pea15  (Human Protein Atlas)

Journal: Heliyon

Article Title: Breast cancer cell secretome analysis to decipher miRNA regulating the tumor microenvironment and discover potential biomarkers

doi: 10.1016/j.heliyon.2023.e15421

Figure Lengend Snippet: Validation of secretome marker gene expression in MCF7-miR526b and MCF7-miR655 cells compared to MCF7-Mock in total cellular mRNA level. Upregulated secretory marker gene expression was high in both miRNA-overexpressed cells ( A ) YWHAB, ( B ) MYL6B , ( C ) TXNDC12 , and ( D ) SFN. Downregulated secretory markers gene expression was low in miRNA-overexpressed cells ( E ) FN1, ( F ) PSMB6 , ( G ) PRDX4 , and ( H ) PEA15. The control gene used was ACTB .

Article Snippet: X: 23,664,260–23,686,399), and PEA15 (Hs00269428_m1, Chromosome Location: Chr.1: 160,205,319–160,215,376), to determine gene expression in total cellular RNA level and cell-free secretions of different breast cancer cell lines.

Techniques: Biomarker Discovery, Marker, Gene Expression, Control

Journal: Heliyon

Article Title: Breast cancer cell secretome analysis to decipher miRNA regulating the tumor microenvironment and discover potential biomarkers

doi: 10.1016/j.heliyon.2023.e15421

Figure Lengend Snippet: Validation of secretome marker mRNA expression in cell-free secretions. All four upregulated secretory markers mRNA expression in the cell-free secretion ( A ) YWHAB, ( B ) MYL6B , ( C ) TXNDC12 , and ( D ) SFN was high in miRNA-overexpressed cells. Among four identified downregulated secretory markers, ( E ) PRDX4 and ( F ) PEA15 are downregulated in both miRNA cell-free secretions. ( G ) PSMB6 is downregulated in MCF7-miR526b cell-free secretions but not in MCF7-miR655. ( H ) FN1 is upregulated in both miRNA cell-free secretions. The control gene used was RPL5 .

Article Snippet: X: 23,664,260–23,686,399), and PEA15 (Hs00269428_m1, Chromosome Location: Chr.1: 160,205,319–160,215,376), to determine gene expression in total cellular RNA level and cell-free secretions of different breast cancer cell lines.

Techniques: Biomarker Discovery, Marker, Expressing, Control

Journal: Heliyon

Article Title: Breast cancer cell secretome analysis to decipher miRNA regulating the tumor microenvironment and discover potential biomarkers

doi: 10.1016/j.heliyon.2023.e15421

Figure Lengend Snippet: Secretome markers immunohistochemical staining data. Immunohistochemistry staining data for secretome marker ( A ) SFN. ( B ) YWHAB. ( C ) PRDX4. ( D ) PEA15. ( E ) FN1. ( F ) PSMB6. ( G ) MYL6B. TXNDC12 has no immunohistochemistry data available. The brown staining indicates where an antibody has been bound to its corresponding antigen, and blue represents counterstaining.

Article Snippet: X: 23,664,260–23,686,399), and PEA15 (Hs00269428_m1, Chromosome Location: Chr.1: 160,205,319–160,215,376), to determine gene expression in total cellular RNA level and cell-free secretions of different breast cancer cell lines.

Techniques: Immunohistochemical staining, Staining, Immunohistochemistry, Marker

Journal: Heliyon

Article Title: Breast cancer cell secretome analysis to decipher miRNA regulating the tumor microenvironment and discover potential biomarkers

doi: 10.1016/j.heliyon.2023.e15421

Figure Lengend Snippet: Gene expression in breast tissues and measurement of correlation between gene and miRNAs clusters. Gene expression in human breast tumor and normal tissue for ( A ) YWHAB , ( B ) TXNDC12 , ( C ) MYL6B , ( D ) SFN , ( E ) FN1 , ( F ) PSMB6 , ( G ) PRDX4 , and ( H ) PEA15 . (T): Breast cancer tumor samples. (N): Normal breast samples. The black line represents the median expression value, and each dot is a patient sample. Pearson's correlation coefficient heatmap for secretome markers in breast cancer subtypes for ( I ) miR526b cluster and ( J ) miR655 cluster. Red: strong positive correlation. Blue: strong negative correlation. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: X: 23,664,260–23,686,399), and PEA15 (Hs00269428_m1, Chromosome Location: Chr.1: 160,205,319–160,215,376), to determine gene expression in total cellular RNA level and cell-free secretions of different breast cancer cell lines.

Techniques: Gene Expression, Expressing

Journal: Heliyon

Article Title: Breast cancer cell secretome analysis to decipher miRNA regulating the tumor microenvironment and discover potential biomarkers

doi: 10.1016/j.heliyon.2023.e15421

Figure Lengend Snippet: Secretome marker mRNA expression in breast cancer patient blood (n = 140) and healthy participant blood (n = 118) for ( A ) MYL6B , ( B ) YWHAB , ( C ) SFN , ( D ) PEA15 , ( E ) PSMB6 , ( F ) TXNDC12 , ( G ) FN1 , and ( H ) PRDX4 . * p < 0.05, **** p < 0.0001.

Article Snippet: X: 23,664,260–23,686,399), and PEA15 (Hs00269428_m1, Chromosome Location: Chr.1: 160,205,319–160,215,376), to determine gene expression in total cellular RNA level and cell-free secretions of different breast cancer cell lines.

Techniques: Marker, Expressing

Journal: iScience

Article Title: PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis

doi: 10.1016/j.isci.2025.113695

Figure Lengend Snippet: Clinical characteristics and prognostic factor PEA15 in the OS autophagy-related model (A) Kaplan-Meier survival analysis of the OS prognostic factor PEA15. (B) Risk survival status plot. (C and D) Univariate and multivariate COX regression analyses of the OS autophagy-related model and various clinical features. (E) mRNA expression levels of PEA15 in the normal osteoblast cell line hFOB1.19 and four osteosarcoma cell lines. (F and G) Validation of knockdown efficiency in U2OS cells and overexpression efficiency in MG63 cells ( n = 3). (H and I) CCK-8 assays of cell proliferation following PEA15 knockdown and overexpression ( n = 3). (J–M) Validation of autophagy activity in human tumor tissues and corresponding statistical analysis ( n = 3). (N and O) Protein expression levels of PEA15 are validated by knockdown and overexpression experiments. The data are presented as mean ± SD. ∗∗ p < 0.01, ∗∗∗ p < 0.001. n.s.: not significant.

Article Snippet: The membrane was blocked with 5% non-fat milk in TBST for 2 h at room temperature, followed by incubation overnight at 4°C with primary antibodies targeting PEA15 (CST, #13091,1:1000), LC3B (CST, #3868,1:1000), ATG5 (CST,#9980,1:1000),Cleaved-Caspase3 (CST,#9664,1:1000),Cleaved-PARP (CST, #9541,1:1000), FABP3 (CST,#14780,1:1000), TNF-α (CST,#3707,1:1000), and GAPDH (CST, #5174,1:1000).

Techniques: Expressing, Biomarker Discovery, Knockdown, Over Expression, CCK-8 Assay, Activity Assay

Journal: iScience

Article Title: PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis

doi: 10.1016/j.isci.2025.113695

Figure Lengend Snippet: PEA15 influences tumor cell growth (A and B) Wound healing assays to evaluate the effects of PEA15 knockdown and overexpression. (C and D) Colony formation assays to assess the impact of PEA15 knockdown and overexpression. (E–G) Migration and invasion assays in U2OS cells with PEA15 knockdown, including statistical analysis and expression levels of migration- and invasion-related proteins ( n = 3). (H–J) Migration and invasion assays in MG63 cells with PEA15 overexpression, along with the corresponding protein expression profiles ( n = 3). The data are presented as mean ± SD. ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: The membrane was blocked with 5% non-fat milk in TBST for 2 h at room temperature, followed by incubation overnight at 4°C with primary antibodies targeting PEA15 (CST, #13091,1:1000), LC3B (CST, #3868,1:1000), ATG5 (CST,#9980,1:1000),Cleaved-Caspase3 (CST,#9664,1:1000),Cleaved-PARP (CST, #9541,1:1000), FABP3 (CST,#14780,1:1000), TNF-α (CST,#3707,1:1000), and GAPDH (CST, #5174,1:1000).

Techniques: Knockdown, Over Expression, Migration, Expressing

Journal: iScience

Article Title: PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis

doi: 10.1016/j.isci.2025.113695

Figure Lengend Snippet: PEA15 modulates autophagy and apoptosis (A and B) Assessment of autophagic activity (autophagosome formation) following PEA15 knockdown and overexpression ( n = 3). (C and D) Apoptosis assays were carried out to evaluate the effects of PEA15 knockdown and overexpression ( n = 3). (E and F) Impact of PEA15 knockdown and overexpression on the expression of autophagy-related proteins. (G and H) Changes in apoptosis-related protein levels after PEA15 knockdown and overexpression. The data are presented as mean ± SD. ∗∗ p < 0.01.

Article Snippet: The membrane was blocked with 5% non-fat milk in TBST for 2 h at room temperature, followed by incubation overnight at 4°C with primary antibodies targeting PEA15 (CST, #13091,1:1000), LC3B (CST, #3868,1:1000), ATG5 (CST,#9980,1:1000),Cleaved-Caspase3 (CST,#9664,1:1000),Cleaved-PARP (CST, #9541,1:1000), FABP3 (CST,#14780,1:1000), TNF-α (CST,#3707,1:1000), and GAPDH (CST, #5174,1:1000).

Techniques: Activity Assay, Knockdown, Over Expression, Expressing

Journal: iScience

Article Title: PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis

doi: 10.1016/j.isci.2025.113695

Figure Lengend Snippet: Mechanistic insights into PEA15 downstream signaling (A) Heatmap of transcriptomic analysis in U2OS cells following PEA15 knockdown. (B) CCK-8 assay was adopted to assess cell proliferation after FABP3 knockdown in U2OS cells ( n = 3). (C) Colony formation assay in U2OS cells with FABP3 knockdown ( n = 3). (D and E) Migration and invasion assays in U2OS cells with FABP3 knockdown, along with the expression levels of related proteins ( n = 3). (F and G) Fluorescence imaging of autophagic activity and expression of autophagy-related proteins following FABP3 knockdown. (K–L) Flow cytometry analysis of apoptosis and expression of apoptosis-related markers after FABP3 knockdown ( n = 3). (M) KEGG pathway analysis of transcriptomic data from U2OS cells with PEA15 knockdown. (N) In U2OS cells with PEA15 knockdown, FABP3 was overexpressed, followed by the detection of ATG5 and LC3B protein expression levels.

Article Snippet: The membrane was blocked with 5% non-fat milk in TBST for 2 h at room temperature, followed by incubation overnight at 4°C with primary antibodies targeting PEA15 (CST, #13091,1:1000), LC3B (CST, #3868,1:1000), ATG5 (CST,#9980,1:1000),Cleaved-Caspase3 (CST,#9664,1:1000),Cleaved-PARP (CST, #9541,1:1000), FABP3 (CST,#14780,1:1000), TNF-α (CST,#3707,1:1000), and GAPDH (CST, #5174,1:1000).

Techniques: Knockdown, CCK-8 Assay, Colony Assay, Migration, Expressing, Fluorescence, Imaging, Activity Assay, Flow Cytometry

Journal: iScience

Article Title: PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis

doi: 10.1016/j.isci.2025.113695

Figure Lengend Snippet: Knockdown of PEA15 Enhances the Anticancer Efficacy of DDP (A) Colony formation assays in control, DDP-treated, Si-PEA15, and DDP/Si-PEA15 combined treatment groups. (B) Migration and invasion assay images for the four treatment groups. (C) Fluorescence imaging of autophagic activity in the four treatment groups. (D and E) Expression levels of migration/invasion-related proteins and autophagy-related proteins in the four treatment groups. (F) Knockdown of PEA15 enhances the anticancer effect of DDP through the TNF signaling pathway. (G) The protein expression of ATG5 and LC3B was assessed in U2OS cells treated with the TNF-α antagonist (R-7050).

Article Snippet: The membrane was blocked with 5% non-fat milk in TBST for 2 h at room temperature, followed by incubation overnight at 4°C with primary antibodies targeting PEA15 (CST, #13091,1:1000), LC3B (CST, #3868,1:1000), ATG5 (CST,#9980,1:1000),Cleaved-Caspase3 (CST,#9664,1:1000),Cleaved-PARP (CST, #9541,1:1000), FABP3 (CST,#14780,1:1000), TNF-α (CST,#3707,1:1000), and GAPDH (CST, #5174,1:1000).

Techniques: Knockdown, Control, Migration, Invasion Assay, Fluorescence, Imaging, Activity Assay, Expressing

Journal: iScience

Article Title: PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis

doi: 10.1016/j.isci.2025.113695

Figure Lengend Snippet: In Vivo Tumor Formation Assay (A) Images of solid tumors from control, DDP-treated, Sh-PEA15, and DDP/Sh-PEA15 combined treatment groups. (B and C) Statistical analysis of tumor volume and tumor weight in the four treatment groups ( n = 3). (D) Hematoxylin and eosin (H&E) staining of tumors from the four treatment groups ( n = 3). (E) Expression of Ki67 in tumors from the four treatment groups in the animal experiment. (F) Expression of LC3B in tumors from the four treatment groups in the animal experiment. The data are presented as mean ± SD. ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: The membrane was blocked with 5% non-fat milk in TBST for 2 h at room temperature, followed by incubation overnight at 4°C with primary antibodies targeting PEA15 (CST, #13091,1:1000), LC3B (CST, #3868,1:1000), ATG5 (CST,#9980,1:1000),Cleaved-Caspase3 (CST,#9664,1:1000),Cleaved-PARP (CST, #9541,1:1000), FABP3 (CST,#14780,1:1000), TNF-α (CST,#3707,1:1000), and GAPDH (CST, #5174,1:1000).

Techniques: In Vivo, Tube Formation Assay, Control, Staining, 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: 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: Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress

doi: 10.3390/ijms24032303

Figure Lengend Snippet: Immunodensities of activated ( A ) Akt and ( B ) Pea15 in cortical and thalamic brain tissue samples from WT (grey bars; n = 9) and PDYN-KO (reddish bars; n = 9) mice. Normalized protein activation was estimated as the ratio between phosphorylated (i.e., p-Ser473 Akt or p-Ser116 Pea15) to non-phosphorylated protein species. Columns are means ± SEM of each experimental group and expressed in percent change from WT animals for each brain region. ( A , B ) Representative immunoblots of cortical and thalamic Akt and Pea15 phosphorylated and non-phosphorylated species (three different animals per group) are shown at the bottom. The indicated molecular weights (in kDaltons, kDa) of the immunoreactive bands were estimated from in-gel-loaded, prestained protein standards.

Article Snippet: Pea15 , Human PEA-15 (peptide containing Leu60) , Rabbit , 2780 , 1 , Cell Signaling, USA.

Techniques: Activation Assay, Western Blot

Journal: International Journal of Molecular Sciences

Article Title: Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress

doi: 10.3390/ijms24032303

Figure Lengend Snippet: Cortical immunodensities of ( A ) activated p-Thr183/Tyr185 JNK1/2, ( B ) activated p-Thr202/Tyr204 ERK1/2, ( C ) dimeric FADD, ( D ) oligomeric p-Ser191 FADD, ( E ) full-length and cleaved PARP, ( F ) activated p-Ser473 Akt, ( G ) p-Ser116 Pea15, and ( H ) activated p-Ser2448 mTOR in WT and PDYN-KO mice exposed to acute restraint ( A , blue bars) or chronic mild ( C , orange bars) stress procedures, as compared to basal ( B , grey bars) stress levels in undisturbed animals. Normalized protein amounts were estimated as the ratio between the corresponding immunoreactive band to total enzyme or α-tubulin. Columns are means ± SEM of n = 7–9 mice per experimental group and expressed in percent change from wildtype-basal (WT-B) mice. All datasets were analyzed by TW-ANOVA (see ). * p < 0.05, ** p < 0.01, and *** p < 0.001, TW-ANOVA followed by Tukey’s post hoc test. ( A – H ) Representative immunoblots of phosphorylated and/or non-phosphorylated species of the indicated proteins are shown at the bottom. The indicated molecular weights (in kDaltons, kDa) of the immunoreactive bands were estimated from in-gel-loaded, prestained protein standards.

Article Snippet: Pea15 , Human PEA-15 (peptide containing Leu60) , Rabbit , 2780 , 1 , Cell Signaling, USA.

Techniques: Western Blot

Journal: International Journal of Molecular Sciences

Article Title: Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress

doi: 10.3390/ijms24032303

Figure Lengend Snippet: Results of TW-ANOVA reporting the effects of the stress procedures, PDYN gene deletion, and their interaction on cortical and thalamic immunodensities of the studied proteins.

Article Snippet: Pea15 , Human PEA-15 (peptide containing Leu60) , Rabbit , 2780 , 1 , Cell Signaling, USA.

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress

doi: 10.3390/ijms24032303

Figure Lengend Snippet: Thalamic immunodensities of ( A ) activated p-Thr183/Tyr185 JNK1/2, ( B ) dimeric FADD, ( C ) oligomeric p-Ser191 FADD, ( D ) activated p-Ser473 Akt, and ( E ) p-Ser116 Pea15 in WT and PDYN-KO mice exposed to acute restraint (A, blue bars) or chronic mild (C, orange bars) stress procedures, as compared to basal (B, grey bars) stress levels in undisturbed animals. Normalized protein amounts were estimated as the ratio between the corresponding immunoreactive band to total enzyme or α-tubulin. Columns are means ± SEM of n = 7–9 mice per experimental group and expressed in percent change from wildtype-basal (WT-B) mice. All datasets were analyzed by TW-ANOVA (see ). * p < 0.05, and *** p < 0.001, TW-ANOVA followed by Tukey’s post hoc test. ( A – E ) Representative immunoblots of phosphorylated and/or non-phosphorylated species of the indicated proteins are shown at the bottom. The indicated molecular weights (in kDaltons, kDa) of the immunoreactive bands were estimated from in-gel-loaded, prestained protein standards.

Article Snippet: Pea15 , Human PEA-15 (peptide containing Leu60) , Rabbit , 2780 , 1 , Cell Signaling, USA.

Techniques: Western Blot

Journal: International Journal of Molecular Sciences

Article Title: Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress

doi: 10.3390/ijms24032303

Figure Lengend Snippet: Antibodies used for the detection and quantification of target proteins.

Article Snippet: Pea15 , Human PEA-15 (peptide containing Leu60) , Rabbit , 2780 , 1 , Cell Signaling, USA.

Techniques: