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JUN — SRC
Text-mined interactions from Literome
Hsia et al., J Cell Biol 2003
(Neoplasm Invasiveness...) :
Cell invasion was linked to transient FAK accumulation at lamellipodia, formation of a
FAK-Src-p130Cas-Dock180 signaling complex, elevated Rac and
c-Jun NH2-terminal kinase
activation , and increased matrix metalloproteinase expression and activity
Funakoshi-Tago et al., Eur J Biochem 2003
:
TRAF6 and
C-SRC induce synergistic
AP-1 activation via PI3-kinase-AKT-JNK pathway ... We found that IL-1 mediated
c-Src activation was
required for
AP-1 activation, but not for NF-kappa B activation and also revealed that c-Src induced AP-1 activation was enhanced synergistically by the coexpression of TNF receptor associated factor 6 (TRAF6) ... During the TRAF6 and
c-Src induced
AP-1 activation, phosphatidylinositol 3 (PI3)-kinase, its downstream signaling molecule, Akt and c-Jun N-terminal kinase (JNK) were significantly activated and inhibition of these kinase activities down-regulated AP-1 activation through the suppression of c-fos expression
Lerner-Marmarosh et al., Arterioscler Thromb Vasc Biol 2003
(Inflammation) :
TNF-alpha mediated JNK,
c-Jun , and NF-kappaB activation
required Src and SHP-2 activity
Chandrasekar et al., J Biol Chem 2005
:
Src kinase inhibitors PP1 and PP2, phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, Akt inhibitor, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, antisense JNK and dominant negative MyD88, interleukin-1 receptor associated kinase ( IRAK)-1, IRAK4, and phosphatidylinositol 3-kinase expression all
attenuated IL-18 mediated
AP-1 binding and reporter activity, CXCL16 promoter-reporter activity, and CXCL16 expression
Zhu et al., Cancer Res 2006
(Cell Transformation, Neoplastic) :
COOH-terminal
Src kinase mediated c-Jun phosphorylation
promotes c-Jun degradation and inhibits cell transformation
Nakuci et al., Exp Cell Res 2006
(Breast Neoplasms) :
However, depletion of
SRC1 or SRC3 instead
reduced c-Jun expression
Jeong et al., Exp Mol Med 2007
:
Interestingly, co-expression of E12A mutant, lack of TRAF6 binding, with cellular
Src ( Src ) results in decreased transcriptional activity of Stat3 and
AP-1 , a novel target of STP-A11 compared to that of wild type
Reinehr et al., Methods Enzymol 2007
:
Hyperosmolarity induced ROS formation then leads to a
Src-family kinase Yes mediated activation of the epidermal growth factor receptor (EGFR) and to an
activation of the
c-Jun-N-terminal kinase (JNK)
Jiao et al., Mol Biol Cell 2008
(Neoplasm Invasiveness) :
c-Jun increased c-Src mRNA abundance and
c-Src promoter activity involving an AP-1 site in the c-Src promoter
Hsieh et al., Biochim Biophys Acta 2008
:
Moreover, thrombin stimulated
activation of NF-kappaB,
AP-1 , and COX-2 promoter activity was blocked by the inhibitors of
c-Src , PKC, EGFR, MEK1/2, AP-1 and NF-kappaB, suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Baichwal et al., Nature 1991
:
Moreover,
induction of
c-Jun activity by
Src and Ras occurs in cell lines containing the c-Jun inhibitor but not in a cell line lacking it
Scodelaro Bilbao et al., Arch Biochem Biophys 2010
:
In this work, we studied the
involvement of PKC and
Src in the phosphorylation of ERK1/2, p38 and JNK1 MAPKs and in the modulation of ATF-1, c-Fos,
c-Jun and Jun D transcription factors by ATP in MCF-7 breast cancer cells
Williams et al., J Innate Immun 2009
:
Finally,
Src64B overexpression
induced F-actin formation and
Jun kinase activation in plasmatocytes
Han et al., FEBS Lett 2011
:
Structural-functional studies suggest that the proline-rich motif in the N-terminus of AFAP is critical for c-Src activation, and subsequent SRE/AP-1 transactivation and the actin binding domain in the AFAP C-terminus is negatively involved in the regulation of
AFAP/c-Src mediated
SRE/AP-1 transactivation
Yang et al., Biochem Pharmacol 2013
:
c-Src dependent
MAPKs/AP-1 activation is involved in TNF-a induced matrix metalloproteinase-9 expression in rat heart derived H9c2 cells
Muppala et al., PloS one 2013
:
In a series of colon and breast cancer cell lines, we found that CD24 activates
Src , and
induces the activation of
c-Jun and expression of c-Jun and c-Fos
Frame et al., Mol Biol Cell 1994
(Cell Transformation, Neoplastic) :
However, in CEF that had been made quiescent by serum deprivation,
v-Src induced stimulation of
AP-1 DNA binding activity was substantially reduced
Fincham et al., Cell Biol Int 1994
(Cell Transformation, Neoplastic) :
Transient early
AP-1 activation
requires proper location of
v-Src at the cell periphery and it is essential for mitogenesis
Jalali et al., Arterioscler Thromb Vasc Biol 1998
:
Thus,
p60src plays a critical role in the shear stress activation of MAPK pathways and induction of
Activating Protein-1 (AP- 1)/TRE and Elk-1/SRE mediated transcription in ECs
Levi et al., Mol Endocrinol 1998
:
Stimulation of
Jun N-terminal kinase (JNK) by gonadotropin releasing hormone in pituitary alpha T3-1 cell line is
mediated by protein kinase C,
c-Src , and CDC42