Gene interactions and pathways from curated databases and text-mining

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CXCL12 — JUN

Text-mined interactions from Literome

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
Florin et al., J Cell Sci 2005 : Increased keratinocyte proliferation by JUN dependent expression of PTN and SDF-1 in fibroblasts
Kremer et al., J Immunol 2007 : IL-10 promoter activity was ablated by mutating two nonpolymorphic binding sites for the AP-1 transcription factor, and chromatin immunoprecipitation assays of primary human T cells revealed that SDF-1 costimulation enhances AP-1 binding to both of these sites
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
Sung et al., Circ Res 2009 (Atherosclerosis...) : Inhibition of Sp1 and AP-1 activations by specific siRNA blocked the homocysteine induced SDF-1 promoter activity and expression
Hsu et al., J Cell Physiol 2012 (Carcinoma, Hepatocellular...) : Inhibition of Sp1 and AP-1 activations by specific siRNAs blocked the uPA induced SDF-1 promoter activity and expression
Huang et al., J Cell Physiol 2012 (Colorectal Neoplasms...) : Analysis of transcription factor binding using ELISA and chromatin immunoprecipitation assays revealed that SDF-1 increased Sp1- and AP-1-DNA binding activities in DLD-1 cells
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
Huang et al., J Cell Physiol 2013 (Colorectal Neoplasms...) : Inhibition of NF-?B and AP-1 activation blocked the visfatin induced expression and activity of the SDF-1 promoter