Literature DB >> 2830575

Reduced protein kinase C activity in a ras-resistant cell line derived from Ki-MSV transformed cells.

T Kamata1, N F Sullivan, M W Wooten.   

Abstract

We have examined phosphatidylinositol turnover and C-kinase distribution in a flat cellular ras-resistant cell line (C11) derived from Kirsten murine sarcoma virus (Ki-MSV) transformed NIH/3T3 cells (DT). This cell type has been shown to express high levels of the p21 Ki-ras gene product yet is resistant to the transforming effects of this protein. Our data indicate that C11 cells have reduced levels of total C-kinase activity when compared to NIH/3T3 cells and do not retain the ability to phosphorylate the growth associated 80-kDa C-kinase substrate either in vivo or in vitro. Furthermore, whilst the steady state levels of diacylglycerol and the sum of inositol phosphates are elevated in DT cells, in C11 cells these levels are reduced to an amount equivalent to that seen in NIH/3T3 cells. These data indicate a correlation between a protein kinase C dependent pathway and resistance to transformation by ras.

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Year:  1987        PMID: 2830575

Source DB:  PubMed          Journal:  Oncogene        ISSN: 0950-9232            Impact factor:   9.867


  23 in total

1.  Purification of two distinct proteins of approximate Mr 80,000 from human epithelial cells and identification as proper substrates for protein kinase C.

Authors:  M Hirai; N Shimizu
Journal:  Biochem J       Date:  1990-09-15       Impact factor: 3.857

2.  Modulation of maturation and ribosomal protein S6 phosphorylation in Xenopus oocytes by microinjection of oncogenic ras protein and protein kinase C.

Authors:  T Kamata; H F Kung
Journal:  Mol Cell Biol       Date:  1990-03       Impact factor: 4.272

3.  Differential pathways (phospholipase C and phospholipase D) of bradykinin-induced biphasic 1,2-diacylglycerol formation in non-transformed and K-ras-transformed NIH-3T3 fibroblasts. Involvement of intracellular Ca2+ oscillations in phosphatidylcholine breakdown.

Authors:  T Fu; Y Okano; Y Nozawa
Journal:  Biochem J       Date:  1992-04-15       Impact factor: 3.857

Review 4.  The biochemistry of ras p21.

Authors:  R J Grand; D Owen
Journal:  Biochem J       Date:  1991-11-01       Impact factor: 3.857

5.  Loss of responsiveness of an AP1-related factor, PEBP1, to 12-O-tetradecanoylphorbol-13-acetate after transformation of NIH 3T3 cells by the Ha-ras oncogene.

Authors:  M Satake; T Ibaraki; Y Yamaguchi; Y Ito
Journal:  J Virol       Date:  1989-09       Impact factor: 5.103

6.  Abnormal protein kinase C down regulation and reduced substrate levels in non-phorbol ester-responsive 3T3-TNR9 cells.

Authors:  H P Biemann; R L Erikson
Journal:  Mol Cell Biol       Date:  1990-05       Impact factor: 4.272

7.  Detection of genes with a potential for suppressing the transformed phenotype associated with activated ras genes.

Authors:  M Noda; H Kitayama; T Matsuzaki; Y Sugimoto; H Okayama; R H Bassin; Y Ikawa
Journal:  Proc Natl Acad Sci U S A       Date:  1989-01       Impact factor: 11.205

8.  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

9.  Thirty years of Oncogene.

Authors:  G Miller; J Stebbing
Journal:  Oncogene       Date:  2017-10-23       Impact factor: 9.867

10.  Regulation of tetradecanoyl phorbol acetate-induced responses in NIH 3T3 cells by GAP, the GTPase-activating protein associated with p21c-ras.

Authors:  M Nori; G L'Allemain; M J Weber
Journal:  Mol Cell Biol       Date:  1992-03       Impact factor: 4.272

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