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Overexpressed IGFBP-1 in transgenic mice shows that its increase produces hyperinsulinaemia accompanied by glucose intolerance, and that this process is dependent upon IGFBP-1 phosphorylation statewhich is increased in diabetes [259]

Interestingly, almost all mutants with a defect in LCA-induced biofilm also had disrupted or altered self-aggregation in YCFA + DMSO, suggesting that the mechanisms underlying these two phenomena may overlap to a large degree

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