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Image Search Results
Journal: Frontiers in immunology
Article Title: RANBP1, a member of the nuclear-cytoplasmic trafficking-regulator complex, is the terminal-striking point of the SGK1-dependent Th17 + pathological differentiation.
doi: 10.3389/fimmu.2023.1213805
Figure Lengend Snippet: FIGURE 3 RANBP1 fluctuations affect Th17+ differentiation markers expression and interfere with SGK1-dependent signal transduction. (A, B) qPCR and immunoblot analysis to assess the expression of RANBP1 (under RANBP1 lentiviral over-expression) and associated Th17+ markers (IL-23R; IL-17A; RORgt for qPCR and IL-23R and RORgt for WB over GAPDH normalization) in CD4+ naïve (Th0) control cells, in basal and under 40mM NaCl stimulation CD4+Th17+ cells, at 5 days of differentiation (n=5 qPCR; n=3 WB). (C, D) qPCR and immunoblot analysis to assess the expression of RANBP1 (under RANBP1 lentiviral mediated Silencing) and associated Th17+ markers (IL-23R; IL-17A; RORgt for qPCR and IL-23R and RORgt for WB over GAPDH normalization) in CD4+ naïve (Th0) control cells, in basal and under 40mM NaCl stimulation CD4+Th17+ cells, at 5 days of differentiation (n=5 qPCR; n=3 WB). (E, F) qPCR and immunoblot analysis to assess the expression of RANBP1 (under SGK1 lentiviral over-expression, +/- concomitant RANBP1 lentiviral mediated silencing) and associated Th17+ markers (IL-23R; IL-17A; RORgt for qPCR and IL-23R and RORgt for WB over GAPDH normalization) in CD4+ naïve (Th0) control cells, in basal and under 40mM NaCl stimulation CD4+Th17+ cells, at 5 days of differentiation (n=5 qPCR; n=3 WB). Data are representative of at least three independent experiments (unless otherwise specified) and are shown as mean ± SD. *p <0.05, **p < 0.01, and ***p < 0.001 determined by one-way ANOVA followed by Bonferroni’s post hoc test.
Article Snippet: RANBP1 silencing was obtained through
Techniques: Expressing, Transduction, Western Blot, Over Expression, Control
Journal: Frontiers in immunology
Article Title: RANBP1, a member of the nuclear-cytoplasmic trafficking-regulator complex, is the terminal-striking point of the SGK1-dependent Th17 + pathological differentiation.
doi: 10.3389/fimmu.2023.1213805
Figure Lengend Snippet: FIGURE 4 RANBP1 regulates FOXO1 nuclear exclusion during Th17+ differentiation, working as an SGK1 down-stream effector. (A) Immunoblot analysis of FOXO1 expression in the separated cytoplasmic and nuclear fractions (cropped gel, SF3 for uncropped version), under RANBP1 lentiviral over- expression in CD4+ naïve (Th0) control cells and in basal CD4+Th17+ cells, at 5 days of differentiation. a-Tubulin and Nucleolin were used as cytoplasmic and nuclear loading controls, respectively. Under the same experimental conditions, the localization of FOXO1 was observed by immunofluorescence (Red Ch FOXO1, Blue Ch=DAPI). (n=2 for WB and n=3 for IF). (B) Immunoblot analysis of FOXO1 expression in the separated cytoplasmic and nuclear fractions (cropped gel, SF3 for uncropped version), under RANBP1 lentiviral silencing in CD4+ naïve (Th0) control cells and in basal CD4+Th17+ cells, at 5 days of differentiation. a-Tubulin and Nucleolin were used as cytoplasmic and nuclear loading controls, respectively. Under the same experimental conditions, the localization of FOXO1 was observed by immunofluorescence (Red Ch FOXO1, Blue Ch=DAPI). (n=2 for WB and n=3 for IF). (C) Immunofluorescence analysis of FOXO1 under SGK1 lentiviral over-expression, +/- concomitant RANBP1 lentiviral mediated silencing, in CD4+ naïve (Th0) control cells and in basal CD4+Th17+ cells, at 5 days of differentiation. (Red Ch=FOXO1, Blue Ch=DAPI, Green Ch=SGK1). (n=3). (D) Graphical representation of the proposed model.
Article Snippet: RANBP1 silencing was obtained through
Techniques: Western Blot, Expressing, Over Expression, Control