Journal: BMC Immunology

Article Title: Establishment and validation of a recurrent prediction model for glioma: extrinsic apoptotic molecules FADD and CASP8 are closely associated with glioma recurrence

doi: 10.1186/s12865-025-00746-z

Figure Lengend Snippet: The association between recurrent score and classical apoptotic genes. (A) The relationship between the 6 genes and recurrent score in CGGA and TCGA database . (B) PPI network of CASP3, CASP9, FADD, CASP7, CASP8, BCL2，and the 9-gene signature from the STRING. (C-D) The expression levels of the 6 apoptotic genes in low- and high-risk levels . (E-J) Correlation between recurrent score and expression levels of apoptotic genes. *P<0.05; ***P<0.001; ns, not significant

Article Snippet: Characterizing the differential expression patterns of CASP8 and FADD in gliomas and normal tissues will play a crucial role in the further development of targeted therapeutic strategies for gliomas Fig. 9 RNA and protein levels of CASP8 and FADD in normal tissues and tumors. (A-B) RNA expression of CASP8 and FADD in normal tissues from the NCBI database (https://www.ncbi.nlm.nih.gov/). (C-D) RNA expression of CASP8 and FADD in normal tissues from the Human Protein Atlas database (https://www.proteinatlas.org/). (E) Protein levels of CASP8 and FADD in normal brain tissues from The Human Protein Atlas database. (F) Protein levels of CASP8 and FADD in normal tissues from The Human Protein Atlas database. (G) Protein levels of CASP8 and FADD in tumors from The Human Protein Atlas database

Techniques: Expressing

Journal: BMC Immunology

Article Title: Establishment and validation of a recurrent prediction model for glioma: extrinsic apoptotic molecules FADD and CASP8 are closely associated with glioma recurrence

doi: 10.1186/s12865-025-00746-z

Figure Lengend Snippet: RNA and protein levels of CASP8 and FADD in normal tissues and tumors. (A-B) RNA expression of CASP8 and FADD in normal tissues from the NCBI database (https://www.ncbi.nlm.nih.gov/). (C-D) RNA expression of CASP8 and FADD in normal tissues from the Human Protein Atlas database (https://www.proteinatlas.org/). (E) Protein levels of CASP8 and FADD in normal brain tissues from The Human Protein Atlas database. (F) Protein levels of CASP8 and FADD in normal tissues from The Human Protein Atlas database. (G) Protein levels of CASP8 and FADD in tumors from The Human Protein Atlas database

Article Snippet: Characterizing the differential expression patterns of CASP8 and FADD in gliomas and normal tissues will play a crucial role in the further development of targeted therapeutic strategies for gliomas Fig. 9 RNA and protein levels of CASP8 and FADD in normal tissues and tumors. (A-B) RNA expression of CASP8 and FADD in normal tissues from the NCBI database (https://www.ncbi.nlm.nih.gov/). (C-D) RNA expression of CASP8 and FADD in normal tissues from the Human Protein Atlas database (https://www.proteinatlas.org/). (E) Protein levels of CASP8 and FADD in normal brain tissues from The Human Protein Atlas database. (F) Protein levels of CASP8 and FADD in normal tissues from The Human Protein Atlas database. (G) Protein levels of CASP8 and FADD in tumors from The Human Protein Atlas database

Techniques: RNA Expression

Journal: Biochemistry and Biophysics Reports

Article Title: Transcriptome analysis of serum biomarker, shared gene signature and pharmacological targets between diabetic cardiomyopathy and nephropathy

doi: 10.1016/j.bbrep.2025.102194

Figure Lengend Snippet: PEA15 and TFPI2 expression in normal heart and kidney tissues is evidenced by the Human Protein Atlas. (A) Representative image: PEA15 and TFPI2 antibody staining in the kidney. (B) Representative image: PEA15 and TFPI2 expression in the kidney, measured using HPA RNA-seq. (C) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney, as measured by HPA RNA-seq. (D) Percentage of cell types expressing PEA15 and TFPI2 in the kidney, determined through HPA RNA-seq. (E) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney cortex and medulla, measured using GTEx RNA-seq. (F) Representative image: PEA15 and TFPI2 antibody staining in cardiomyocytes. (G) Representative image: PEA15 and TFPI2 expression in heart muscle, measured with HPA RNA-seq. (H) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in heart muscle, as measured by HPA RNA-seq. (I) Percentage of cell types expressing PEA15 and TFPI2 in heart muscle, determined through HPA RNA-seq. (J) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the atrial appendage and left ventricle, measured using GTEx RNA-seq.

Article Snippet: PEA15 and TFPI2 expression in normal heart and kidney tissues is evidenced by the Human Protein Atlas. (A) Representative image: PEA15 and TFPI2 antibody staining in the kidney. (B) Representative image: PEA15 and TFPI2 expression in the kidney, measured using HPA RNA-seq. (C) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney, as measured by HPA RNA-seq. (D) Percentage of cell types expressing PEA15 and TFPI2 in the kidney, determined through HPA RNA-seq. (E) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney cortex and medulla, measured using GTEx RNA-seq. (F) Representative image: PEA15 and TFPI2 antibody staining in cardiomyocytes. (G) Representative image: PEA15 and TFPI2 expression in heart muscle, measured with HPA RNA-seq. (H) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in heart muscle, as measured by HPA RNA-seq. (I) Percentage of cell types expressing PEA15 and TFPI2 in heart muscle, determined through HPA RNA-seq. (J) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the atrial appendage and left ventricle, measured using GTEx RNA-seq.

Techniques: Expressing, Staining, RNA Sequencing

Journal: Biochemistry and Biophysics Reports

Article Title: Transcriptome analysis of serum biomarker, shared gene signature and pharmacological targets between diabetic cardiomyopathy and nephropathy

doi: 10.1016/j.bbrep.2025.102194

Figure Lengend Snippet: Association of shared gene signatures and progressed cell death involving apoptosis and ferroptosis. (A) Expression levels of apoptosis-related genes in cardiomyocytes under a hyperglycemic environment (GSE 62203). (B) Expression levels of apoptosis-related genes in diabetic tubules (GSE 30122). (C) Correlation of the expression of two shared genes (PEA15 and TFPI2) and selected apoptosis-related genes in cardiomyocytes under a hyperglycemic environment (GSE 62203). (D) Correlation of the expression of two shared genes (PEA15 and TFPI2) and selected apoptosis-related genes in diabetic tubules (GSE 30122). (E) Expression levels of ferroptosis-related genes in diabetic cardiomyocytes (GSE 62203) and kidneys (GSE 30122). (F) Correlation of the expression of two shared genes (PEA15 and TFPI2) and selected ferroptosis-related genes in diabetic cardiomyocytes (GSE 62203) and kidneys (GSE 30122). (G) Expression levels of ferroptosis-related genes in the peripheral blood of patients with type II diabetes (GSE 23561) and glomeruli of diabetic nephropathy (GSE 96804). (H) Correlation of the expression of two shared genes (PEA15 and TFPI2) and selected ferroptosis-related genes in the peripheral blood of patients with type II diabetes (GSE 23561) and glomeruli of diabetic nephropathy (GSE 96804). The data has been normalized, and batch effects have been handled. A T-statistic test was employed to compare the expression levels of shared genes between the two groups. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.01 denotes statistical significance. DCM: diabetic cardiomyopathy; DT: diabetic tubuli; DNT: diabetic nephropathy tubuli; DNG: diabetic nephropathy glomeruli; DM: diabetes mellitus

Article Snippet: PEA15 and TFPI2 expression in normal heart and kidney tissues is evidenced by the Human Protein Atlas. (A) Representative image: PEA15 and TFPI2 antibody staining in the kidney. (B) Representative image: PEA15 and TFPI2 expression in the kidney, measured using HPA RNA-seq. (C) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney, as measured by HPA RNA-seq. (D) Percentage of cell types expressing PEA15 and TFPI2 in the kidney, determined through HPA RNA-seq. (E) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney cortex and medulla, measured using GTEx RNA-seq. (F) Representative image: PEA15 and TFPI2 antibody staining in cardiomyocytes. (G) Representative image: PEA15 and TFPI2 expression in heart muscle, measured with HPA RNA-seq. (H) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in heart muscle, as measured by HPA RNA-seq. (I) Percentage of cell types expressing PEA15 and TFPI2 in heart muscle, determined through HPA RNA-seq. (J) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the atrial appendage and left ventricle, measured using GTEx RNA-seq.

Techniques: Expressing

Journal: Biochemistry and Biophysics Reports

Article Title: Transcriptome analysis of serum biomarker, shared gene signature and pharmacological targets between diabetic cardiomyopathy and nephropathy

doi: 10.1016/j.bbrep.2025.102194

Figure Lengend Snippet: Clinical significance of shared genes in the Nephroseq database is illustrated through the following associations. (A) the relationship between PEA15 expression and glomerular filtration rate across all measured samples. (B) The correlation between PEA15 expression and serum creatinine levels in living donors. (C) The association of TFPI2 expression with glomerular filtration rate across all measured samples, and (D) The relationship between TFPI2 expression and serum creatinine levels in samples from patients with diabetic nephropathy.

Article Snippet: PEA15 and TFPI2 expression in normal heart and kidney tissues is evidenced by the Human Protein Atlas. (A) Representative image: PEA15 and TFPI2 antibody staining in the kidney. (B) Representative image: PEA15 and TFPI2 expression in the kidney, measured using HPA RNA-seq. (C) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney, as measured by HPA RNA-seq. (D) Percentage of cell types expressing PEA15 and TFPI2 in the kidney, determined through HPA RNA-seq. (E) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney cortex and medulla, measured using GTEx RNA-seq. (F) Representative image: PEA15 and TFPI2 antibody staining in cardiomyocytes. (G) Representative image: PEA15 and TFPI2 expression in heart muscle, measured with HPA RNA-seq. (H) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in heart muscle, as measured by HPA RNA-seq. (I) Percentage of cell types expressing PEA15 and TFPI2 in heart muscle, determined through HPA RNA-seq. (J) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the atrial appendage and left ventricle, measured using GTEx RNA-seq.

Techniques: Expressing, Filtration

Journal: Biochemistry and Biophysics Reports

Article Title: Transcriptome analysis of serum biomarker, shared gene signature and pharmacological targets between diabetic cardiomyopathy and nephropathy

doi: 10.1016/j.bbrep.2025.102194

Figure Lengend Snippet: Molecular docking of candidate compounds and shared genes, including transcription factor s. (A) Affinities of candidate compounds with RUNX2 (a transcription factor for PEA15), PEA15, and TFPI2. (B) Affinities of candidate compounds with transcription factors (HBA1, HBA2, and HBB) corresponding to the three hemoglobin subunits.

Article Snippet: PEA15 and TFPI2 expression in normal heart and kidney tissues is evidenced by the Human Protein Atlas. (A) Representative image: PEA15 and TFPI2 antibody staining in the kidney. (B) Representative image: PEA15 and TFPI2 expression in the kidney, measured using HPA RNA-seq. (C) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney, as measured by HPA RNA-seq. (D) Percentage of cell types expressing PEA15 and TFPI2 in the kidney, determined through HPA RNA-seq. (E) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the kidney cortex and medulla, measured using GTEx RNA-seq. (F) Representative image: PEA15 and TFPI2 antibody staining in cardiomyocytes. (G) Representative image: PEA15 and TFPI2 expression in heart muscle, measured with HPA RNA-seq. (H) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in heart muscle, as measured by HPA RNA-seq. (I) Percentage of cell types expressing PEA15 and TFPI2 in heart muscle, determined through HPA RNA-seq. (J) Average normalized transcripts per million (nTPM) of PEA15 and TFPI2 in the atrial appendage and left ventricle, measured using GTEx RNA-seq.

Techniques:

Journal: International journal of molecular sciences

Article Title: Reovirus μ2 Protein Impairs Translation to Reduce U5 snRNP Protein Levels.

doi: 10.3390/ijms24010727

Figure Lengend Snippet: Figure 2. The µ2 protein impairs translation: (A) WB of newly synthesized proteins in HEK 293T cells expressing GFP, µ2-GFP, or GFP- µ2. Cells were transfected for 48 h, newly synthesized proteins were metabolically labeled with AHA for 4 h (or DMSO for control), a biotin moiety was added using CLICK chemistry and revealed using streptavidin-HRP. A loading control (actin) was loaded and a WB against GFP was realized to validate the expression of GFP and fusion protein between GFP and µ2; (B) quantification of three independent experiments. Biological replicates, n = 3, one-way ANOVA with Dunnett’s multiple comparisons test against the GFP alone condition (***, p ≤0.001); (C) polysome profiles for control GFP or µ2-expressing cells. Polysome to monosome ratio (P/M) and heavy to light ratio (H/L) were calculated as described in the material and methods section. Respective profiles were overlapped by aligning the 40S to the same height; (D) polysome to monosome ratio (P/M) and heavy to light ratio (H/L) from three independent experiments for control GFP or µ2-expressing cells. Biological replicates, n = 3, one-way ANOVA with Dunnett’s multiple comparisons test against the GFP alone condition (***, p ≤0.001); (E) relative mRNA level determined by qPCR for EFTUD2, PRPF8, SNRNP200, and GAPDH in 40S + 60S, 80S, and polysomal (P1 + P2 + P3) fractions from GFP or µ2-GFP expressing cells at 48 h post-transfection. Lysates were prepared, separated on a 5–50% sucrose gradient, and 30% of each fraction was subjected to RNA extraction using Qiazol. RNA was reverse transcribed using a fixed volume for each sample and subjected to qPCR with U6 snRNA as the housekeeping gene, as it was stable between all fractions. The relative expression is calculated against the first sample in the GFP condition for the 40S + 60S fraction. n = 3, biological replicates, two-way ANOVA with Dunnett’s multiple comparisons test against the GFP control for each fraction (ns, p > 0.05); and (F) WB against GFP, RPL19 (large subunit), RPS2 (small subunit), and actin in polysomal fractions from control GFP or µ2-expressing cells at 48 h post-transfection in HEK 293T cells. Results presented are mean ± standard deviation.

Article Snippet: The antibodies used in this study are the following: Actin (Sigma, A5441, 1:10,000), EFTUD2 (Abcam, ab188327, 1:2000), FLAG (Sigma, F1804, 1:1000), GFP (Santa Cruz Biotechnology, sc-9996, 1:8000), PRPF8 (Abcam, ab79237, 1:1000), Streptavidin-HRP (ThermoFisher Scientific, N100, 1:5000), RPL19 (Santa Cruz Biotechnology, 1:1000), RPS2 (1:2000, a kind gift from the Mark Bedford lab), Vinculin (Santa Cruz Biotechnology, sc-73614, 1:1000).

Techniques: Synthesized, Expressing, Transfection, Metabolic Labelling, Labeling, Control, RNA Extraction, Reverse Transcription, Standard Deviation