◀ Back to EGR1
EGR1 — IL1A
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Granet et al., Cytokine 2004
:
IL-1 and TNF-alpha
induced egr-1 and all AP-1 member expression, except fosB and junD
Hoffmann et al., J Biol Chem 2008
(MAP Kinase Signaling System) :
Transcriptional
activation of the
EGR-1 promoter by JNK-MKK7 or by
IL-1 required a single upstream AP-1 site and three distal serum-response elements ( SRE )
Rangnekar et al., J Biol Chem 1991
:
IL-1 caused persistent steady state elevation of gro mRNA but only transient induction of c-jun. Northern analysis using gene probes for the transcription factors c-fos and Egr-1 revealed that
IL-1 induced c-fos but not
Egr-1 expression in these cells
Gurgui et al., Cell Signal 2010
:
Using RNA interference we found that
Egr-1 is
required primarily for S1P induced expression of
IL-1 and COX2
Zayed et al., J Rheumatol 2011
:
Treatment with VA did not alter
IL-1 induced
Egr-1 expression, or its recruitment to the mPGES-1 promoter, but prevented its transcriptional activity
Nebbaki et al., Arthritis Res Ther 2012
(Osteoarthritis) :
Overexpression of Egr-1 potentiated, whereas overexpression of Sp1 alleviated, the suppressive effect of IL-1 on the PPAR? promoter, suggesting that
Egr-1 may
mediate the suppressive effect of
IL-1
Sanchez-Guerrero et al., PloS one 2012
:
Further,
IL-1beta activates
Egr-1 via the epidermal growth factor receptor (EGFR)
Wu et al., J Surg Res 2013
(Reperfusion Injury) :
Inhibition of
Egr-1 significantly attenuated lung IR injury and the inflammation response caused by IR or hypoxia/reoxygenation, as shown by the alleviated lung pathologic changes, decreased pulmonary malondialdehyde content, wet/dry ratio, reduced release of the cytokines tumor necrosis factor-a, IL-6, and IL-8 in the bronchoalveolar lavage, and
reduced Egr-1,
IL-1ß , and HO-1 protein expression and HO-1 activity