Title : Evidence of two mechanisms for the activation of the glucose transporter GLUT1 by anisomycin: p38(MAP kinase) activation and protein synthesis inhibition in mammalian cells.

Pub. Date : 1997 Nov 1

PMID : 9401960






4 Functional Relationships(s)
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1 In contrast, stimulation by anisomycin, a potent Jun-NH2-terminal kinase (JNK) agonist, exhibited no lag phase. Anisomycin mitogen-activated protein kinase 8 Homo sapiens
2 In contrast, stimulation by anisomycin, a potent Jun-NH2-terminal kinase (JNK) agonist, exhibited no lag phase. Anisomycin mitogen-activated protein kinase 8 Homo sapiens
3 The stimulation of transport by a low concentration of anisomycin (0.3 microM) was transient, peaked at 30-60 min and it was inhibited (IC50 < 1 microM) by SB203580, which indicates that its mediator is not JNK, but the homologous p38(MAP kinase) (p38(MAPK)). Anisomycin mitogen-activated protein kinase 8 Homo sapiens
4 The stimulation of transport by a low concentration of anisomycin (0.3 microM) was transient, peaked at 30-60 min and it was inhibited (IC50 < 1 microM) by SB203580, which indicates that its mediator is not JNK, but the homologous p38(MAP kinase) (p38(MAPK)). SB 203580 mitogen-activated protein kinase 8 Homo sapiens