junb antibody  (NSJ Bioreagents)

Journal: bioRxiv

Article Title: Ischemic stroke induces persistent alteration to brain stromal progenitor cells linked to chronic vascular dysfunction

doi: 10.64898/2025.12.10.693193

Figure Lengend Snippet: (a) Representative image of AP-1 member JunB in six weeks post-stroke peri-infarct tissue and in no stroke. Scale bar = 50 µm. (b) Percentage of JunB+ tdTomato cells is significantly higher in peri-infarct tissue compared to no stroke. (c) Representative images of immunocytochemical labelling of JunB in SPCs (expressing tdTomato and GFP via the endogenous Pdgfra promoter) treated with TNFα, TNFα and the AP-1 inhibitor T5224 or vehicle. Scale bar = 50 μm. Treatment with TNFα resulted in increased, (d) SPC migration, (e) increased GFP intensity (proxy for Pdgfra promoter activity) and (f) nuclear JunB; all of which were abolished by pre-treatment with the AP-1 inhibitor T5224. Conversely, TNFα treatment did not result in a significant increase in (g) nuclear Jun, * = P > 0.05; ** = P > 0.01 (j) Representative images of uninjured carotid artery, carotid artery one week post FeCl 3 -induced injury and carotid artery three weeks post injury in Pdgfrb-CreER T2 transgenic mice that were bred with membrane-Tomato (mT) membrane-Green Fluorescent Protein (mG) transgenic mice immunolabelled with anti-PDGFRα or (k) anti-JunB. Scale bar = 50 μm. (l) The percentage of PDGFRα-expressing cells was significantly increased at seven days post carotid artery injury and (m) the percentage of JunB+ cells was significantly elevated at 7 days post injury. (b) Repeated measures one-way ANOVA with Tukey’s post hoc test. (d-i). Mixed effects two-way ANOVA with Tukey’s multiple comparisons test. (l-m) ANOVA with Geisser-greenhouse correction and Dunnett’s multiple comparisons test. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.

Article Snippet: After blocking, SPCs were exposed to primary antibodies against either JunB (Cell Signaling, Cat#: 3753, diluted 1:300), Jun (Cell Signaling, Cat#: 9165, diluted 1:300), cFos (invitrogen, Cat#: PA5-143600, diluted 1:2000) or NF-κB (invitrogen, Cat#: PA5-143600, diluted 1:500) diluted in antibody buffer (0,5% λ-carrageenan and 0,02% sodium azide in PBS) over night at 4° C shaking at 70rpm.

Techniques: Expressing, Migration, Activity Assay, Transgenic Assay, Membrane

Journal: bioRxiv

Article Title: Ischemic stroke induces persistent alteration to brain stromal progenitor cells linked to chronic vascular dysfunction

doi: 10.64898/2025.12.10.693193

Figure Lengend Snippet: AP-1 signaling related changes in SPCs are not mediated by IL-17. (a) Representative images of immunocytochemical labelling of JunB in SPCs (expressing tdTomato and GFP via the endogenous Pdgfra promoter) treated with IL-17, IL-17 and the AP-1 inhibitor T5224 or vehicle. Treatment with IL-17 had no effect on (b) SPC migration, (c) GFP intensity (proxy for Pdgfra promoter activity) and (d) nuclear JunB, (f) nuclear cFos or (g) nuclear Nf-κB. (e) only nuclear intensity of the AP-1 member Jun was significantly reduced upon IL-17 exposure as well as after co-treatment with the AP-1 inhibitor T5224. Scale bar = 50 μm. ANOVA with Geisser-greenhouse correction and Dunnett’s multiple comparisons test. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.

Article Snippet: After blocking, SPCs were exposed to primary antibodies against either JunB (Cell Signaling, Cat#: 3753, diluted 1:300), Jun (Cell Signaling, Cat#: 9165, diluted 1:300), cFos (invitrogen, Cat#: PA5-143600, diluted 1:2000) or NF-κB (invitrogen, Cat#: PA5-143600, diluted 1:500) diluted in antibody buffer (0,5% λ-carrageenan and 0,02% sodium azide in PBS) over night at 4° C shaking at 70rpm.

Techniques: Expressing, Migration, Activity Assay