Matches in Nanopublications for { ?s ?p "The treatment of rat lung epithelial cells with nicotine for various periods differentially mobilizes multiple intracellular pathways [64]. Protein kinase C and PI3-OH-kinase are transiently activated after the treatment. Also, Ras and its downstream effector ERK1/2 are activated after long-term exposure to nicotine. The activation of Ras by nicotine treatment is responsible for the subsequent perturbation of the methotrexate (MTX)-mediated G1 cell cycle restriction, as well as an increase in production of reactive oxygen species [64]." ?g. }
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- _4 value "The treatment of rat lung epithelial cells with nicotine for various periods differentially mobilizes multiple intracellular pathways [64]. Protein kinase C and PI3-OH-kinase are transiently activated after the treatment. Also, Ras and its downstream effector ERK1/2 are activated after long-term exposure to nicotine. The activation of Ras by nicotine treatment is responsible for the subsequent perturbation of the methotrexate (MTX)-mediated G1 cell cycle restriction, as well as an increase in production of reactive oxygen species [64]." provenance.
- _4 value "The treatment of rat lung epithelial cells with nicotine for various periods differentially mobilizes multiple intracellular pathways [64]. Protein kinase C and PI3-OH-kinase are transiently activated after the treatment. Also, Ras and its downstream effector ERK1/2 are activated after long-term exposure to nicotine. The activation of Ras by nicotine treatment is responsible for the subsequent perturbation of the methotrexate (MTX)-mediated G1 cell cycle restriction, as well as an increase in production of reactive oxygen species [64]." provenance.
- _4 value "The treatment of rat lung epithelial cells with nicotine for various periods differentially mobilizes multiple intracellular pathways [64]. Protein kinase C and PI3-OH-kinase are transiently activated after the treatment. Also, Ras and its downstream effector ERK1/2 are activated after long-term exposure to nicotine. The activation of Ras by nicotine treatment is responsible for the subsequent perturbation of the methotrexate (MTX)-mediated G1 cell cycle restriction, as well as an increase in production of reactive oxygen species [64]." provenance.
- _3 value "The treatment of rat lung epithelial cells with nicotine for various periods differentially mobilizes multiple intracellular pathways [64]. Protein kinase C and PI3-OH-kinase are transiently activated after the treatment. Also, Ras and its downstream effector ERK1/2 are activated after long-term exposure to nicotine. The activation of Ras by nicotine treatment is responsible for the subsequent perturbation of the methotrexate (MTX)-mediated G1 cell cycle restriction, as well as an increase in production of reactive oxygen species [64]." provenance.