Gene interactions and pathways from curated databases and text-mining

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CXCL1 — IFNG

Text-mined interactions from Literome

Hardaker et al., FASEB J 2004 (Inflammation...) : In primary cultured hASM cells taken from normal donors, CXCL10 protein expression was induced by IFN-gamma and TNF-alpha, cytokines reported as elevated in COPD, and a synergistic response was obtained when they were combined
Hillyer et al., Clin Exp Immunol 2003 : In combination with TNF-alpha, IFN-gamma suppressed CXCL8 but enhanced CCL5 and CXCL10, whereas transforming growth factor ( TGF ) -beta reduced secretion of all chemokines
Thomas et al., J Immunol 2004 (Bronchial Hyperreactivity) : In lymphocytes restimulated with CXCL9 and allergen in vitro, CXCL9 down-regulated IL-4 expression and up-regulated IFN-gamma expression, suggesting that CXCL9 is able to direct activated lymphocytes toward a Th1-type phenotype
Omari et al., Brain 2005 (Hypertrophy...) : CXCL8 and CXCL1 production by human astrocytes at both the RNA and protein levels could be induced by interleukin (IL)-1beta, while CXCL10 was induced by both IL-1beta and interferon-gamma
Traidl-Hoffmann et al., Int Arch Allergy Immunol 2006 : Keratinocyte cultures established from normal skin of healthy donors were activated by IFN-gamma in the absence or presence of desloratadine and loratadine, and tested for the release of CCL5/RANTES, CXCL8/IL-8 , CCL17/TARC and CXCL10/IP-10 ... Desloratadine and loratadine inhibited the constitutive and IFN-gamma induced release of CCL5, CXCL8 and CXCL10 from keratinocytes, while the low release of CCL17 remained unchanged
Bandyopadhyay et al., Biochem Pharmacol 2006 : In addition, apigenin inhibits IFNgamma stimulated secretion of monokines, CXCL-9 , and -10 in MC3T3-E1 cells
Kanda et al., Endocrinology 2007 (MAP Kinase Signaling System...) : Prolactin enhances interferon-gamma induced production of CXC ligand 9 (CXCL9), CXCL10 , and CXCL11 in human keratinocytes ... Although prolactin alone was ineffective, it enhanced IFN-gamma induced secretion and mRNA expression of CXCL9, CXCL10 , and CXCL11 in parallel to the activation of STAT1, NF-kappaB, and IRF-1 ... These results suggest that prolactin may enhance IFN-gamma induced CXCL9, CXCL10 , and CXCL11 production in keratinocytes via activation of STAT1, NF-kappaB, and IRF-1 through JAK2 and MEK/ERK pathways
Kanda et al., Eur J Immunol 2007 : IL-18 enhances IFN-gamma induced production of CXCL9, CXCL10 , and CXCL11 in human keratinocytes ... We examined the in vitro effects of IL-18 on IFN-gamma induced CXCL9, CXCL10 , and CXCL11 production in human keratinocytes ... IL-18 enhanced the IFN-gamma induced secretion and mRNA expression of CXCL9, CXCL10 , and CXCL11 in parallel to the activation of NF-kappaB, STAT1, and IFN-regulatory factor (IRF)-1 ... These results suggest that IL-18 may potentiate IFN-gamma induced CXCL9, CXCL10 , and CXCL11 production in keratinocytes by activating NF-kappaB, STAT1, or IRF-1 through PI3 K/Akt and MEK/ERK pathways
Taubert et al., Vet Res Commun 2008 : Furthermore, IFNgamma-stimulation led to a strong upregulation in the transcription of VCAM-1, ICAM-1, CXCL10 and CCL2 genes and to a low to moderate increase in the E- and P-selectin, CXCL1, CXCL8 , CCL5, COX-2 and iNOS gene transcripts, but failed to enhance GM-CSF gene transcription ... Furthermore, IFNgamma-stimulation led to a strong upregulation in the transcription of VCAM-1, ICAM-1, CXCL10 and CCL2 genes and to a low to moderate increase in the E- and P-selectin, CXCL1 , CXCL8, CCL5, COX-2 and iNOS gene transcripts, but failed to enhance GM-CSF gene transcription
Xu et al., Stem Cells 2009 : C/EBPbeta knockdown also inhibited the synergistic expression of CXCL1 , inducible nitric oxide synthase, and CCL5 in response to concomitant IFNgamma and TNFalpha ... Furthermore, while STAT1 is critical in IFNgamma signaling, we found that STAT1 knockdown in MSCs did not affect C/EBPbeta expression or the synergistic induction of IL-6 and CXCL1 by IFNgamma and TNFalpha
Milks et al., Liver Int 2009 (Disease Models, Animal...) : Ifng is dichotomous in the regulation of distinct chemokine subfamilies : specifically, Ifng is critical for overexpression of specific CXCL genes but dispensable for overexpression of specific CCL genes