Journal: Experimental and Therapeutic Medicine

Article Title: PDK1 inhibition reduces autophagy and cell senescence through the PI3K/AKT signalling pathway in a cigarette smoke mouse emphysema model

doi: 10.3892/etm.2023.11922

Figure Lengend Snippet: Expression of p16 protein in the airway epithelial tissues. (A) Immunofluorescence staining for the analysis of p16 protein expression in airway epithelial tissues. Magnification, x400. (B) Comparison of p16 protein expression among the experimental groups. aP<0.05 vs. control. bP<0.05 vs. emphysema. CS + CSE, emphysema group; CS3, PI3K inhibitor group; CS1, PDK1 inhibitor group; PDK1, phosphoinositide dependent protein kinase 1; p16, cyclin-dependent kinase inhibitor 2A.

Article Snippet: Slices were incubated with anti-LC3B (1:100; cat. no. APG8B; Abcepta) and anti-p16 antibodies (1:100; cat. no. Bs-11652R; BIOSS) overnight at 4˚C.

Techniques: Expressing, Immunofluorescence, Staining, Comparison, Control

Journal: Experimental and Therapeutic Medicine

Article Title: PDK1 inhibition reduces autophagy and cell senescence through the PI3K/AKT signalling pathway in a cigarette smoke mouse emphysema model

doi: 10.3892/etm.2023.11922

Figure Lengend Snippet: PI3K, PDK1, AKT, LC3B II and p16 protein expression levels. Western blotting for (A) PI3K, (B) PDK1, (C) AKT, (D) LC3B and (E) p16 expression in the airway epithelial tissues. GAPDH as an internal control. Semi-quantification of PI3K, PDK1, AKT, LC3B and p16 protein expression in airway epithelial tissues in each group. aP<0.05 vs. control. bP<0.05 vs. emphysema. The protein expression levels were expressed as the ratio of band intensity for the target protein relative to that for the internal control GAPDH. Values are expressed as the mean ± standard deviation. CS + CSE, emphysema group; CS3, PI3K inhibitor group; CS1, PDK1 inhibitor group; PDK1, phosphoinositide dependent protein kinase 1; p16, cyclin-dependent kinase inhibitor 2A.

Article Snippet: Slices were incubated with anti-LC3B (1:100; cat. no. APG8B; Abcepta) and anti-p16 antibodies (1:100; cat. no. Bs-11652R; BIOSS) overnight at 4˚C.

Techniques: Expressing, Western Blot, Control, Standard Deviation

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 1 Abnormally high expression of ARPC5 in glioma. (A) Differential expression of ARPC5 in various tumor types was analyzed based on the TIMER online website. (B) The distinct upregulation of ARPC5 in glioma was demonstrated in GEPIA online website. (C) Box plot based on the expression of ARPC5 in the GSE2223 (Glioma = 50, Normal = 4). (D) Box plot based on the expression of ARPC5 in the GSE29796 (Glioma = 52, Normal = 20). (E) Box plot based on the expression of ARPC5 in the GSE116520 (Glioma = 34, Normal = 8). (F) Box plot based on the protein expression of ARPC5 in the CPTAC samples (Glioma = 99, Normal = 10). (G) ARPC5 protein expression was detected in cerebral cortex (Patient id: 1582), low grade glioma (Patient id: 3365), and high-grade glioma (Patient id: 3251) tissues from HPA dataset. (H) Representative images of ARPC5 expression in glioma and its surrounding tissues. *p < 0.05, **p < 0.01, ***p < 0.001

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Expressing, Quantitative Proteomics

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 2 Correlation between different status of ARPC5 expression and prognosis of glioma patients. (A) Survival analysis of ARPC5 in CGGA database. (B) ROC curve analysis of ARPC5 at 1, 3, and 5 years in CGGA database. (C) Survival analysis of ARPC5 in TCGA database. (D) ROC curve analysis of ARPC5 at 1, 3, and 5 years in TCGA database. Survival analysis of the signature in patients stratified by grade (E, F), gender (G, H), age (I, J), IDH mutation status (K, L), 1p/19q codeletion status (M, N), and MGMTp methylation status (O, P) in CGGA database

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Expressing, Mutagenesis, Methylation

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 3 Prognostic significance of ARPC5 and its association with drug sensitivity in glioma. (A) Univariate regression analysis of prognosis in CGGA data base. (B) Multivariate analysis of prognosis in CGGA database. (C) The nomogram to predict the association between ARPC5 expression and OS was de veloped using the CGGA dataset. (D) The calibration curve for the nomogram-predicted OS. ARPC5 affects the sensitivity to 5-fluorouracil (E), bleomycin (F), etoposide (G), crizotinib (H), sorafenib (I), and erlotinib (J)

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Expressing

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 4 Enrichment analysis identifies ARPC5-associated signaling pathways. (A) Heatmap for DEGs generated by compare the difference of ARPC5 ex pression in glioma from the CGGA dataset. (B) Volcano plots illustrated all DEGs. Barplot showing the GO (C) and KEGG (D) analysis for ARPC5 in glioma. (E) GO functional annotation of ARPC5 in glioma from GSEA. (F) KEGG pathway analysis of ARPC5 in glioma from GSEA.

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Protein-Protein interactions, Generated, Functional Assay

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 5 Investigations the expression of ARPC5 in glioma through single-cell analysis. (A) Through dimension reduction analysis of CGGA single-cell data, TSNE plot depicted that 6,148 cells were classified into 16 clusters. (B) The violin plot showed the expression of ARPC5 in each type of cluster. (C) Sixteen clusters were divided into 5 types of cells: astrocyte, macrophage, monocyte, epithelial and T cell. (D) The scatter plot shows the expression of ARPC5 in each cell

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Expressing, Single-cell Analysis

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 6 Correlations of ARPC5 expression with immunity-related indexes. (A) Violin plot showed the correlation between immune classification and tumor purity. The immune infiltration models of low- and high-ARPC5 were detected through ssGSEA methods in glioma from the TCGA database. (C) Violin plot showed the correlation between ARPC5 with stromal scores, immune scores, and ESTIMATE scores. (D) Lollipop showed the correlation between ARPC5 with infiltrating immune cells. Scatter plot showed the correlation between ARPC5 with TMB (E) and MSI (F). (G-J) Violin plot showed the correla tion between ARPC5 with immunotherapy

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Expressing

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 7 Effect of ARPC5 on the expression of CD3 and prognosis. (A) Representative images revealed the relationships between the ARPC5 expression and T cell marker CD3 in gliomas. (B) Survival analysis of ARPC5 in glioma chip ZL-BraG180sur01.

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Expressing, Marker

Journal: BMC cancer

Article Title: ARPC5 acts as a potential prognostic biomarker that is associated with cell proliferation, migration and immune infiltrate in gliomas.

doi: 10.1186/s12885-023-11433-w

Figure Lengend Snippet: Fig. 8 Effect of ARPC5 on the proliferation and migration of glioma cells. (A) The expression level of ARPC5 protein was detected in LN229 and U251 cells after shRNA interference, GAPDH was used to confirm equal protein loading. (B) RT-qPCR verified the expression efficiency of ARPC5 in LN229 and U251 cells after shRNA interference. Growth curve assessing the effect of ARPC5 on the proliferation of LN229 (C) and U251 (D) cells. (E) The representa tive image showed the clone formation ability of LN229 and U251 cells after transfection. (F) Transwell analysis was further used to examine the effect of ARPC5 on migration of LN229 and U251 cells, and the number of migrating cells was quantitatively analyzed. *p < 0.05, **p < 0.01, ***p < 0.001

Article Snippet: Glioma tissue samples and glioma chip ZLBraG180sur01 were incubated with ARPC5 antibody (16717-1-AP, proteintech, Wuhan, China) and CD3 antibody (17617-1-AP, proteintech, Wuhan, China).

Techniques: Migration, Expressing, shRNA, Quantitative RT-PCR, Transfection

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: ( A ) Gene set enrichment analysis (GSEA) of RNA-seq data from hearts of sham and septic mice, highlighting enrichment of senescence-related genes. ( B ) Heat map showing differential expression of selected senescence-associated genes. ( C ) Expression levels of representative senescence-related genes (Cdkn1a/p21, Cxcl2, Mmp9, Thbs1, Cxcl1) based on RNA-seq analysis of hearts from sham and septic mice. ( D ) Western blot analysis of senescence markers p16, p21, and acetylated p53 in sham and septic heart tissues (n=6 mice/group). ( E ) qRT-PCR analysis of senescence markers in sham and septic heart tissues (n=6-8 mice/group). ( F, G ) Western blot analysis and quantification of senescence markers p16, p21, and acetylated p53 in heart tissues from sham mice, septic non-survivors (body temperature < 30L°C), and septic survivors (> 30L°C) at 24 hours post-CLP (n=6 mice/group). ( H) qRT-PCR analysis of senescence associated genes (Cxcl9, Il-1A, Serpine1, Thbs1) in heart tissues from sham mice, septic survivors, and septic non-survivors. All data are presented as mean ± SD. Statistical significance was determined using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: RNA Sequencing, Quantitative Proteomics, Expressing, Western Blot, Quantitative RT-PCR, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Cardiac endothelial cells are the predominant senescent population during sepsis . ( A-D ) Co-immunostaining of senescence markers p21 and p16 with the endothelial cell marker CD31, and their quantification in heart sections from sham and septic mice (n=6 mice/group). Scale bars, 50Lμm. ( E-F ) Co-immunostaining of the cellular proliferation marker Ki67 with the endothelial marker CD31 in heart tissues from sham controls and septic mice at 24 hours post-CLP, along with corresponding quantification. (n=8/group). Scale bars, 50Lμm. ( G ) β-gal staining of HUVECs treated with plasma (1:200) from sham or septic (CLP 24 h) mice for 24 hours (n=6/group). Scale bars, 100Lμm. ( H ) Quantification of β-gal staining in HUVECs, as shown in ( G ). ( I ) BrdU incorporation assay in HUVECs from the indicated treatment groups (n=6/group). Scale bars, 100Lμm. ( J) Quantification of BrdU incorporation in HUVECs, as shown in ( H ). All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Immunostaining, Marker, Staining, Clinical Proteomics, BrdU Incorporation Assay, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Cardiac endothelial senescence impairs proliferation in sepsis . ( A-B ) Immunofluorescent co-staining and quantification of the senescence marker p21 (red) and the endothelial marker CD31 (green) in heart sections from the indicated groups (n=6 mice/group). Scale bars, 50Lμm. ( C-D ) Immunofluorescent co-staining and quantification of the senescence marker p16 (red) and the endothelial marker CD31 (green) in heart sections from the indicated groups (n=6 mice/group). Scale bars, 50Lμm. ( E, F ) Immunofluorescent co-staining and quantification of the proliferation marker Ki67 (red) and the endothelial marker CD31 (green) in heart sections from sham, septic survivors, and septic non-survivors (n=6-8 mice/group). Scale bars, 50Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Staining, Marker, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Elevated heme levels correlate with cardiac endothelial senescence and dysfunction in sepsis . ( A ) Plasma heme levels in sham mice, septic non-survivors (body temperature < 30L°C), and septic survivors (> 30L°C) at 24 hours post-CLP (n=6–8 mice/group). ( B, C ) Mice with higher circulating heme levels exhibited increased cardiac endothelial senescence, as indicated by elevated expression of senescence markers p21 and p16. ( D, E ) Co-immunostaining of p21 with endothelial cells marker CD31 and quantification in heart tissues from sham and septic mice with or without heme treatment (n=6 mice/group). Scale bars, 50Lμm. ( F–H ) Echocardiographic assessment of ejection fraction (EF) and fractional shortening (FS) in sham and septic mice treated with or without heme (n=6 mice/group). ( I, J ) Western blot analysis and quantification of senescence markers p16, p21, and acetylated p53 in heart tissues from sham and septic mice with or without heme treatment (n=6 mice/group). All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Clinical Proteomics, Expressing, Immunostaining, Marker, Western Blot, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Heme administration enhances cardiac endothelial senescence and impairs endothelial proliferation . ( A, B ) Immunofluorescent co-staining and quantification of the senescence marker p16 (red) and the endothelial marker CD31 (green) in heart sections from the indicated groups (n=6 mice/group). Scale bars, 50Lμm. ( C, D ) Immunofluorescent co-staining and quantification of the proliferation marker Ki67 (red) and the endothelial marker CD31 (green) in heart sections from the indicated groups (n=6 mice/group). Scale bars, 50Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Staining, Marker, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Heme exacerbates bacterial induced endothelial senescence . ( A, B ) β-galactosidase staining and quantification of HUVECs treated with heme (10LµM), heat-killed E. coli (MOI:10), or both for 24 hours (n=6/group). Scale bars, 100Lμm. ( C, D ) Western blot analysis and quantification of senescence markers p16, p21, and acetylated p53 in the indicated HUVEC groups (n=4/group). ( E, F ) Immunofluorescent staining and quantification of p21 in the indicated HUVEC groups (n=6/group). Scale bars, 50Lμm. ( G, H ) BrdU incorporation assay and quantification in the indicated HUVEC groups (n=6/group). Scale bars, 100Lμm. ( I ) qRT-PCR analysis of senescence-associated genes in the indicated HUVEC groups (n=6/group). All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Staining, Western Blot, BrdU Incorporation Assay, Quantitative RT-PCR, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: STING activation contributes to sepsis induced cardiac endothelial senescence . ( A, B ) Co-immunofluorescent staining and quantification of the senescence marker p21 with the endothelial cell marker CD31 in cardiac tissues from sham and septic mice treated with a STING inhibitor or vehicle control at 24 hours post-CLP (n=6 mice/group). Scale bars, 50Lμm. ( C ) Representative echocardiographic images assessing ejection fraction (EF) and fractional shortening (FS) at 24 hours, 7 days, and 14 days post-CLP in mice treated with vehicle or STING inhibitor. ( D ) Western blot analysis of p-STING/STING, p-TBK1/TBK1, and p-IRF3/IRF3 in HUVECs treated with heme + heat-killed E. coli , with or without the STING inhibitor C-176 (2.5LμM) (n=6/group). ( E, F ) Echocardiographic assessment of EF and FS in septic mice treated with STING inhibitor or vehicle control at 24 hours, 7 days, and 14 days post-CLP, as shown in (C) (n=6 mice/group). ( G ) Quantification of Western blot analysis of p-STING/STING, p-TBK1/TBK1, and p-IRF3/IRF3 in the indicated HUVEC groups, as shown in ( D ) (n=4/group). ( H, I ) Western blot analysis and quantification of senescence markers p16, p21, and acetylated p53 in the indicated HUVEC groups (n=6/group). ( J, K ) β-galactosidase (β-gal) staining and quantification of HUVECs treated with combined heme and E. coli with or without the STING inhibitor C-176 (n=6/group). Scale bars, 100Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Activation Assay, Staining, Marker, Control, Western Blot, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: STING inhibition attenuates sepsis-induced cardiac endothelial senescence . ( A, B ) Immunofluorescent co-staining and quantification of the senescence marker p16 with the endothelial marker CD31 in heart tissues from sham and septic mice treated with a STING inhibitor or vehicle at 24 hours post-CLP (n=5-6 mice/group). Scale bars, 50Lμm. ( C–E ) Immunofluorescent co-staining and quantification of senescence markers p16 or p21 with the endothelial marker CD31 in heart tissues from sham and septic mice treated with a STING inhibitor or vehicle at 14 days post-CLP (n=4-6 mice/group). Scale bars, 50Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: **PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Inhibition, Staining, Marker, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Increased hemopexin expression attenuates sepsis-induced cardiac endothelial senescence . ( A–D ) Immunostaining and quantification of the senescence markers p21 or p16 with endothelial cell markers in sham and septic heart tissues from AAV-HPX and AAV-Con mice at 24 hours post-CLP (n=6-7/group). Scale bars, 50Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: **PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Expressing, Immunostaining, Two Tailed Test

Journal: bioRxiv

Article Title: Heme drives cardiac endothelial senescence in sepsis via STING activation

doi: 10.1101/2025.06.18.660159

Figure Lengend Snippet: Increased hemopexin expression attenuates sepsis-induced cardiac endothelial senescence and enhances endothelial proliferative capacity . ( A, B ) Co-immunostaining and quantification of the cellular proliferation marker Ki67 with the endothelial marker CD31 in sham and septic heart tissues from AAV–HPX and AAV–Con mice at 24 hours post-sepsis. Scale bars, 50Lμm. ( C, D ) Co-immunostaining and quantification of the senescence marker p16 with the endothelial marker CD31 in heart tissues from AAV–HPX and AAV–Con mice at 14 days post-sepsis. Scale bars, 50Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL

Article Snippet: Anti-p16 (Cat: A8571), Anti-AP53 (Cat: A19836), Anti-Hemopexin (HPX) (Cat: A5603), Anti-DDDDK-Tag (Cat: AE005) were purchased from Abclonal.

Techniques: Expressing, Immunostaining, Marker, Two Tailed Test

Journal: Frontiers in Neurology

Article Title: Preconditioning With Intermittent Hypobaric Hypoxia Attenuates Stroke Damage and Modulates Endocytosis in Residual Neurons

doi: 10.3389/fneur.2021.750908

Figure Lengend Snippet: GO annotation list of significantly different proteins ( n = 3).

Article Snippet: The antibodies used in the study were anti-CHMP1a antibody (1:2000, ab167412, Abcam, Cambridge, MA, USA); anti-HSPA2 antibody (1:5000, ab108416, Abcam, Cambridge, MA, USA); anti-ARPC5 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA); and anti-RABEP1 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA).

Techniques: Ubiquitin Proteomics

Journal: Frontiers in Neurology

Article Title: Preconditioning With Intermittent Hypobaric Hypoxia Attenuates Stroke Damage and Modulates Endocytosis in Residual Neurons

doi: 10.3389/fneur.2021.750908

Figure Lengend Snippet: KEGG pathway annotation list ( n = 3).

Article Snippet: The antibodies used in the study were anti-CHMP1a antibody (1:2000, ab167412, Abcam, Cambridge, MA, USA); anti-HSPA2 antibody (1:5000, ab108416, Abcam, Cambridge, MA, USA); anti-ARPC5 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA); and anti-RABEP1 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA).

Techniques:

Journal: Frontiers in Neurology

Article Title: Preconditioning With Intermittent Hypobaric Hypoxia Attenuates Stroke Damage and Modulates Endocytosis in Residual Neurons

doi: 10.3389/fneur.2021.750908

Figure Lengend Snippet: Cluster analysis of significantly different protein expressions and western blot analysis of selected key proteins. (A) Cluster analysis (H6M vs. M). Red represents up-regulation and blue represents down-regulation. (B) Western blotting results of four differentially expressed endocytosis-related proteins. (C) A western blotting gray value analysis of Rabep1. One-way ANOVA showed differences among the five groups, F = 7.34, p = 0.0008. Results are presented as mean ± SD ( n = 5). (D) A western blotting gray value analysis of Hspa2. One-way ANOVA showed differences among the five groups, F = 19.29, p < 0.0001. Results are presented as mean ± SD ( n = 5). (E) A western blotting gray value analysis of Chmp1a. One-way ANOVA showed differences among the five groups, F = 15.43, p < 0.0001. Results are presented as mean ± SD ( n = 5). (F) A western blotting gray value analysis of Arpc5. One-way ANOVA showed differences among the five groups, F = 13.04, p < 0.0001. Results are presented as mean ± SD ( n = 5). ANOVA, analysis of variance.

Article Snippet: The antibodies used in the study were anti-CHMP1a antibody (1:2000, ab167412, Abcam, Cambridge, MA, USA); anti-HSPA2 antibody (1:5000, ab108416, Abcam, Cambridge, MA, USA); anti-ARPC5 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA); and anti-RABEP1 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA).

Techniques: Western Blot

Journal: Frontiers in Neurology

Article Title: Preconditioning With Intermittent Hypobaric Hypoxia Attenuates Stroke Damage and Modulates Endocytosis in Residual Neurons

doi: 10.3389/fneur.2021.750908

Figure Lengend Snippet: The main biological process changed in preconditioned MCAO rats' cortex based on KEGG pathways. After combining clathrin and adaptor proteins on the cytoplasmic side of the cell membrane, the signal receptors were collected on the surface of the cell membrane into clathrin-coated pits. Next, the pits were invaginated and pinched off the clathrin-surrounded membrane, the uncoated vesicle fused with the early endosome using Hspa2. This process included two factors, Arpc5 and Rabep1, which were up-regulated in the intermittent hypobaric hypoxia preconditioned group. In the case of CDE, the main outcomes were: (1) return to the cell membrane through the endosomal recycling compartment, and (2) entry into late endosomes and multivesicular bodies, and degradation by the lysosomal pathway. ESCRTs play a pivotal role during this process, and Chmp1a is essential for its function. KEGG, Kyoto Encyclopedia of Genes and Genomes; MCAO, middle cerebral artery occlusion.

Article Snippet: The antibodies used in the study were anti-CHMP1a antibody (1:2000, ab167412, Abcam, Cambridge, MA, USA); anti-HSPA2 antibody (1:5000, ab108416, Abcam, Cambridge, MA, USA); anti-ARPC5 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA); and anti-RABEP1 antibody (1:2,000, Novus Biologicals, Briarwood Avenue Centennial, USA).

Techniques: Membrane