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Figure 9 | Cell Communication and Signaling

Figure 9

From: The signaling pathway of Campylobacter jejuni-induced Cdc42 activation: Role of fibronectin, integrin beta1, tyrosine kinases and guanine exchange factor Vav2

Figure 9

Downregulation, elimination or i nterference with important Vav2 functions reduces the uptake of C. jejuni in host cells. (A) INT-407 cells were transfected with siRNA against Vav2 or a scrambled siRNA as control. After 48 hours, cells were infected with wt C. jejuni 81-176 for 6 hours. Intracellular bacteria were quantified by gentamicin protection assays. (B) The presence of active Rac1-GTP and Cdc42-GTP was quantified by CRIB-GST pulldowns. One hundred % of activity corresponds to the highest amount of detected GTPase-GTP level. (C) INT-407 cells were transfected with indicated Myc-tagged or (D) GFP-tagged Vav2 constructs. After 48 hours, cells were infected with wt C. jejuni 81-176 for 6 hours. Intracellular bacteria were quantified by gentamicin protection assays. Expression of the individual Vav2 constructs was verified by Western blot analysis. GAPDH expression levels were determined as control. (E) Vav2-deficient cells (Vav1/2-/-) or Vav2-expressing control fibroblasts (Vav1/2+/+) were infected for 6 hours with C. jejuni. Intracellular and cell-associated bacteria were quantified by gentamicin protection assays. (*) P ≤ 0.05 and (**) P ≤ 0.005 were considered as statistically significant.

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