Journal: eLife

Article Title: Molecular architecture of the tumor microenvironment caused by BRCA1 and BRCA2 somatic mutations in human lung adenocarcinoma

doi: 10.7554/eLife.110662

Figure Lengend Snippet: ( A–B ) Survival analysis of BRCA2 mutation-related signature score in TCGA-LUAD ( A ) and ICB-treated ( B ) cohorts. ( C ) Comparison of BRCA1 / 2 mutation-related signature score between responders ( R ) and non-responders (NR) after ICB treatment. ( D ) Immunofluorescence staining for S100A10 (red) and DAPI (blue) on lung tumor ( T ) and adjacent ( N ) tissues from a patient with BRCA1 mutations. Scale bars, 100 µm. ( E ) Quantification and estimation of the relative intensity of the S100A10 + cells. The p value was computed with the two-sided Welch’s t test (ns, p>0.05; *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001). ( F ) Survival analysis of GAPDH (left) and MYL12A (right) in TCGA-LUAD cohort according to the expression median. ( G–H ) Average cell replicate level after being treated with entinostat and vorinostat in different LUAD cell lines. ( I ) Expression dynamics of S100A10 (left) and MYL12A (right) after treatment with different concentrations of HDAC inhibitors.

Article Snippet: The following antibodies were used: GAPDH Rabbit mAb (#A19056, 1:100,000; Abclonal), S100A10 Rabbit mAb (#A13634, 1:1000; Abclonal), LDHA Rabbit mAb (#A0861, 1:1000; Abclonal), β-Tubulin Rabbit mAb (#A12289, 1:10000; Abclonal), and HRP-conjugated Goat Anti-Rabbit IgG (H+L) (#111-035-003, 1:10000; Jackson).

Techniques: Mutagenesis, Comparison, Immunofluorescence, Staining, Expressing

Journal: eLife

Article Title: Molecular architecture of the tumor microenvironment caused by BRCA1 and BRCA2 somatic mutations in human lung adenocarcinoma

doi: 10.7554/eLife.110662

Figure Lengend Snippet: ( A–B ) Survival analysis of BRCA1 -mutant signature score in TCGA-LUAD ( A ) and ICB treated ( B ) cohorts. ( C ) Survival analysis of S100A10 (left) and LDHA (right) in TCGA-LUAD cohort according to the expression median. ( D ) The effects of sh- LDHA , S100A10 , and GAPDH on protein levels in A549 cell line. ( E ) The effects of sh- LDHA , S100A10 , GAPDH , and vector on cell proliferation were determined by a cell proliferation assay in A549 LUAD cell line. ( F ) The molecular perturbations of 4 R genes in A549 cell line at 10 µM concentration (24 hr) from the LINCS data resource. NCS: Normalized connectivity score. ( G ) The effects of HDAC inhibitors concentration on cell proliferation in A549 cell line. ( H ) Cell replication levels after treatment with different concentrations of entinostat (left) and vorinostat (right) in LUAD cell lines. Error bars, means ± SEM. Significance level was calculated by Kruskal-Wallis test. ( I ) The protein levels of LDHA , S100A10 , and GAPDH after treatment with vorinostat (left) and belinostat (right) in A549 cell line were measured using western blotting. ( J ) The mRNA levels of LDHA and GAPDH after treatment (3 µM) with vorinostat (left) and belinostat (right) in A549 cell line were measured using qPCR (n=4 per group). Error bars, means ± SEM. Significance levels were determined by Student’s t-test. For all statistical tests, *p≤0.05; **p≤0.01; ***p≤0.001. Figure 7—source data 1. PDF file containing original western blots for . Figure 7—source data 2. Original files for western blot analysis displayed in .

Article Snippet: The following antibodies were used: GAPDH Rabbit mAb (#A19056, 1:100,000; Abclonal), S100A10 Rabbit mAb (#A13634, 1:1000; Abclonal), LDHA Rabbit mAb (#A0861, 1:1000; Abclonal), β-Tubulin Rabbit mAb (#A12289, 1:10000; Abclonal), and HRP-conjugated Goat Anti-Rabbit IgG (H+L) (#111-035-003, 1:10000; Jackson).

Techniques: Mutagenesis, Expressing, Plasmid Preparation, Proliferation Assay, Concentration Assay, Western Blot

Journal: Journal of Neuroinflammation

Article Title: Porcine plasma-derived extracellular vesicles orchestrate multi-target neuroimmune reconfiguration to alleviate Alzheimer’s disease pathology in a 5×FAD mouse model

doi: 10.1186/s12974-026-03866-4

Figure Lengend Snippet: PpSEVs modulate pathological astrogliosis state. A-C Representative IF images of brain sections collected from treated mice co-stained with anti-C3 and anti-GFAP antibody ( A ), and quantification of C3 ( B ) and C3 intensity within GFAP-positive astrocytes ( C ). Scale bars, 100 μm ( n = 4 replicates per group). D-F Representative IF images of brain sections collected from treated mice co-stained with anti-S100A10 and anti-GFAP antibody ( D ), and quantification of S100A10 ( E ) and S100A10 intensity within GFAP-positive astrocytes ( F ). Scale bars, 100 μm ( n = 4 replicates per group). G , K Immunoblot analysis of GFAP, C3, and S100A10 in cortex ( G ) and hippocampus ( K ) tissue lysates ( n = 6 replicates per group). H-J Quantitative analysis of immunoblot protein bands in cortex ( G ) by ImageJ: GFAP ( H ), C3 ( I ) and S100A10 ( J ) ( n ≥ 6 replicates per group). L-N Quantitative analysis of immunoblot protein bands in hippocampus ( K ) by ImageJ: GFAP ( L ), C3 ( M ) and S100A10 ( N ) ( n ≥ 6 replicates per group). Data are presented as mean ± SD. For (B, C, E, F), statistical significance was determined using multiple unpaired two-tailed Student’s t -tests, with corrections for multiple comparisons performed using the False Discovery Rate (FDR) approach. Other was determined using an ordinary one-way ANOVA followed by Tukey’s post hoc test to correct for multiple comparisons

Article Snippet: Anti-S100A10 (ABclonal, A14658) was sourced from ABclonal, while anti-PSD-95 (Santa Cruz Biotechnology, sc-71934) was purchased from Santa Cruz Biotechnology.

Techniques: Staining, Western Blot, Two Tailed Test