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Fig. 3. Rac changes the redox state of the cell through the engagement of multiple superoxide sources to modulate signal transduction. Downstream of several cell-surface receptors, Rac is activated to shift the intracellular redox state by triggering superoxide generation from several alternative sources. Tyrosine phosphatases are one of the known targets for superoxide, which are inactivated upon oxidation of a catalytic cysteine residue, thus increasing phosphotyrosine content of several effector proteins in Rac-mediated signal transduction pathways.





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