Reactive oxygen species receptor tyrosine kinases

Fig. 6.4 Proposed scheme for ATj-mediated transactivation of the EGF receptor and the subsequent activation of ERK1/2. The interaction of angiotensin II with the ATi receptor stimulates several pathways that result in the transactivation of the EGF receptor. In one pathway, phospholipase C (PLC) is activated, which in turn promotes the production of reactive oxygen species (ROS). ATj receptor activation also elevates [Ca2+]j, contributing to the stimulation of a Ca2+-dependent tyrosine kinase, of which Src and proline-rich tyrosine kinase-2 (Pyk2) are the preferred targets. Both ROS and the Ca2+-dependent tyrosine kinase activate a metalloprotease, presumably ADAM17, which proteolytically activates the EGF ligand. The Ca2+-dependent tyrosine kinase, as well as a Ca2+-independent kinase, also phosphorylate the EGF receptor. The activation of the EGF receptor triggers a cascade leading to the activation of ERK1/2. EGF receptor transactivation also proceeds via a G-protein-independent pathway (see text).

Esposito, F., G. Chirico, G.N. Montesano, I. Posadas, R. Ammendola, T. Russo, G. Cirino, and F. Cimino. 2003. Protein kinase B activation by reactive oxygen species is independent of tyrosine kinase receptor phosphorylation and requires SRC activity. J. Biol. Chem. 278 20828-20834. 

RNAP, DNA-dependent RNA polymerase RNAS, RNA synthesis ROS, reactive oxygen species rRIP, recombinant RIP RRL, rabbit reticulocyte lysate (for in vitro PSI measurement) rRNA, ribosomal RNA RT, reverse transcriptase RTK, receptor tyrosine kinase RY-R, ryanodine receptor,... 

Protein kinases C transduce the of signals mediated by phospholipid hydrolysis. Activation of G protein coupled receptors, tyrosine kinase receptors, and nonreceptor tyrosine kinases can activate protein kinase C, by stimulation of either phospholipases C to yield diacylglycerol or phospholipase D to yield phosphatidic acid and then diacylglycerol. Phospholipase D has been implicated in the process of generation of reactive oxygen species by neutrophil granulocytes (for review see Exton 2002, p. 53). 

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