Literature DB >> 3360787

Protein kinase C and its substrates in tumor promoter-sensitive and -resistant cells.

B M Smith1, N H Colburn.   

Abstract

Calcium- and phospholipid-dependent protein kinase C activity and substrates were characterized in cell lysates of preneoplastic JB6 cells, a model system of genetic variants for sensitivity to tumor promoter-induced neoplastic transformation. Protein kinase C activity was similar for sensitive and resistant variants, as measured by calcium- and phospholipid-dependent phosphorylation of an exogenous substrate (histone HIII). Of 13 endogenous protein kinase C substrates, identified by labeling proteins with [gamma-32P] ATP, at least two (80 and 23 kDa) are potential candidates for mediating events on the pathway for promotion of transformation. 32P incorporation into the 80-kDa protein kinase C substrate was stimulated by tetradecanoylphorbol acetate and correlated with phenotype: the highest incorporation was found in promotion-insensitive cells, an intermediate level in promotion-sensitive cells and the lowest in the transformed cells. The phosphorylation of an 80-kDa protein, found by labeling intact cells in monolayer growth with [32P]orthophosphate, was also stimulated by tetradecanoylphorbol acetate and correlated inversely with phenotype. The 80 kDa protein kinase C substrate from cell lysates and the 80-kDa phosphoprotein from intact cells appear to be identical, as indicated by peptide mapping with protease V8 from Staphylococcus aureus. This finding suggests that the 80-kDa substrate is relevant to promoter-induced signal transduction in the intact cell. The 23-kDa protein kinase C substrate exhibited a band shift in sodium dodecyl sulfate gels in response to another transformation promoter in JB6 cells, the calcium analog, lanthanum (Smith, B. M., Gindhart, T. D., and Colburn, N. H. (1986) Carcinogenesis 7, 1949-1956). In summary, there are no unique substrates that distinguish the variants. Quantitative differences in certain substrates or their phosphorylation may, however, account for the difference in promotion sensitivity among the variants.

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Year:  1988        PMID: 3360787

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  6 in total

1.  Differential expression of an 80-kDa protein kinase C substrate in preneoplastic and neoplastic mouse JB6 cells.

Authors:  S L Simek; D Kligman; J Patel; N H Colburn
Journal:  Proc Natl Acad Sci U S A       Date:  1989-10       Impact factor: 11.205

2.  Promotion-resistant JB6 mouse epidermal cells exhibit defects in phosphatidylethanolamine synthesis and phorbol ester-induced phosphatidylcholine hydrolysis.

Authors:  Z Kiss; B Guyer; Z Dong
Journal:  Biochem J       Date:  1997-04-15       Impact factor: 3.857

3.  Shortage of mitogen-activated protein kinase is responsible for resistance to AP-1 transactivation and transformation in mouse JB6 cells.

Authors:  C Huang; W Y Ma; M R Young; N Colburn; Z Dong
Journal:  Proc Natl Acad Sci U S A       Date:  1998-01-06       Impact factor: 11.205

4.  Phenolic fraction of tobacco smoke condensate potentiates benzo[a]pyerene diol epoxide-induced cell transformation: role of protein kinase C.

Authors:  Jagat J Mukherjee; Subodh Kumar
Journal:  Mutat Res       Date:  2009-12-16       Impact factor: 2.433

Review 5.  Gene regulation and genetic susceptibility to neoplastic transformation: AP-1 and p80 expression in JB6 cells.

Authors:  L R Bernstein; E T Ben-Ari; S L Simek; N H Colburn
Journal:  Environ Health Perspect       Date:  1991-06       Impact factor: 9.031

6.  The mitogenic signaling pathway but not the plasminogen activator-inducing pathway of basic fibroblast growth factor is mediated through protein kinase C in fetal bovine aortic endothelial cells.

Authors:  M Presta; J A Maier; G Ragnotti
Journal:  J Cell Biol       Date:  1989-10       Impact factor: 10.539

  6 in total

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