Fig. 6.
Fig. 6. Parasite death leads to Csk recruitment to GEMs, which accounts for down-regulation of AP-1 transactivation. / (A) PAG was immunoprecipitated from lysates of untreated TpM409 (TpM), of cured cells (cured), or of resting B cells (Bc) and probed by Western blotting with anti-PAG (top) and anti-Csk (bottom) antibodies. (B) TpM409 cells were cotransfected with wild-type (wt) Csk, or a kinase-dead mutant of Csk (R222), together with the 3xTRE-luciferase AP1 reporter construct. Effects of transient expression of wt Csk and CskR222 on AP-1 activation were assayed by monitoring luciferase activity in lysates of transfected cells. Percentage of luciferase activity and standard deviation relative to vector control of 3 experiments is shown.

Parasite death leads to Csk recruitment to GEMs, which accounts for down-regulation of AP-1 transactivation.

(A) PAG was immunoprecipitated from lysates of untreated TpM409 (TpM), of cured cells (cured), or of resting B cells (Bc) and probed by Western blotting with anti-PAG (top) and anti-Csk (bottom) antibodies. (B) TpM409 cells were cotransfected with wild-type (wt) Csk, or a kinase-dead mutant of Csk (R222), together with the 3xTRE-luciferase AP1 reporter construct. Effects of transient expression of wt Csk and CskR222 on AP-1 activation were assayed by monitoring luciferase activity in lysates of transfected cells. Percentage of luciferase activity and standard deviation relative to vector control of 3 experiments is shown.

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