rad23b  (Proteintech)

Journal: International Journal of Molecular Medicine

Article Title: Novel Hsp90 inhibitor JD-02 inhibits HSV-1 infection via the Raf/MEK/ERK signaling pathway

doi: 10.3892/ijmm.2026.5810

Figure Lengend Snippet: JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein VP5 (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.

Article Snippet: Antibodies against GAPDH (cat. no. GTX100118) were purchased from GeneTex, Inc. Antibodies against phospho-ERK1/2 (cat. no. 4370S), ERK1/2 (cat. no. 4695S), phospho-MEK1/2 (cat. no. 9154T), phospho-B-Raf (cat. no. 2696T), HA (cat. no. 3724S) and Flag (cat. no. 14793S) were obtained from Cell Signaling Technology, Inc. Antibodies against VP5 (cat. no. sc-13525), gB (cat. no. sc-56987) and Raf-B (C-19) (cat. no. sc-166) were obtained from Santa Cruz Biotechnology, Inc. Antibodies against MEK1/2 (cat. no. AF6385) were obtained from Affinity Biosciences.

Techniques: Infection, Western Blot, Viral Plaque Assay, Immunofluorescence, Virus

Journal: Neuroscience research

Article Title: The potential mechanism maintaining transactive response DNA binding protein 43 kDa in the mouse stroke model.

doi: 10.1016/j.neures.2025.01.006

Figure Lengend Snippet: Fig. 5. Total number of positive cells and pixel intensity of proteasomal degradation marker RAD23B were upregulated after tMCAO. (a) Immunohistochemistry for RAD23B at the peri-ischemic lesion. (b) Quantitative analyses of total number of RAD23B-positive cells. (c) Quantitative analyses of RAD23B pixel intensity. Scale bar = 200 μm. (d) Representative double immunofluorescence captures for TDP-43 and RAD23B showed colocalization of TDP-43 and RAD23B at 24 h post reperfusion, either in the 30 min or 60 min tMCAO group. The small panels display a representative double-positive cell. Scale bar = 50 μm. (e) Quantitative analysis of TDP-43/RAD23B double-positive cells per visual field. There were significant differences between 24 h after 30 min tMCAO compared with the sham operation group, and between 1 h, 6 h, 24 h after 60 min tMCAO compared with the sham operation group (** and ***, P < 0.01 and P < 0.001 in 30 min tMCAO group versus sham group; &, &&&, and &&&&, P < 0.05, P < 0.001, and P < 0.0001, respectively, in 60 min tMCAO group versus sham group; # and ##, P < 0.05 and P < 0.01 in 60 min versus 30 min tMCAO group; § and §§, P < 0.05 and P < 0.01 in 60 min tMCAO group; two-way ANOVA with the Tukey-Kramer multiple compari sons test).

Article Snippet: These were then incubated at 4°C overnight with the following primary antibodies: mouse anti-TDP-43 antibody (1:100, Santa Cruz, sc-376532), rabbit anti-G3BP1 antibody (1:500, Proteintech, 13057–2-AP), and rabbit anti-RAD23B antibody (1:300, Proteintech, 12121–1-AP).

Techniques: Marker, Immunohistochemistry, Immunofluorescence