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CALM3 — CREB3

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Sée et al., J Biol Chem 2001 (Necrosis) : Oxidative stress activated a caspase independent but calpain dependent decline of calcium/calmodulin dependent protein kinase IV and cAMP- responsive element binding protein ( CREB ) ... Calpain inhibitors restored calcium/calmodulin dependent protein kinase IV and CREB but did not influence phosphorylated CREB levels or survival, indicating recruitment of an additional dephosphorylation process
Mbebi et al., J Biol Chem 2002 : Further analysis of the molecular mechanisms revealed a calpain- and calcineurin dependent proteolysis of the neuroprotective calcium/calmodulin dependent protein kinase IV and its nuclear target protein cAMP responsive element binding protein
Huang et al., J Neurosci 2006 : These Ng-/- mice, as compared with Ng+/+, respond poorly after treatment of their hippocampal slices with agents that activate signaling molecules important for learning and memory, including Ca2+/calmodulin dependent protein kinase II ( alphaCaMKII ), PKC, protein kinase A (PKA), extracellular signal regulated kinase ( ERK ), and cAMP response element binding protein ( CREB )
Mishra et al., Neurochem Res 2006 (Anoxia) : Nuclear Ca ( ++ ) -influx, Ca ( ++ ) /calmodulin dependent protein kinase IV activity and CREB protein phosphorylation during post-hypoxic reoxygenation in neuronal nuclei of newborn piglets : the role of nitric oxide ... We propose that hypoxia induced increase in CaM Kinase IV activity leads to increased phosphorylation of CREB protein and transcription of proapoptotic genes during post-Hx reox resulting in Hx neuronal death
Jiao et al., J Neurochem 2007 : NMDA induced activation of the NMDA-receptor R1 subunit ( NR1 ), Ca ( 2+ ) /calmodulin dependent protein kinase II and the cAMP-response element binding protein ( CREB ), and cocaine induced CREB activation in the CPu are also oppositely regulated by dopamine D ( 1 ) and D ( 3 ) receptors
Takeda et al., Brain Res 2007 : We examined the role of the phosphorylation of calcium/calmodulin dependent protein kinase II ( CaMKII ) and cyclic AMP-response element binding protein ( CREB ) in N-methyl-d-aspartate ( NMDA ) -induced neurotoxicity in the rat retina
Tsakiri et al., Br J Pharmacol 2008 : We demonstrate that IL-1beta induced Src kinase activation triggers the phosphorylation of the NMDA receptor NR2B subunit, leading to activation of Ca ( 2+ ) /calmodulin dependent protein kinase II ( CamKII ) and the nuclear transcription factor CREB
Francis et al., Am J Physiol Cell Physiol 2008 : In several cells : 1 ) activation of HRH1 increases intracellular Ca ( 2+ ) concentration levels ; and 2 ) increased [ Ca ( 2+ ) ] ( i ) levels are coupled with calmodulin dependent stimulation of calmodulin dependent protein kinase ( CaMK ) and activation of cAMP-response element binding protein ( CREB )
Takasaki et al., Glia 2008 : ATP induced CREB phosphorylation was repressed by P2Y antagonists, BAPTA-AM, and CaM kinase inhibitors
Yamin et al., J Neurosci Res 2009 (Alzheimer Disease...) : Furthermore, these studies suggest that A beta specifically interferes with several major signaling pathways downstream of the NMDA receptor, including the Ca ( 2+ ) -dependent protein phosphatase calcineurin, Ca ( 2+ ) /calmodulin dependent protein kinase II ( CaMKII ), protein phosphatase 1, and cAMP response element binding protein ( CREB )
Zhang et al., Anesth Analg 2009 (Neuroblastoma) : Calmodulin (CaM) activation by Ca ( 2+ ), its translocation to the nucleus, and stimulation of phosphorylation of cyclic adenosine monophosphate response element binding protein ( CREB ) ( P-CREB ) are necessary for new gene expression and have been linked to long-term potentiation, a process important in memory formation
Liu et al., Arch Toxicol 2010 (Calcium Signaling) : Ca ( 2+ ) /calmodulin dependent protein kinase IIalpha ( CaMKIIalpha ), cAMP-response element binding protein ( CREB ), c-fos, and c-jun, which are important down-stream molecules of calcium signaling in describing neuron cells structure and function in the CNS, were examined in the paper with the purpose to evaluate the effect of PFOS exposure on brain and approach the molecular mechanisms involved in the neurotoxicity induced by PFOS
Wang et al., Pain 2010 (Disease Models, Animal) : Activation of several cell-type-specific kinase transcription factor cascades is required to mediate this tolerance, including calcium/calmodulin dependent protein kinase II ( CaMKII ) and cAMP response element binding protein ( CREB ) in neurons, p38 and nuclear factor kappa B ( NF?B ) in microglia and extracellular signal regulated protein kinase ( ERK ) and signal transducer and activator of transcription 1 and 3 ( Stat1/3 ) in astrocytes, because inhibitors of CaMKII, p38 and ERK pathways correspondingly reduced the increases in phosphorylated CREB, acetylated-NF?B and phosphorylated Stat1/3 levels and attenuated the development of tolerance
Guo et al., Exp Cell Res 2012 : Also, ERK and CREB phosphorylation was not mediated by protein kinase A (PKA) or calmodulin kinase ( CaMK )
Nakamura et al., Arterioscler Thromb Vasc Biol 2012 (Acidosis...) : In human CNS pericytes, low extracellular Na ( + ) or low pH generated Ca ( 2+ ) oscillation and subsequently phosphorylated Ca ( 2+ ) /calmodulin dependent kinase II ( CaMKII ) and CREB in a time dependent manner
Sheriff et al., Mol Pharmacol 1997 : These results suggest that calcium/calmodulin dependent protein kinase II induced phosphorylation of CREB may be involved in regulating feeding behavior induced by NPY