Calcium/calmodulin-dependent kinase family member

Xie et al. found that activation of the calcium/calmodulin-dependent kinase II family member (CaMKII) following NMDAR activation directly phosphory-lates kalirin-7 on its N-terminus, thereby stimulating its GEF activity (Xie et al.,... 

Anthrax toxin is composed of three proteins protective antigen (PA 83kDa), lethal factor (LF 90kDa), and edema factor (EF 89kDa). Individually, none of the three proteins are toxic but interact synergistically with at least one of the others. PA and LF (called LeTx) can cause lethal shock in experimental animals, and a mixture of PA and EF (edema toxin, EdTx) induces edema at the site of injection. Since two discrete units of the toxin are required for its action, the term binary toxin has been used to this and other bacterial toxins. Anthrax is unique from other binary toxins in that the binary moieties (EF and LF) interact only after being secreted from the bacteria. Further, EF and LF enter the cell via a single PA protein. Assembly of the three toxin proteins is initiated when PA binds to a proteinaceous cellular receptor and is activated by a member of the furin family of cellular proteases. The exact mechanisms of internalization of the toxin moieties are subject of scientific enquiry. Inside the cellular cytoplasm, EF (a calcium and calmodulin-dependent adenylate cyclase) causes a dramatic increase in intracellular cAMP concentrations and LF acts proteolytically to cleave certain MAPK kinases. 

Ryanodine receptors are a family of intracellular Ca release channels that were originally identified in the sarcoplasmic reticulum of skeletal muscle cells. Three members of the family were distinguished, RyR2 ryanodine receptors in the cardiac muscle. RyRl (in the skeletal muscle) and RyR2 function as Ca release chaimels from the sarcoplasmic reticulum intracellular calcium store and play a crucial role in the exdtation-contraction cycle. They bind and calmodulin and become phosphorylated by various protein kinases including Ca /calmodulin- and cAMP-dependent kinases (Lokuta etal. 1995, Mayrleitner etal. 1995). 

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