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Neither BIS I nor BIS V treatment alone significantly altered the levels of aggrecan and type II collagen mRNA.
30 43 Consistently, PMA activates MAPK and AP-1 in AGS cells, and BIS I abolishes this effect.
BIS I, but not siRNAs against PKCα, PKCδ or PKCθ, inhibited PMA-induced cell migration (supplementary figure 6A,C).
To substantiate that the phosphorylation of PKC substrates reflects PKC catalytic activity, bisindolylmaleimide I (BIS I), a selective inhibitor of conventional and novel PKC, was used.
Importantly, BIS I demonstrated no toxicity towards H pylori, in contrast to many other PKC inhibitors, including rottlerin (supplementary figure 3) and calphostin C (data not shown).
However, PMA-induced AGS cell spreading was completely blocked by BIS I but not by siRNAs against PKCα, PKCδ or PKCθ (supplementary figure 7).
Similar(29)
The phosphorylation of PKC substrates and MARCKS in response to H pylori or PMA was completely abolished in BIS I-treated cells (figure 2F).
Quantitative analysis of CD19 mRNA demonstrated normal levels, even in cd81 pre-BII cells.
Yamagami, T. et al. Four of five RAG-expressing JCκ−/− small pre-BII cells have no L chain gene rearrangements: detection by high-efficiency single cell PCR.
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