The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Protein Kinase Cδ Targets Mitochondria, Alters Mitochondrial Membrane Potential, and Induces Apoptosis in Normal and Neoplastic Keratinocytes When Overexpressed by an Adenoviral Vector
Open accessAbstract
Inactivation of protein kinase Cdelta (PKCdelta) is associated with resistance to terminal cell death in epidermal tumor cells, suggesting that activation of PKCdelta in normal epidermis may be a component of a cell death pathway. To test this hypothesis, we constructed an adenovirus vector carrying an epitope-tagged PKCdelta under a cytomegalovirus promoter to overexpress PKCdelta in normal and neoplastic keratinocytes. While PKCdelta overexpression was detected by immunoblotting in keratinocytes, the expression level of other PKC isozymes, including PKCalpha, PKCepsilon, PKCzeta, and PKCeta, did not change. Calcium-independent PKC-specific kinase activity increased after infection of keratinocytes with the PKCdelta adenovirus. Activation of PKCdelta by 12-O-tetradecanoylphorbol-13-acetate (TPA) at a nanomolar concentration was lethal to normal and neoplastic mouse and human keratinocytes overexpressing PKCdelta. Lethality was inhibited by PKC selective inhibitors, GF109203X and Ro-32-0432. TPA-induced cell death was apoptotic as evidenced by morphological criteria, TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay, DNA fragmentation, and increased caspase activity. Subcellular fractionation indicated that PKCdelta translocated to a mitochondrial enriched fraction after TPA activation, and this finding was confirmed by confocal microscopy of cells expressing a transfected PKCdelta-green fluorescent protein fusion protein. Furthermore, activation of PKCdelta in keratinocytes altered mitochondrial membrane potential, as indicated by rhodamine-123 fluorescence. Mitochondrial inhibitors, rotenone and antimycin A, reduced TPA-induced cell death in PKCdelta-overexpressing keratinocytes. These results indicate that PKCdelta can initiate a death pathway in keratinocytes that involves direct interaction with mitochondria and alterations of mitochondrial function.
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Green, D. R., & Reed, J. C. (1998) · Science · doi:10.1126/science.281.5381.1309 · Cited by 8,965
Caspases: Intracellular Signaling by Proteolysis
Salvesen, G. S., & Dixit, V. M. (1997) · Cell · doi:10.1016/s0092-8674(00)80430-4 · Cited by 2,117
Bcl-xL Regulates the Membrane Potential and Volume Homeostasis of Mitochondria
Vander Heiden, M. G., Chandel, N. S., Williamson, E. K., Schumacker, P. T., & Thompson, C. B. (1997) · Cell · doi:10.1016/s0092-8674(00)80450-x · Cited by 1,378
Proteolytic activation of protein kinase C delta by an ICE-like protease in apoptotic cells.
Emoto, Y., Manome, Y., Meinhardt, G., Kisaki, H., Kharbanda, S., Robertson, M., Ghayur, T., Wong, W. W., Kamen, R., & Weichselbaum, R. (1995) · The EMBO Journal · doi:10.1002/j.1460-2075.1995.tb00305.x · Cited by 670
Protein Kinase C δ Activates the MEK-ERK Pathway in a Manner Independent of Ras and Dependent on Raf
Ueda, Y., Hirai, S.-I., Osada, S.-I., Suzuki, A., Mizuno, K., & Ohno, S. (1996) · Journal of Biological Chemistry · doi:10.1074/jbc.271.38.23512 · Cited by 572
Mischak, H., Goodnight, J. A., Kolch, W., Martiny-Baron, G., Schaechtle, C., Kazanietz, M. G., Blumberg, P. M., Pierce, J. H., & Mushinski, J. F. (1993) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)53223-3 · Cited by 541
Self-citationThe Sevenfold Way of PKC Regulation
Liu, W. S., & Heckman, C. A. (1998) · Cellular Signalling · doi:10.1016/s0898-6568(98)00012-6 · Cited by 487
Implication of Mitochondrial Hydrogen Peroxide Generation in Ceramide-induced Apoptosis
Quillet-Mary, A., Jaffrézou, J.-P., Mansat, V., Bordier, C., Naval, J., & Laurent, G. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.34.21388 · Cited by 476
Ghayur, T., Hugunin, M., Talanian, R. V., Ratnofsky, S., Quinlan, C., Emoto, Y., Pandey, P., Datta, R., Huang, Y., Kharbanda, S., et al. (1996) · The Journal of Experimental Medicine · doi:10.1084/jem.184.6.2399 · Cited by 472
Ruvolo, P. P., Deng, X., Carr, B. K., & May, W. S. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.39.25436 · Cited by 452
Cited by
Protein kinase C and other diacylglycerol effectors in cancer
Griner, E. M., & Kazanietz, M. G. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2110 · Cited by 978
Cell Signaling through Protein Kinase C Oxidation and Activation
Cosentino-Gomes, D., Rocco-Machado, N., & Meyer-Fernandes, J. R. (2012) · International Journal of Molecular Sciences · doi:10.3390/ijms130910697 · Cited by 269
Inhibition of δ-Protein Kinase C Protects Against Reperfusion Injury of the Ischemic Heart In Vivo
Inagaki, K., Chen, L., Ikeno, F., Lee, F. H., Imahashi, K.-I., Bouley, D. M., Rezaee, M., Yock, P. G., Murphy, E., & Mochly-Rosen, D. (2003) · Circulation · doi:10.1161/01.cir.0000101682.24138.36 · Cited by 265
Eckert, R. L., Efimova, T., Dashti, S. R., Balasubramanian, S., Deucher, A., Crish, J. F., Sturniolo, M., & Bone, F. (2002) · Journal of Investigative Dermatology Symposium Proceedings · doi:10.1046/j.1523-1747.2002.19634.x · Cited by 125
Kim, T.-S., Jeong, D.-W., Yun, B. Y., & Kim, I. Y. (2002) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(02)00612-5 · Cited by 51
Metadata
- Authors
- Li, L., Lorenzo, P. S., Bogi, K., Blumberg, P. M., & Yuspa, S. H.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1999-12-01
- Volume
- 19
- Issue
- 12
- Pages
- 8547-8558
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W1806836340
- Cited by
- 281
- References
- 44
- FWCI
- 6.74
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Protein Kinase Cδ Targets Mitochondria, Alters Mitochondrial Membrane Potential, and Induces Apoptosis in Normal and Neoplastic Keratinocytes When Overexpressed by an Adenoviral Vector. https://app.cochat.ai/papers/10.1128/mcb.19.12.8547
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- Li, L., Lorenzo, P. S., Bogi, K., Blumberg, P. M., & Yuspa, S. H. (1999). Protein Kinase Cδ Targets Mitochondria, Alters Mitochondrial Membrane Potential, and Induces Apoptosis in Normal and Neoplastic Keratinocytes When Overexpressed by an Adenoviral Vector. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.19.12.8547
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