Title : Role of protein kinase C isoforms in locomotion of Walker 256 carcinosarcoma cells.

Pub. Date : 1999 Apr 12

PMID : 10188728






6 Functional Relationships(s)
Download
Sentence
Compound Name
Protein Name
Organism
1 Treatment with low (nanomolar) concentrations of phorbol-12-myristate-13-acetate (PMA) for 5 to 30 min suppresses locomotion of Walker 256 carcinosarcoma cells, suggesting that activation of protein kinase C (PKC) is a stop signal for tumor cell locomotion. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
2 Treatment with low (nanomolar) concentrations of phorbol-12-myristate-13-acetate (PMA) for 5 to 30 min suppresses locomotion of Walker 256 carcinosarcoma cells, suggesting that activation of protein kinase C (PKC) is a stop signal for tumor cell locomotion. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
3 Long-term incubation with PMA (0.1 microM, 6 hr) resulted in significant reduction of expression of conventional PKCs alpha, betaI, betaII and gamma and of the novel PKC eta to 10% to 26% of controls. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
4 Long-term incubation with PMA (0.1 microM, 6 hr) resulted in significant reduction of expression of conventional PKCs alpha, betaI, betaII and gamma and of the novel PKC eta to 10% to 26% of controls. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
5 Motility and polarized shape of the down-regulated cells were no longer susceptible to short-term treatment with PMA, showing that active PKC is indeed responsible for the inhibitory effects of PMA. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
6 Motility and polarized shape of the down-regulated cells were no longer susceptible to short-term treatment with PMA, showing that active PKC is indeed responsible for the inhibitory effects of PMA. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus