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JUN — SPP1

Text-mined interactions from Literome

Bidder et al., J Biol Chem 2002 : Osteopontin transcription in aortic vascular smooth muscle cells is controlled by glucose regulated upstream stimulatory factor and activator protein-1 activities ... Expression of either USF or AP1 activates the proximal OPN promoter in A7r5 VSMCs in part via the CCTCATGAC element ... Thus, OPN gene transcription is regulated by USF and AP1 in aortic VSMCs, entrained to changes in cellular glucose metabolism
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) : Overexpression of NIK enhances OPN induced c-Jun expression, whereas overexpressed NIK had no role in OPN induced JNK1 phosphorylation and activation ... OPN stimulated both NIK and MEKK1 dependent c-Jun expression, leading to AP-1 activation, whereas NIK dependent AP-1 activation is independent of JNK1 ... 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 stimulates NIK- or JNK1 dependent c-Jun expression ... 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
Camalier et al., Cancer prevention research (Philadelphia, Pa.) 2010 (Cell Transformation, Neoplastic...) : Supplementation of medium with phosphate increased anchorage independent transformation and proliferation of BALB/c mouse JB6 epidermal cells, activation of N-ras, ERK1/2, and activator protein-1 , and increased gene expression of Fra-1, COX-2, and osteopontin in a dose dependent manner
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