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CALM3 — JUN

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
Botez et al., Neuropathol Appl Neurobiol 2001 (Brain Ischemia) : We conclude that : ( 1 ) the presence of C-Jun and Bcl-2 within the glucose polymer mass of CAm may be related to mitochondrial damage and/or a transient overload of proteolytic systems during cellular injury ; and ( 2 ) repetitive cellular stress during life may cause the age related increase of CAm in elderly subjects
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 ... 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
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 ... 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
Li et al., J Biol Chem 2013 (MAP Kinase Signaling System) : Wingless-type Mammary Tumor Virus Integration Site Family, Member 5A ( Wnt5a ) Regulates Human Immunodeficiency Virus Type 1 ( HIV-1 ) Envelope Glycoprotein 120 (gp120) induced Expression of Pro-Inflammatory Cytokines via the Ca2+/Calmodulin dependent Protein Kinase II ( CaMKII ) and c-Jun N-terminal Kinase (JNK) Signaling Pathways