By J. Hofmann, M. Sommer, E. Jarosch, U. Lenk, L. Hein

During this quantity of stories of body structure we current 3 articles on modulation of PKC in antitumor remedy, compartment-specific services of the ubiquitin-proteasome pathway and transgenic versions of alpha2-adrenergic receptor subtype functionality.

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Additional resources for Reviews of Physiology, Biochemistry, and Pharmacology Volume 142 (Reviews of Physiology, Biochemistry, and Pharmacology)

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1999). The tyrosine kinase and oncogene src promoted cell proliferation and DNA synthesis. , 1999). , 1994). , 1999). , 1997). Calphostin C and TNF-ot were found to induce apoptosis in U937 histiocytic lymphoma cells. Treatment with TPA prevented apoptosis induced by these compounds. A peptide derived from the V1 region of PKCg specifically blocked translocation of PKC~ and blocked also the inhibitory effect on apoptosis by TPA (Mayne and Murray, 1998). These results indicate that PKCg is activated during apoptosis.

These results indicate that PKCg is activated during apoptosis. However, R6 cells stably transfected with PKCa were shown to prevent cis-platin-induced apoptosis (Basu and Cline, 1995). PKC0 is cleaved by caspase 3 during apoptosis induced by diverse agents (Datta et al, 1997). In Jurkat cells, induction of apoptosis by activation of Fas inhibited the TPA-induced translocation of PKC0 from the cytosol to the membrane (Chen and Failer, 1999). In murine thymocytes treatment with the diterpene diester, ingenol-3,-20-dibenzoate induced selective translocation of nPKCS, 8, 0 and ~t from the cytosolic fraction to the particulate fraction and induced apoptosis.

Staurosporine, H-7, calphostin C and chelerythrine were found to enhance ara-C-induced apoptosis in HL-60 and U937 cells (Grant et al, 1994). Staurosporine potentiated ara-Crelated degradation of DNA to oligonucleosomal fragments in HL-60 and U937 cells, but was ineffective when given alone at these concentrations. , 1994). apoptosis. Treatment with bryostatin 1 alone failed to induce DNA damage, but promoted substantial time- and concentration-related increases in the extent of apoptosis induced by a subsequent exposure to ara-C.

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