Journal: Frontiers in Immunology

Article Title: CD4 + T-cell-dependent differentiation of CD23 + follicular B cells contributes to the pulmonary pathology in a primary Sjögren’s syndrome mouse model

doi: 10.3389/fimmu.2023.1217492

Figure Lengend Snippet: FB cells in pSS model mice. (A) F (CD23 + CD21 − ) and MZ (CD23 − CD21 + ) B cells among the CD19 + cells identified in the spleen, the salivary glands, and the lungs of 10-week-old control and pSS model. Representative results are shown. (B) Proportions and numbers of follicular B cells in the spleen of 10-week-old control mice and pSS model mice. Data are presented as mean ± SD of four to five mice per group. (C) Proportions and numbers of follicular B cells in the salivary gland tissues of 12-week-old control and SS model mice. Data are presented as mean ± SD of four mice per group. (D) Population of follicular B cells in the lungs of 8- and 16-week-old control mice and SS model mice. Data are presented as mean ± SD of three to eight mice per group. * p < 0.05, ** p < 0.01. (E) CD23 + cells were detected through immunohistochemical analysis by using lung sections of 8-week-old control and SS model mice. Scale bar: 100 μm. (F) B220 + B cells and CD23 + cells were detected through immunofluorescence analysis by using lung sections obtained from 8-week-old control and pSS model mice. Nuclei were stained with DAPI. Scale bar: 50 μm.

Article Snippet: Anti-mouse B220 (eBioscience), anti-mouse CD3 (Cell Signaling Technology) monoclonal antibodies (mAbs), and anti-mouse CD23 (Boster Biological Technology) polyclonal Ab were applied to the sections overnight, at 4°C.

Techniques: Control, Immunohistochemical staining, Immunofluorescence, Staining

Journal: Frontiers in Immunology

Article Title: CD4 + T-cell-dependent differentiation of CD23 + follicular B cells contributes to the pulmonary pathology in a primary Sjögren’s syndrome mouse model

doi: 10.3389/fimmu.2023.1217492

Figure Lengend Snippet: CD23 + B-cell differentiation via IL-4 in the lungs of the pSS model mice. (A) Il4 mRNA expressions were analyzed through qRT-PCR, by using spleen and lung tissues of 8-week-old control and SS model mice. Data are presented as mean ± SD of four mice per group. * p < 0.05. (B) Gata3 (upper panel) and Tbx21 (lower panel) mRNA expressions were analyzed through qRT-PCR, by using spleen, salivary gland, and lung tissues of 8-week-old control and SS model mice. Data are presented as mean ± SD of three to four mice per group. * p < 0.05. (C) CD19 + B cells isolated from the lungs of control and SS model mice were stimulated in vitro with an anti-CD40 mAb (5 µg/ml) and recombinant IL-4 (100 ng/ml) for 7 days. The relative cell number of CD23 + B cells to the unstimulated cells was evaluated. Data are presented as mean ± SD of triplicates per group. * p < 0.05, ** p <0.01.

Article Snippet: Anti-mouse B220 (eBioscience), anti-mouse CD3 (Cell Signaling Technology) monoclonal antibodies (mAbs), and anti-mouse CD23 (Boster Biological Technology) polyclonal Ab were applied to the sections overnight, at 4°C.

Techniques: Cell Differentiation, Quantitative RT-PCR, Control, Isolation, In Vitro, Recombinant

Journal: Frontiers in Immunology

Article Title: CD4 + T-cell-dependent differentiation of CD23 + follicular B cells contributes to the pulmonary pathology in a primary Sjögren’s syndrome mouse model

doi: 10.3389/fimmu.2023.1217492

Figure Lengend Snippet: CD23 + FB cell differentiation within the lungs of anti-CD4 mAb-treated pSS model mice. (A) Anti-CD4 mAb was intraperitoneally administered to pSS model mice between their sixth to eighth week of their lives. We assessed the proportions of CD4 + T cells in the spleen and of CD4 + T and CD19 + B cells in the lungs of isotype control mAb-treated and of anti-CD4 mAb-treated pSS model mice. Data are presented as mean ± SD of seven mice per group. * p < 0.05. (B) Number of CD4 + T cells in the spleen and of CD4 + T and CD19 + B cells in the lungs of isotype control mAb- and of anti-CD4 mAb-treated pSS model mice. Data are presented as mean ± SD of seven mice per group. ** p < 0.01. (C) Pulmonary lesions in anti-CD4 mAb-treated pSS model mice were histologically evaluated. Representative images of HE-stained lung tissues sections of isotype control mAb-treated and anti-CD4 mAb-treated pSS model mice. Scale bar: 100 μm. (D) The number of foci in the pulmonary lesions was counted by using HE-stained sections. Data are presented as mean ± SD of seven mice per group. (E) CD23 + cells in the pulmonary lesions were evaluated immunohistochemically. Representative images are shown for each group. Scale bar: 100 μm. (F) CD23 + CD19 + FB cells and CD23 − CD19 + B cells were evaluated through flow cytometric analysis by using lung tissues. Representative results are shown for each group. (G) The proportions of CD23 + CD19 + FB cells and of CD23 − CD19 + B cells were analyzed through flow cytometry. Data are presented as mean ± SD of seven mice per group. * p < 0.05.

Article Snippet: Anti-mouse B220 (eBioscience), anti-mouse CD3 (Cell Signaling Technology) monoclonal antibodies (mAbs), and anti-mouse CD23 (Boster Biological Technology) polyclonal Ab were applied to the sections overnight, at 4°C.

Techniques: Cell Differentiation, Control, Staining, Flow Cytometry

Journal: Frontiers in Immunology

Article Title: CD4 + T-cell-dependent differentiation of CD23 + follicular B cells contributes to the pulmonary pathology in a primary Sjögren’s syndrome mouse model

doi: 10.3389/fimmu.2023.1217492

Figure Lengend Snippet: Preventive effect of the anti-CD4 mAb in the pulmonary lesions of pSS model mice. (A) Anti-CD4 mAb was intraperitoneally administered to pSS model mice between their fourth to sixth week of their lives. Pulmonary lesions in anti-CD4 mAb-treated pSS model mice were histologically evaluated. Representative images of HE-stained lung tissues sections of isotype control mAb-treated and anti-CD4 mAb-treated pSS model mice. Scale bar: 100 μm. (B) The area of foci in the pulmonary lesions was measured by using HE-stained sections. Data are presented as mean ± SD of seven to eight mice per group. ** p <0.01. (C) We assessed the proportions of CD4 + T cells in the spleen and lung of isotype control mAb-treated and of anti-CD4 mAb-treated pSS model mice. Data are presented as mean ± SD of seven to eight mice per group. ** p < 0.01. (D) Number of CD4 + T, CD19 + B, and CD19 + CD23 + FB cells in the lung of isotype control mAb-treated and of anti-CD4 mAb-treated pSS model mice. Data are presented as mean ± SD of seven to eight mice per group. ** p <0.01.

Article Snippet: Anti-mouse B220 (eBioscience), anti-mouse CD3 (Cell Signaling Technology) monoclonal antibodies (mAbs), and anti-mouse CD23 (Boster Biological Technology) polyclonal Ab were applied to the sections overnight, at 4°C.

Techniques: Staining, Control

Journal: Biochemical pharmacology

Article Title: TP53 R175H mutation promotes breast cancer cell proliferation through CORO1A-P38 MAPK pathway regulation.

doi: 10.1016/j.bcp.2024.116047

Figure Lengend Snippet: Fig. 4. TP53R175H regulates the expression of coronin 1A protein. (a) Visual analysis of IGV for p53-R175H mutation. (b) Cluster heat map:red indicates high expression genes; green indicates low expression genes. (c) Bubble plot of GO enrichment analysis for Control group and p53-R175H group. (d) Bubble plot of GO enrichment analysis for NC group and p53-R175H group. (e) Bubble plot of GO enrichment analysis for NC and Control groups. (f) Sequencing results analysis of CORO1A gene FPKM values. (g-j) Western Blot detection of coronin 1A protein expression. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The primary antibodies included p53 antibody (AF0879, Affinity Biosciences, US), p38 antibody (BS3566, bioworld, Nanjing, China), pp38 antibody (BS4635, bioworld, Nanjing, China), CORO1A Antibody (A04245-2, Boster, Wuhan, China), and anti-GAPDH (BM1623, Boster, Wuhan, China).

Techniques: Expressing, Mutagenesis, Control, Sequencing, Western Blot

Journal: Biochemical pharmacology

Article Title: TP53 R175H mutation promotes breast cancer cell proliferation through CORO1A-P38 MAPK pathway regulation.

doi: 10.1016/j.bcp.2024.116047

Figure Lengend Snippet: Fig. 5. Coronin 1A protein promotes cell proliferation by regulating the P38 MAPK pathway. (a-d) CCK8 assay for cell proliferation following overexpression of the CORO1A gene. (e-h) Western Blot to detect the expression of coronin 1A, p38 and p-p38 proteins in cells after transfection with CORO1A gene overexpression.

Article Snippet: The primary antibodies included p53 antibody (AF0879, Affinity Biosciences, US), p38 antibody (BS3566, bioworld, Nanjing, China), pp38 antibody (BS4635, bioworld, Nanjing, China), CORO1A Antibody (A04245-2, Boster, Wuhan, China), and anti-GAPDH (BM1623, Boster, Wuhan, China).

Techniques: CCK-8 Assay, Over Expression, Western Blot, Expressing, Transfection

Journal: Biochemical pharmacology

Article Title: TP53 R175H mutation promotes breast cancer cell proliferation through CORO1A-P38 MAPK pathway regulation.

doi: 10.1016/j.bcp.2024.116047

Figure Lengend Snippet: Fig. 6. Tea polyphenols inhibit the proliferation of breast cancer by promoting coronin 1A protein expression. (a) Docking results for the maximum binding energy of epicatechin and p53 protein. (b) Docking results for the maximum binding energy of epigallocatechin and p53 protein. (c) Docking results for the maximum binding energy of epicatechin gallate and p53 protein. (d) Docking results for the maximum binding energy of epigallocatechin gallate and p53 protein. (e-h) Western Blot detection of coronin 1A protein expression in cells after the effect of tea polyphenols. (i-j) CCK8 assay of the inhibition rate of TP53R175H mutant cells after the action of different concentration of tea polyphenols.

Article Snippet: The primary antibodies included p53 antibody (AF0879, Affinity Biosciences, US), p38 antibody (BS3566, bioworld, Nanjing, China), pp38 antibody (BS4635, bioworld, Nanjing, China), CORO1A Antibody (A04245-2, Boster, Wuhan, China), and anti-GAPDH (BM1623, Boster, Wuhan, China).

Techniques: Expressing, Binding Assay, Western Blot, CCK-8 Assay, Inhibition, Mutagenesis, Concentration Assay

Journal: Science Advances

Article Title: MAIA, Fc receptor–like 3, supersedes JUNO as IZUMO1 receptor during human fertilization

doi: 10.1126/sciadv.abn0047

Figure Lengend Snippet: ( A ) OBOC library structure (c, d -cysteine; X, 19 l -eukaryotic amino acids except l -cysteine). ( B ) Sperm-OBOC assay. ( C ) Sperm-bead binding (inset: human egg). ( D ) Sperm-bead binding (higher magnification). ( E ) Peptide hits and proportions assigned to functions. ( F ) Sperm (five donors) consistently bound to four specific bead aliquots incubated under specific conditions (fig. S1). Bead 16 hit for FcRL3. ( G ) Sperm bound to resynthesized cAMWNEDc peptide–beads during incubation. ( H ) Sperm-bound bead (higher magnification, bottom left corner; representative sperm highlighted by green cross) and “naked” bead (*). ( I ) IZUMO1 on human sperm. ( J ) Acrosomal antigen 18.6 on human sperm (control). ( K ) Antibody inhibition of sperm binding to resynthesized beads ( n = repetitions) . ( L ) Antibody inhibition of sperm fusion to zona-free hamster eggs ( n = animals, each of 10 to 15 oocytes). ( M ) Gamete interaction proteins on sperm (IZUMO1, SPACA6, DCST1, TMEM95, DCST2, and FIMP) and egg (JUNO, FcRL1, and FcRL3) experienced similar gene evolutionary histories, as shown by ERC sequence analysis. Color intensity reflects the strength of ERC value for that pair of genes. NA, not available.

Article Snippet: HEK293T cells were transfected with FcRL3 plasmid (Origene, SC125617), IZUMO 1R (Origene, SC329497), or a combination of both.

Techniques: Binding Assay, Incubation, Inhibition, Sequencing

Journal: Iranian Journal of Basic Medical Sciences

Article Title: Quinazoline derivative compound (11d) as a novel angiogenesis inhibitor inhibiting VEGFR2 and blocking VEGFR2-mediated Akt/mTOR /p70s6k signaling pathway

doi:

Figure Lengend Snippet: Inhibition of VEGFR2 kinase activity by quinazoline derivative 11d and SU6668 was analyzed using an in vitro HTScan® VEGF receptor 2 kinase kit (Cell Signaling Technology, Danvers, MA, USA) combined with colorimetric ELISA detection according to the manufacturer’s instructions. Values are mean ± SEM (n = 6) of three independent experiments

Article Snippet: In vitro VEGFR2 kinase inhibition assay was performed using recombinant human VEGFR2 (Sino Biological Inc., USA) and VEGFR2 kinase assay Kit (GENMED SCIENTIFICS INC., USA).

Techniques: Inhibition, Activity Assay, In Vitro, Enzyme-linked Immunosorbent Assay

Journal: Iranian Journal of Basic Medical Sciences

Article Title: Quinazoline derivative compound (11d) as a novel angiogenesis inhibitor inhibiting VEGFR2 and blocking VEGFR2-mediated Akt/mTOR /p70s6k signaling pathway

doi:

Figure Lengend Snippet: mRNA expression of VEGF and VEGFR2. Compound 11d reduced the mRNA expression of VEGFA and VEGFR2 in a dosedependent manner. HUVECs were treated with increasing concentrations of compound 11d for 24 hr

Article Snippet: In vitro VEGFR2 kinase inhibition assay was performed using recombinant human VEGFR2 (Sino Biological Inc., USA) and VEGFR2 kinase assay Kit (GENMED SCIENTIFICS INC., USA).

Techniques: Expressing

Journal: Iranian Journal of Basic Medical Sciences

Article Title: Quinazoline derivative compound (11d) as a novel angiogenesis inhibitor inhibiting VEGFR2 and blocking VEGFR2-mediated Akt/mTOR /p70s6k signaling pathway

doi:

Figure Lengend Snippet: (A) Compound 11d inhibited HepG-2 cell growth. Values are expressed as mean ± SEM ( n = 6) of three independent experiments; P < 0.05 versus vehicle control. (B) Compound 11d inhibited the VEGFR2-mediated AKT/mTOR/P70S6K pathway in HCC cells

Article Snippet: In vitro VEGFR2 kinase inhibition assay was performed using recombinant human VEGFR2 (Sino Biological Inc., USA) and VEGFR2 kinase assay Kit (GENMED SCIENTIFICS INC., USA).

Techniques: