◀ Back to JUN
CXCL1 — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Wang et al., Oncogene 2000
(Cell Transformation, Neoplastic...) :
The
effects of
MGSA/GRO on
AP-1 activation could be mimicked by over-expression of wild-type M-Ras or a constitutively activated M-Ras mutant in control melan-a cells as monitored by an AP-1-luciferase reporter, while expression of a dominant negative M-Ras blocked AP-1-luciferase activity in MGSA/GRO transformed melan-a clones
Cinatl et al., Int J Mol Med 2005
(Colonic Neoplasms...) :
High hydrocortisone concentrations ( > or =50 microg/ml ) completely prevented increased DNA binding activity of
AP-1 and NF-kappaB and
inhibited up-regulation of
CXCL8 and CXCL10, but did not reduce chemokine expression to basal levels
D'Aversa et al., J Neurosci Res 2008
(AIDS Dementia Complex...) :
Gel shift analyses demonstrated that NFkappaB and
AP-1 , but not C/EBPbeta,
mediate microglial
CXCL8 production
Li et al., J Clin Endocrinol Metab 2011
(Inflammation...) :
In IL-1ß- or TNF-a stimulated first trimester decidual cells, NF?B inhibitor suppressed production of all six chemokines ;
JUN NH2-terminal kinase inhibitor
inhibited secretion of CCL2, CCL4, and CCL5 ; and MAPK kinase and p38 inhibitor decreased production of
CXCL8