Skip to main content
Fig. 2 | BMC Genomics

Fig. 2

From: Nur77-deficiency in bone marrow-derived macrophages modulates inflammatory responses, extracellular matrix homeostasis, phagocytosis and tolerance

Fig. 2

Nur77 represses SDF-1α expression through binding to an NBRE in the SDF-1α promoter. a The activation of the non-canonical NFκB pathway was measured in Nur77-KO and WT BMM by determining active p52 levels in the presence of LPS or CD40 activating antibody. b Analysis of the SDF-1α promoter region revealed the presence of an NBRE. Mutation analysis showed involvement of this NBRE in Nur77-dependent repression of SDF1α expression as measured by luciferase activity. Data were normalized for transfection efficiency by corresponding Renilla luciferase activity and in the right panel are depicted relative to the luciferase activity in the absence of Nur77. dNBRE, mutation of NBRE. c Nur77 binding to the SDF-1α promoter was determined by ChIP analyses using SDF-1α promoter-specific primers and Nur77-specific antibodies (M210) or control IgG in BMM after lentiviral overexpression of Nur77. Data are representative of at least three independent experiments performed in triplicate. Values represent mean ± S.D. *p < 0.05, **p < 0.01

Back to article page