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CTGF — RELA
Text-mined interactions from Literome
Gao et al., Cell communication and signaling : CCS 2005
:
Activation of
nuclear factor kappa B (NF-kappaB) by
connective tissue growth factor ( CCN2 ) is involved in sustaining the survival of primary rat hepatic stellate cells
Wu et al., Kidney Int 2006
:
CTGF enhanced the mRNA expression and protein release of fractalkine, MCP-1, and RANTES, the expression of phospho ( P ) -p42/44 mitogen activated protein kinase ( MAPK ), P-phosphoinositide 3-kinase (PI3-K), P-Akt, and activity of
nuclear factor-kappaB (NF-kappaB) in mesangial cells ... P-p42/44 MAPK blockade inhibited the
CTGF induced expression of P-p42/44 MAPK but not
NF-kappaB , and partially decreased the levels of the above chemokines in supernatants ... P-PI3-K blockade downregulated the
CTGF stimulated expression of P-PI3-K, P-Akt, and
NF-kappaB but not P-p42/44 MAPK, and partially decreased the release of the above chemokines ... LXA ( 4 ) dose-dependently inhibited the
CTGF stimulated mRNA expression and protein release of the above chemokines, and the expression of P-p42/44MAPK, P-PI3-K, P-Akt, and
NF-kappaB
Chen et al., Br J Pharmacol 2008
:
Curcumin
inhibits connective tissue growth factor gene expression in activated hepatic stellate cells in vitro by blocking
NF-kappaB and ERK signalling
Terada et al., J Am Soc Nephrol 2008
(Fibrosis) :
Furthermore, aldosterone augmented the promoter activity and protein expression of intercellular adhesion molecule-1 ( ICAM-1 ), which modulates the inflammatory response, and the profibrotic cytokine
connective tissue growth factor (CTGF) in an SGK1- and
NF-kappaB dependent manner
Karger et al., Cell Signal 2008
:
CTGF stimulated binding of
NF-kappaB to the IL-6 promoter, and siRNA targeting the NF-kappaB subunit RelA interfered with CTGF induced IL-6 expression, implicating the NF-kappaB pathway in the mediation of the CTGF effect
Wu et al., Growth Factors 2008
:
CTGF enhanced the mRNA expressions and protein release of fractalkine, MCP-1 and RANTES, and the expressions of phosphorylated ERK1/2, PI3-K and PKB, and activities of
NF-KB