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CALM3 — FOS

Text-mined interactions from Literome

Abe et al., Am J Respir Cell Mol Biol 2000 : In accord with promoter analyses, an electrophoretic mobility shift assay showed that CAM repressed AP-1 binding in TNF-alpha treated BET-1A cells ; however, TNF-alpha induced both AP-1 and NF-kappaB binding activities in BET-1A cells
Ekokoski et al., J Cell Physiol 2001 : The ATP stimulated expression of c-Fos and c-Jun was dependent on Ca ( 2+ ), and protein kinase C, but not on calmodulin or Ca ( 2+ ) /calmodulin dependent protein kinase II
Yamaji et al., Biochim Biophys Acta 2003 : The inhibition of Ca ( 2+ ) /calmodulin dependent protein kinases or c-Jun/AP-1 activation caused a significant decrease in the activation of GAPDH mRNA by hypoxia
Jomphe et al., Naunyn Schmiedebergs Arch Pharmacol 2003 (Second Messenger Systems) : The induction of Fos expression was blocked by tetrodotoxin, BAPTA and KN-93, thus showing that it is activity- and calcium dependent and requires the activation of a calmodulin dependent kinase ( CaMK )
Mishra et al., J Biol Chem 2005 (Calcium Signaling) : Differential involvement of calmodulin dependent protein kinase II-activated AP-1 and c-Jun N-terminal kinase activated EGR-1 signaling pathways in tumor necrosis factor-alpha and lipopolysaccharide induced CD44 expression in human monocytic cells
Falktoft et al., Neuropeptides 2009 (Neuroblastoma) : Calmodulin interacts with PAC1 and VPAC2 receptors and regulates PACAP induced FOS expression in human neuroblastoma cells ... The immediate early response gene FOS is a well-known marker of neuronal activation, so we used a human neuroblastoma cell line NB-1 to explore the role of calmodulin in PACAP induced FOS gene expression
Holloway-Erickson et al., Frontiers in behavioral neuroscience 2012 : The alpha isoform of the Calcium/Calmodulin dependent protein kinase II ( CaMKIIa ) and the immediate early gene c-Fos are involved in long-term potentiation and memory