The antibodies to the following proteins were used: CaMK
II delta (1: 1000, Abcam Corporation.), phospho-CaMK II (1: 1000, Cell Signaling Technology Inc.), PLB (G-18) (1:200, Santa Cruz Biotechnology Inc.), p-phospholamban-R (1: 200, Santa Cruz Biotechnology Inc.), and ryanodine receptor 2 (1: 1000, Millipore Corporation.).
The activation of CaMK
, protein kinase C (PKC) and tyrosine kinase (TK), through the Ca2+ influx, leads to the activation of retrograde messengers that send signals to the presynaptic neuron.
CREB mediates the activity of several signaling cascades, including cyclic-AMP-dependent protein kinase A, [Ca.sup.2+]/ calmodulin-dependent protein kinases (CaMKs
), and mitogen-activated protein kinase (Lonze and Ginty 2002; Pandey 2004).
Previous reports demonstrated that treatment of cultured hippocampal neurons with the CaMK
kinase inhibitor STO-609 (2-5 [micro]M) inhibits CaMKI but not CaMKII (Wayman et al.
The Mb pathway involves signaling of the [Ca.sup.2+] concentration variance from muscle cells being transducted to nuclear factor of activated T cells (NFATc1) and myocyte enhancer factor 2 (MEF2) in the nucleus by activating calcineurin (CaN) or calmodulin- dependent protein kinases (CaMK
); this modulates the transcription of downstream genes, including the Mb gene [16,17].
Ang II-mediated podocyte injury can be induced by CREB which carries signal from calmodulin-dependent protein kinase II (CaMK
II) to downstream Wnt/[beta]-catenin signaling pathway to increase Wnt mRNA expression and [beta]-catenin phosphorylation leading to inhibition of podocin and nephrin expression.
Tang et al., "Calcium/calmodulin-dependent protein kinase (CaMK
) IV mediates nucleocytoplasmic shuttling and release of HMGB1 during lipopolysaccharide stimulation of macrophages," The Journal of Immunology, vol.
Leptin facilitates learning and memory performance and enhances hippocampal CAI long-term potentiation nad CaMK
II phosphorylation in rats.
Classification and regression tree (CART) analysis for deriving variable importance of parameters influencing average flexibility of CaMK
Mechanistically, an increase in the cytoplasmic [Ca.sup.2+] concentration triggers activation of [Ca.sup.2+]-calmodulin kinase (CaMK
) II, consequently leading to RIP1 phosphorylation and ROS production.
Involvement of Ca2+, CaMK
II and PKA in EGb 761-induced insulin secretion in INS-1 cells.
Stimulation of NMDAR as well as stimulation of GluA2-lacking-AMPAR results in the Ca2+ influx and induction of intracellular signaling pathways including: [Ca.sup.2+]-calmodulin-dependent protein kinase (CaMK
), cAMP response element binding protein (CREB), BDNF and its receptor, tropomyosin-related kinase B (TrkB) .