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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