Title : MEK/ERK pathway mediates cell-shape-dependent plasminogen activator inhibitor type 1 gene expression upon drug-induced disruption of the microfilament and microtubule networks.

Pub. Date : 2002 Aug 1

PMID : 12118065






5 Functional Relationships(s)
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1 PAI-1 transcript levels in quiescent R22 cells increased rapidly and in a CD-concentration-dependent fashion, with kinetics of expression paralleling the morphological changes. Cytochalasin D serpin family E member 1 Rattus norvegicus
2 Colchicine concentrations that effectively disrupted microtubule structure and reduced the cellular "footprint" area (to approximately that of CD treatment) also stimulated PAI-1 synthesis. Cytochalasin D serpin family E member 1 Rattus norvegicus
3 Unlike the mechanism of induction in growth-factor-stimulated cells, CD- and colchicine-induced PAI-1 expression required on-going protein synthesis (i.e. it was a secondary response). Cytochalasin D serpin family E member 1 Rattus norvegicus
4 Reduced PAI-1 mRNA levels upon exposure to genistein prior to CD addition correlated with inhibition of ERK1/2 activity, implicating a tyrosine kinase in shape-dependent MEK activation. Cytochalasin D serpin family E member 1 Rattus norvegicus
5 Src-family kinases, moreover, appeared to be specific upstream elements in the CD- and colchicine-dependent pathways of PAI-1 transcription since both agents effectively activated pp60(c-src) kinase activity in quiescent R22 cells. Cytochalasin D serpin family E member 1 Rattus norvegicus