◀ Back to FOS

FOS — SPP1

Text-mined interactions from Literome

Kim et al., J Cell Biochem 2002 : Okadaic acid stimulates osteopontin expression through de novo induction of AP-1
Renault et al., Circ Res 2003 : AP-1 is involved in UTP induced osteopontin expression in arterial smooth muscle cells
Das et al., J Biol Chem 2004 (Breast Neoplasms...) : Furthermore, OPN induces alpha(v)beta(3) integrin/EGFR mediated ERK1/2 phosphorylation and AP-1 activation ... OPN induced ERK phosphorylation, AP-1 activation, uPA secretion, and cell motility were suppressed when cells were transfected with dn c-Src or pretreated with alpha(v)beta(3) integrin antibody, c-Src kinase inhibitor ( pp2 ), EGFR tyrosine kinase inhibitor ( PD153035 ), and MEK-1 inhibitor ( PD98059 ) ... To our knowledge, this is the first report that OPN induces alpha(v)beta(3) integrin mediated AP-1 activity and uPA secretion by activating c-Src/EGFR/ERK signaling pathways and further demonstrates a functional molecular link between OPN induced integrin/c-Src dependent EGFR phosphorylation and ERK/AP-1 mediated uPA secretion, and all of these ultimately control the motility of breast cancer cells
Rangaswami et al., J Biol Chem 2005 (Neoplasm Invasiveness) : To our knowledge this is first report that OPN induces NIK/MEKK1 mediated JNK1 dependent/independent AP-1 mediated pro-MMP-9 activation and regulates the negative crosstalk between NIK/ERK1/2 and MEKK1/JNK1 pathways that ultimately controls the cell motility, invasiveness, and tumor growth
Takeshita et al., J Oral Sci 2005 (Second Messenger Systems) : Sphingosine 1-phosphate ( SPP ) actually induced expression of these oncogenes and activated AP-1
Hartl et al., Oncogene 2006 (Cell Transformation, Neoplastic...) : Electrophoretic mobility shift assays, chromatin immunoprecipitation and transcriptional reporter gene analyses showed that c-Fos and c-Jun bind specifically to this site and that c-Fos efficiently transactivates the OPN promoter
Jalvy et al., Circ Res 2007 (MAP Kinase Signaling System) : We previously demonstrated that osteopontin (OPN) expression is a key step for UTP mediated migration of arterial SMCs and that activator protein (AP)-1 , nuclear factor kappaB, and upstream stimulatory transcription factors are involved in this OPN expression
Rangaswami et al., Oncol Rep 2007 (Lung Neoplasms...) : OPN triggers NIK- and MEKK1 dependent AP-1 activation whereas NIK dependent AP-1 activation is independent of JNK1 that leads to pro-MMP-9 activation
Ahmed et al., Molecular cancer 2010 (Breast Neoplasms) : Moreover, overexpression of mTOR inhibits OPN induced NF-kappaB and AP-1-DNA binding and transcriptional activity
Sharma et al., Molecular cancer 2010 : Silencing HDAC1 followed by stimulation with PMA resulted in significant decrease in OPN promoter activity suggesting that HDAC1 but not HDAC3 or HDAC4 was required for AP-1 mediated OPN transcription
Tachibana et al., J Am Soc Nephrol 2012 (Diabetes Mellitus, Experimental...) : In vitro, LXR activation suppressed osteopontin expression in proximal tubular epithelial cells by inhibiting AP-1 dependent transcriptional activation of the osteopontin promoter