EN
The protein serina/threonine kinases which are highly expressed in the central nervous system (CNS) are severely affected by brain ischemia.Irrespective of substantial differences among the particular members of this group of kinases, their responses to ischemic stress show a lot of similarities.Initially they are switched on fy faciliated interaction with their specific activators/second messengers like cyclic AMP, 1,2 -sn-diacylglicrol and particularly Ca2+, then they are translocated to highly specific regions of plasma membranes.After phosphorylation of target proteins, the kinases are deactivated by means access to cAMP. In the case of CaMKII, it is probably achieved by its extensive, inhibitory autophosphorylations, while PKC seems to be proteolytically degraded.These biphasic changes in serine/threonine kinases activity may play a critical role in the evolution of postichemic brain injury and provide a mechanism for a variety of short- and long-term signalling events.