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CISH — RELA

Text-mined interactions from Literome

Park et al., DNA Cell Biol 2003 : Regulatory effect of SOCS on NF-kappaB activity in murine monocytes/macrophages
Frobøse et al., Mol Endocrinol 2006 : Suppressor of cytokine signaling (SOCS)-3 was shown to inhibit IL-1 induced transcription and activation of NFkappaB and the MAPKs JNK and p38, but the mechanism is unknown
Dai et al., J Invest Dermatol 2006 : However, SOCS1 did not affect NF-kappaB signaling
Kaneko et al., J Immunol 2008 : In addition, activation of NF-kappaB and lipid peroxidation were induced by cis-UCA and SSR, but not trans-UCA, suggesting possible upstream events of the gene expression changes
Hu et al., J Immunol 2009 (Cryptosporidiosis...) : Moreover, gain-of-function ( by overexpression of CIS ) and loss-of-function ( by siRNA interference ) studies revealed that CIS could enhance IkappaBalpha degradation and regulate NF-kappaB activation in cholangiocytes in response to LPS stimulation or C. parvum infection
Hommelberg et al., Lipids 2010 (Insulin Resistance) : Of all tested unsaturated FAs, only elaidic acid ( 3-fold ), cis9,trans11-CLA ( 3-fold ) and trans10,cis12-CLA ( 13-fold ) increased NF-kappaB transactivation in myotubes
Hernandez-Flores et al., BMC cancer 2011 (Uterine Cervical Neoplasms) : CIS induces important levels of senescence and phosphorylation of ERK1/2, p38, p65/RELA , and I?Ba, and decreased the expression of anti-apoptotic protein Bcl-XL
Strebovsky et al., Frontiers in bioscience (Landmark edition) 2012 : A model is presented that integrates the current, partly conflicting, data on the role of SOCS proteins in innate immunity 's NFkappaB signaling