PLD expression [22].
  • Considering that PKC-beta I and -beta II are coexpressed with PKC-alpha in mouse medullary collecting duct, the present results indicate that conventional PKC isoenzymes cannot fully compensate for each other [19].
  • Over-expression of PKC alpha down-regulated GnRH promoter activity, indicating that PKC activation was sufficient to inhibit GnRH gene expression [23].

Other interactions of Prkca

  • In wild-type mice, diabetes increased the translocation of PKC-alpha and -beta1 to the membrane, whereas only PKC-alpha was elevated in PKC-beta(-/-) mice [24].
  • At the functional level, DN PKC-alpha overexpression strongly inhibited LPS-induced interleukin-1alpha mRNA accumulation, and to a lesser extent inducible nitric oxide synthase and tumor necrosis factor-alpha expression [17].
  • This inhibition was not related to defective NF-kappaB nuclear translocation, suggesting that PKC-alpha might be involved in the modulation of other LPS-inducible transcription factors [20].
  • In the present study, we have investigated the impact of PKC-alpha on the activation of AP-1 and NF-IL6 in LPS-treated RAW 264.7 macrophages [20].
  • In a mouse neuroblast cell line, Neuro 2a, down modulation of mRNAs for both PKC alpha and nPKC epsilon was observed in association with in vitro differentiation [5].

Analytical, diagnostic and therapeutic context of Prkca


  1. Inhibition of protein kinase C-alpha expression in mice after systemic administration of phosphorothioate antisense oligodeoxynucleotides. Dean, N.M., McKay, R. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  2. Characterization of conventional protein kinase C (PKC) isotype expression during F9 teratocarcinoma differentiation. Overexpression of PKC alpha alters the expression of some differentiation-dependent genes. Kindregan, H.C., Rosenbaum, S.E., Ohno, S., Niles, R.M. J. Biol. Chem. (1994) [Pubmed]
  3. Alterations in protein kinase C isozymes alpha and beta 2 in activated Ha-ras containing papillomas in the absence of an increase in diacylglycerol. Mills, K.J., Bocckino, S.B., Burns, D.J., Loomis, C.R., Smart, R.C. Carcinogenesis (1992) [Pubmed]
  4. Relation of the induction of epidermal ornithine decarboxylase and hyperplasia to the different skin tumor-promotion susceptibilities of protein kinase C alpha, -delta and -epsilon transgenic mice. Jansen, A.P., Dreckschmidt, N.E., Verwiebe, E.G., Wheeler, D.L., Oberley, T.D., Verma, A.K. Int. J. Cancer (2001) [Pubmed]
  5. Cell type-specific expression of the genes for the protein kinase C family: down regulation of mRNAs for PKC alpha and nPKC epsilon upon in vitro differentiation of a mouse neuroblastoma cell line neuro 2a. Wada, H., Ohno, S., Kubo, K., Taya, C., Tsuji, S., Yonehara, S., Suzuki, K. Biochem. Biophys. Res. Commun. (1989) [Pubmed]
  6. Role of protein kinase C-alpha in the control of infection by intracellular pathogens in macrophages. St-Denis, A., Caouras, V., Gervais, F., Descoteaux, A. J. Immunol. (1999) [Pubmed]
  7. Alterations of protein kinase C isozyme and substrate proteins in mouse brain after electroconvulsive seizures. Chen, C.C. Brain Res. (1994) [Pubmed]
  8. p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells. Kawasaki, H., Song, J., Eckner, R., Ugai, H., Chiu, R., Taira, K., Shi, Y., Jones, N., Yokoyama, K.K. Genes Dev. (1998) [Pubmed]
  9. 12(S)-hydroxyeicosatetraenoic acid and 13(S)-hydroxyoctadecadienoic acid regulation of protein kinase C-alpha in melanoma cells: role of receptor-mediated hydrolysis of inositol phospholipids. Liu, B., Khan, W.A., Hannun, Y.A., Timar, J., Taylor, J.D., Lundy, S., Butovich, I., Honn, K.V. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  10. Diminished loss of proteoglycans and lack of albuminuria in protein kinase C-alpha-deficient diabetic mice. Menne, J., Park, J.K., Boehne, M., Elger, M., Lindschau, C., Kirsch, T., Meier, M., Gueler, F., Fiebeler, A., Bahlmann, F.H., Leitges, M., Haller, H. Diabetes (2004) [Pubmed]
  11. Increased expression of protein kinase C alpha plays a key role in retinoic acid-induced melanoma differentiation. Gruber, J.R., Ohno, S., Niles, R.M. J. Biol. Chem. (1992) [Pubmed]
  12. Apoptosis of murine melanoma B16-BL6 cells induced by quercetin targeting mitochondria, inhibiting expression of PKC-alpha and translocating PKC-delta. Zhang, X.M., Chen, J., Xia, Y.G., Xu, Q. Cancer Chemother. Pharmacol. (2005) [Pubmed]
  13. Human melanoma metastasis is inhibited following ex vivo treatment with an antisense oligonucleotide to protein kinase C-alpha. Dennis, J.U., Dean, N.M., Bennett, C.F., Griffith, J.W., Lang, C.M., Welch, D.R. Cancer Lett. (1998) [Pubmed]
  14. Genomic organization and chromosomal localization of the mouse protein kinase C alpha gene. Hara, T., Chida, K. Gene (2002) [Pubmed]
  15. Roles of specific isoforms of protein kinase C in the transcriptional control of cyclin D1 and related genes. Soh, J.W., Weinstein, I.B. J. Biol. Chem. (2003) [Pubmed]
  16. Dose-dependent differential expression of protein kinase C isozymes in mouse lymphocytes after gamma irradiation in vivo and ex vivo. Varadkar, P.A., Krishna, M., Verma, N.C. Radiat. Res. (2003) [Pubmed]
  17. Protein kinase C-alpha modulates lipopolysaccharide-induced functions in a murine macrophage cell line. St-Denis, A., Chano, F., Tremblay, P., St-Pierre, Y., Descoteaux, A. J. Biol. Chem. (1998) [Pubmed]
  18. Deletion of Protein Kinase C-{beta} Isoform In Vivo Reduces Renal Hypertrophy but Not Albuminuria in the Streptozotocin-Induced Diabetic Mouse Model. Meier, M., Park, J.K., Overheu, D., Kirsch, T., Lindschau, C., Gueler, F., Leitges, M., Menne, J., Haller, H. Diabetes (2007) [Pubmed]
  19. Evidence for a role of protein kinase C-alpha in urine concentration. Yao, L., Huang, D.Y., Pfaff, I.L., Nie, X., Leitges, M., Vallon, V. Am. J. Physiol. Renal Physiol. (2004) [Pubmed]
  20. Modulation of lipopolysaccharide-induced NF-IL6 activation by protein kinase C-alpha in a mouse macrophage cell line. Chano, F., Descoteaux, A. Eur. J. Immunol. (2002) [Pubmed]
  21. Retinoic acid-induced transition from protein kinase C beta to protein kinase C alpha in differentiated F9 cells: correlation with altered regulation of proto-oncogene expression by phorbol esters. Khuri, F.R., Cho, Y., Talmage, D.A. Cell Growth Differ. (1996) [Pubmed]
  22. Phospholipase D-mediated hydrolysis of phosphatidylcholine: role in cell signalling. Liscovitch, M., Ben-Av, P., Danin, M., Faiman, G., Eldar, H., Livneh, E. Journal of lipid mediators. (1993) [Pubmed]
  23. Suppression of GnRH gene expression in GT1-1 hypothalamic neuronal cells: action of protein kinase C. Sun, W., Choe, Y.S., Lee, Y.J., Kim, K. Neuroreport (1997) [Pubmed]
  24. Reduction of Diabetes-Induced Oxidative Stress, Fibrotic Cytokine Expression, and Renal Dysfunction in Protein Kinase C{beta}-Null Mice. Ohshiro, Y., Ma, R.C., Yasuda, Y., Hiraoka-Yamamoto, J., Clermont, A.C., Isshiki, K., Yagi, K., Arikawa, E., Kern, T.S., King, G.L. Diabetes (2006) [Pubmed]
  25. Differential expression of protein kinase C alpha and delta in testes of mouse at various stages of development. Feng, C., Zhang, J., Gasana, V., Fu, W., Liu, Y., Zong, Z., Yu, B. Cell Biochem. Funct. (2005) [Pubmed]
  26. Growth hormone and phorbol esters require specific protein kinase C isoforms to activate mitogen-activated protein kinases in 3T3-F442A cells. MacKenzie, S., Fleming, I., Houslay, M.D., Anderson, N.G., Kilgour, E. Biochem. J. (1997) [Pubmed]
  27. Nuclear import of factors involved in signaling is inhibited in C3H/10T1/2 cells treated with tetradecylthioacetic acid. Bjørndal, B., Helleland, C., Bøe, S.O., Gudbrandsen, O.A., Kalland, K.H., Bohov, P., Berge, R.K., Lillehaug, J.R. J. Lipid Res. (2002) [Pubmed]
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