Review

rabbit anti arpc5 (Novus Biologicals)

Novus Biologicals is a verified supplier

Novus Biologicals manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Novus Biologicals rabbit anti arpc5
Rabbit Anti Arpc5, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti-arpc5/ARPC5+Antibody/pm37382373-197-4-6
Average 91 stars, based on 5 article reviews

rabbit anti arpc5 - by Bioz Stars, 2026-10

91/100 stars

Images

Electrophoresis:

Article Title: ARPC5 deficiency leads to severe early-onset systemic inflammation and mortality.
Article Snippet: Proteins were detected with rabbit anti-ARPC5 (Novus, #NBP2-67350, lot #HL0702, 1:1000), rabbit anti-ARPC5L (Abcam, #ab169763, lot #GR121833-4, 1:2000) or mouse anti-ARPC3 (anti-Arp2/3 Complex Antibody Clone 13c9, Millipore, #MILL-MABT95, lot3283230, 1:5000).

Saline:

Image Search Results

( 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<L0.05, **PL<L0.01, ***PL<L0.001, ****PL<L0.0001.

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

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<L0.05, **PL<L0.01, ****PL<L0.0001.

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

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<L0.05, **PL<L0.01, ****PL<L0.0001.

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

$Elevated heme levels correlate with cardiac endothelial senescence and dysfunction in sepsis . ( A ) Plasma heme levels in sham mice, septic non-survivors (body temperature < 30L°C), and septic survivors (> 30L°C) at 24 hours post-CLP (n=6–8 mice/group). ( B, C ) Mice with higher circulating heme levels exhibited increased cardiac endothelial senescence, as indicated by elevated expression of senescence markers p21 and p16. ( D, E ) Co-immunostaining of p21 with endothelial cells marker CD31 and quantification in heart tissues from sham and septic mice with or without heme treatment (n=6 mice/group). Scale bars, 50Lμm. ( F–H ) Echocardiographic assessment of ejection fraction (EF) and fractional shortening (FS) in sham and septic mice treated with or without heme (n=6 mice/group). ( I, J ) Western blot analysis and quantification of senescence markers p16, p21, and acetylated p53 in heart tissues from sham and septic mice with or without heme treatment (n=6 mice/group). All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL<L0.05, **PL<L0.01, ***PL<L0.001, ****PL<L0.0001.$

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

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<L0.05, **PL<L0.01, ****PL<L0.0001.

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

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<L0.05, **PL<L0.01, ***PL<L0.001, ****PL<L0.0001.

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

$STING activation contributes to sepsis induced cardiac endothelial senescence . ( A, B ) Co-immunofluorescent staining and quantification of the senescence marker p21 with the endothelial cell marker CD31 in cardiac tissues from sham and septic mice treated with a STING inhibitor or vehicle control at 24 hours post-CLP (n=6 mice/group). Scale bars, 50Lμm. ( C ) Representative echocardiographic images assessing ejection fraction (EF) and fractional shortening (FS) at 24 hours, 7 days, and 14 days post-CLP in mice treated with vehicle or STING inhibitor. ( D ) Western blot analysis of p-STING/STING, p-TBK1/TBK1, and p-IRF3/IRF3 in HUVECs treated with heme + heat-killed E. coli , with or without the STING inhibitor C-176 (2.5LμM) (n=6/group). ( E, F ) Echocardiographic assessment of EF and FS in septic mice treated with STING inhibitor or vehicle control at 24 hours, 7 days, and 14 days post-CLP, as shown in (C) (n=6 mice/group). ( G ) Quantification of Western blot analysis of p-STING/STING, p-TBK1/TBK1, and p-IRF3/IRF3 in the indicated HUVEC groups, as shown in ( D ) (n=4/group). ( H, I ) Western blot analysis and quantification of senescence markers p16, p21, and acetylated p53 in the indicated HUVEC groups (n=6/group). ( J, K ) β-galactosidase (β-gal) staining and quantification of HUVECs treated with combined heme and E. coli with or without the STING inhibitor C-176 (n=6/group). Scale bars, 100Lμm. All data are presented as mean ± SD. Statistical analysis was performed using the unpaired two-tailed Student’s t-test: *PL<L0.05, **PL<L0.01, ***PL<L0.001, ****PL<L0.0001.$

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

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<L0.01, ***PL<L0.001, ****PL<L0.0001.

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

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<L0.01, ****PL<L0.0001.

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

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<L0.05, **PL<L0.01, ****PL<L0.0001.

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

The expression levels of APRC5 in different cancers, normal tissues, and cells. (A) The differential expression of ARPC5 in pan-cancer tissues from TCGA datasets. (B) The differential expression of ARPC5 in pan-cancer tissues based on TCGA and GTEx datasets. (C) ARPC5 expression in paired cancer tissues and adjacent normal tissues from TCGA datasets. (D) The mRNA expression levels of ARPC5 in different normal tissues from HPA database. (E) The mRNA expression of ARPC5 in cancer cell lines from HPA database. (F) ARPC5 mRNA expression in different single cell types from HPA database. ns: no significance; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: The expression levels of APRC5 in different cancers, normal tissues, and cells. (A) The differential expression of ARPC5 in pan-cancer tissues from TCGA datasets. (B) The differential expression of ARPC5 in pan-cancer tissues based on TCGA and GTEx datasets. (C) ARPC5 expression in paired cancer tissues and adjacent normal tissues from TCGA datasets. (D) The mRNA expression levels of ARPC5 in different normal tissues from HPA database. (E) The mRNA expression of ARPC5 in cancer cell lines from HPA database. (F) ARPC5 mRNA expression in different single cell types from HPA database. ns: no significance; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: After the antigen retrieval, the rabbit anti-human ARPC5(1:500, T553316S, Abmart) primary antibody was applied to the slides and incubated at 4°C overnight and followed by the secondary anti–horseradish peroxide for 30 min. Next, the slides were stained with DAB chromogenic reagent and hematoxylin.

Techniques: Expressing, Quantitative Proteomics

Genetic alteration of ARPC5 in pan-cancer. (A) Mutation type and mutation frequency of ARPC5 obtained from the cBioPortal website. (B) The expression levels of ARPC5 in various CNV status of pan-cancer, CNV, copy number variations; *p < 0 . 0 5 ; * *p < 0.01; ****p < 0.0001.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: Genetic alteration of ARPC5 in pan-cancer. (A) Mutation type and mutation frequency of ARPC5 obtained from the cBioPortal website. (B) The expression levels of ARPC5 in various CNV status of pan-cancer, CNV, copy number variations; *p < 0 . 0 5 ; * *p < 0.01; ****p < 0.0001.

Techniques: Mutagenesis, Expressing

Prognosis analyses of ARPC5 in pan-cancer based on univariate Cox regression method. (A) The correlation between ARPC5 expression and OS. (B) The correlation between ARPC5 expression and PFI. (C) The correlation between ARPC5 expression and DSS. OS: overall survival; PFI: progression-free interval; DSS: disease-specific survival.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: Prognosis analyses of ARPC5 in pan-cancer based on univariate Cox regression method. (A) The correlation between ARPC5 expression and OS. (B) The correlation between ARPC5 expression and PFI. (C) The correlation between ARPC5 expression and DSS. OS: overall survival; PFI: progression-free interval; DSS: disease-specific survival.

Techniques: Expressing

ARPC5 expression significantly correlated with OS based on Kaplan–Meier analysis. (A) The correlation in ESCA. (B) The correlation in HNSC. (C) The correlation in KIRC. (D) The correlation in KIRP. (E) The correlation in LIHC. (F) The correlation in LGG. (G) The correlation in OV. (H) The correlation in SKCM. The optimal cutoff of ARPC5 expression were used to divide patients into high- and low-expression groups.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: ARPC5 expression significantly correlated with OS based on Kaplan–Meier analysis. (A) The correlation in ESCA. (B) The correlation in HNSC. (C) The correlation in KIRC. (D) The correlation in KIRP. (E) The correlation in LIHC. (F) The correlation in LGG. (G) The correlation in OV. (H) The correlation in SKCM. The optimal cutoff of ARPC5 expression were used to divide patients into high- and low-expression groups.

Techniques: Expressing

The correlation between ARPC5 expression and clinical stage, histologic grade, and tumor molecular subtypes in various cancers based on Spearman’s correlation analysis (the correlation with p < 0.05 were displayed). (A) The correlation between ARPC5 expression and clinical stage in pan-cancer. (B–C) The expression levels of ARPC5 in different clinical stages of KIRC (B) and KIRP (C) . (D) The correlation between ARPC2 expression and histologic grade in pan-cancer. (E–H) The expression levels of ARPC5 in different histologic grades of KIRC (E) , LGG (F) , LIHC (G) , and UCEC (H) . (I–R) The correlation between ARPC5 expression and molecular subtypes in ACC (I) , BRCA (J) , LGG (K) , HNSC (L) , KIRP (M) , OV (N) , LUSC (O) , PCPG (P) , STAD (Q) , UCEC (R) . rho; rank coefficient of Spearman. Pv; p -value. NS, no significance.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: The correlation between ARPC5 expression and clinical stage, histologic grade, and tumor molecular subtypes in various cancers based on Spearman’s correlation analysis (the correlation with p < 0.05 were displayed). (A) The correlation between ARPC5 expression and clinical stage in pan-cancer. (B–C) The expression levels of ARPC5 in different clinical stages of KIRC (B) and KIRP (C) . (D) The correlation between ARPC2 expression and histologic grade in pan-cancer. (E–H) The expression levels of ARPC5 in different histologic grades of KIRC (E) , LGG (F) , LIHC (G) , and UCEC (H) . (I–R) The correlation between ARPC5 expression and molecular subtypes in ACC (I) , BRCA (J) , LGG (K) , HNSC (L) , KIRP (M) , OV (N) , LUSC (O) , PCPG (P) , STAD (Q) , UCEC (R) . rho; rank coefficient of Spearman. Pv; p -value. NS, no significance.

Techniques: Expressing

The correlation between ARPC5 expression and immune scores and stromal scores of tumor microenvironments in pan-cancer.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: The correlation between ARPC5 expression and immune scores and stromal scores of tumor microenvironments in pan-cancer.

Techniques: Expressing

The correlation between ARPC5 and immune infiltration cells in pan-cancer based on TIMER algorithm. (A) Heatmap displayed the correlation between ARPC5 expression and the proportions of B cell, CD4 + T cell, CD8 + T cell, neutrophil, macrophage, and DC cell. (B) The top five cancer types (including KIRC, LGG, PRAD, THCA, and THYM) with most significant correlation between ARPC5 and immune infiltration cells were displayed with scatterplots. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: The correlation between ARPC5 and immune infiltration cells in pan-cancer based on TIMER algorithm. (A) Heatmap displayed the correlation between ARPC5 expression and the proportions of B cell, CD4 + T cell, CD8 + T cell, neutrophil, macrophage, and DC cell. (B) The top five cancer types (including KIRC, LGG, PRAD, THCA, and THYM) with most significant correlation between ARPC5 and immune infiltration cells were displayed with scatterplots. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques: Expressing

The correlation between ARPC5 expression and immune subtypes in pan-cancer using TISIDB. The cancers with significant correlation were displayed. (A) In BLCA. (B) In BRCA. (C) In CESC. (D) In KICH. (E) In KIRC. (F) In LGG. (G) In LIHC. (H) In LUAD. (I) In PAAD. (J) In OV. (K) PCPG. (L) PRAD. (M) In READ. ( N) In SARC. (O) In SKCM. (P) In STAD. (Q) In TGCT. (R) In THCA. (S) In UCS. (T) In UCEC. Pv; p -value. C1, wound healing; C2, IFN-gamma dominant; C3, inflammatory; C4, lymphocyte depleted; C5, immunologically quiet; C6, TGF-b dominant.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: The correlation between ARPC5 expression and immune subtypes in pan-cancer using TISIDB. The cancers with significant correlation were displayed. (A) In BLCA. (B) In BRCA. (C) In CESC. (D) In KICH. (E) In KIRC. (F) In LGG. (G) In LIHC. (H) In LUAD. (I) In PAAD. (J) In OV. (K) PCPG. (L) PRAD. (M) In READ. ( N) In SARC. (O) In SKCM. (P) In STAD. (Q) In TGCT. (R) In THCA. (S) In UCS. (T) In UCEC. Pv; p -value. C1, wound healing; C2, IFN-gamma dominant; C3, inflammatory; C4, lymphocyte depleted; C5, immunologically quiet; C6, TGF-b dominant.

Techniques: Expressing

The relationship between ARPC5 and immune-checkmate inhibitors biomarkers in pan-cancer. (A) The heatmap showing the co-expression relationship between ARPC5 and 47 immune checkpoint–related genes. (B) Radar plot showing the relationship between ARPC5 and tumor mutation burden (TMB). (C) Radar plot showing the correlation of ARPC5 with microsatellite instability (MSI). (D) Radar plot showing the correlation of ARPC5 with neoantigens. The number in radar plot represents Spearman’s correlation coefficient. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: The relationship between ARPC5 and immune-checkmate inhibitors biomarkers in pan-cancer. (A) The heatmap showing the co-expression relationship between ARPC5 and 47 immune checkpoint–related genes. (B) Radar plot showing the relationship between ARPC5 and tumor mutation burden (TMB). (C) Radar plot showing the correlation of ARPC5 with microsatellite instability (MSI). (D) Radar plot showing the correlation of ARPC5 with neoantigens. The number in radar plot represents Spearman’s correlation coefficient. * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Expressing, Mutagenesis, Immunopeptidomics

Correlation analysis between ARPC5 expression and RNA modification-related genes, DNA methyltransferases, and tumor stemness score in 33 cancer types. (A) Co-expression of ARPC5 with m1A-related genes. (B) Co-expression of ARPC5 with m5C-related genes. (C) Co-expression of ARPC5 with m6A-related genes. (D) Co-expression of ARPC5 with DNA methyltransferases. (E) The correlation between ARPC5 expression and Tumor Stemness score (DNAss). (F) The correlation between ARPC5 expression and Tumor Stemness score (RNAss). * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: Correlation analysis between ARPC5 expression and RNA modification-related genes, DNA methyltransferases, and tumor stemness score in 33 cancer types. (A) Co-expression of ARPC5 with m1A-related genes. (B) Co-expression of ARPC5 with m5C-related genes. (C) Co-expression of ARPC5 with m6A-related genes. (D) Co-expression of ARPC5 with DNA methyltransferases. (E) The correlation between ARPC5 expression and Tumor Stemness score (DNAss). (F) The correlation between ARPC5 expression and Tumor Stemness score (RNAss). * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Expressing, RNA modification

ARPC5 is upregulated in HCC cells and primary HCC tissues. (A) qPCR analysis of ARPC5 mRNA expression in four HCC cell lines (MHCC97-H, Huh7, HCC-LM3, and HepG2) and normal liver cell line (LO2). GAPDH was used as an internal control error bars represent M ± SEM (triplicate experiments). (B, C) The protein expression of ARPC5 was detected in four HCC cell lines and normal liver cell line with Western blot analysis. Error bars represent M ± SD of triplicate measurements. (D) The mRNA expression of ARPC5 in 40 pairs HCC tissues and adjacent para-carcinoma tissues was evaluated using qPCR. (E) Western blot analysis of ARPC5 protein expression in 10 paired HCC tissues and adjacent normal tissues. The number presented the relative protein expression levels of ARPC5. (F) Representative images of ARPC5 immunohistochemical staining analysis in the HCC tissue and adjacent normal liver tissue, original magnifications: ×40 and ×200. Scale bars, 50 μm. (G) Quantitative analysis of ARPC5 expression in HCC tissues based on mean optical density of immunohistochemical staining. Error bars represent the M ± SD of multiple tissues. (H) Kaplan–Meier curves showed that higher expression of ARPC5 was associated with poor DFS in HCC patients. * p < 0.05; ** p < 0.01; *** p < 0.001. ns, no significance.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: ARPC5 is upregulated in HCC cells and primary HCC tissues. (A) qPCR analysis of ARPC5 mRNA expression in four HCC cell lines (MHCC97-H, Huh7, HCC-LM3, and HepG2) and normal liver cell line (LO2). GAPDH was used as an internal control error bars represent M ± SEM (triplicate experiments). (B, C) The protein expression of ARPC5 was detected in four HCC cell lines and normal liver cell line with Western blot analysis. Error bars represent M ± SD of triplicate measurements. (D) The mRNA expression of ARPC5 in 40 pairs HCC tissues and adjacent para-carcinoma tissues was evaluated using qPCR. (E) Western blot analysis of ARPC5 protein expression in 10 paired HCC tissues and adjacent normal tissues. The number presented the relative protein expression levels of ARPC5. (F) Representative images of ARPC5 immunohistochemical staining analysis in the HCC tissue and adjacent normal liver tissue, original magnifications: ×40 and ×200. Scale bars, 50 μm. (G) Quantitative analysis of ARPC5 expression in HCC tissues based on mean optical density of immunohistochemical staining. Error bars represent the M ± SD of multiple tissues. (H) Kaplan–Meier curves showed that higher expression of ARPC5 was associated with poor DFS in HCC patients. * p < 0.05; ** p < 0.01; *** p < 0.001. ns, no significance.

Techniques: Expressing, Control, Western Blot, Immunohistochemical staining, Staining

Silencing of ARPC5 inhibits cell proliferation and promotes cell apoptosis of HCC. (A) The knockdown efficiency of siRNA–ARPC5 was examined in HCC-LM3 and MHCC97-H cells with qPCR. (B) The knockdown efficiency of siRNA-ARPC5 was examined in HCC-LM3 and MHCC97-H cells with Western blot. The number presented as relative protein expression levels of ARPC5. ( C–D ) EdU assays for HCC-LM3 and MHCC 97-H were performed to evaluate cell proliferation ability after transfecting siRNA-ARPC5#1. Representative images (C) and the number of proliferative cells were calculated (D) ; original magnification, ×200. (E–F) Cellular growth curves were evaluated by CCK-8 assays in HCC-LM3 and MHCC97-H cells. (G – H) Flow cytometry was applied to test the apoptosis of HCC cells transfected with si-ARPC5 #1 in HCC-LM3 and MHCC 97-H cells. All data are presented as the M ± SD of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001. ns, no significance.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: Silencing of ARPC5 inhibits cell proliferation and promotes cell apoptosis of HCC. (A) The knockdown efficiency of siRNA–ARPC5 was examined in HCC-LM3 and MHCC97-H cells with qPCR. (B) The knockdown efficiency of siRNA-ARPC5 was examined in HCC-LM3 and MHCC97-H cells with Western blot. The number presented as relative protein expression levels of ARPC5. ( C–D ) EdU assays for HCC-LM3 and MHCC 97-H were performed to evaluate cell proliferation ability after transfecting siRNA-ARPC5#1. Representative images (C) and the number of proliferative cells were calculated (D) ; original magnification, ×200. (E–F) Cellular growth curves were evaluated by CCK-8 assays in HCC-LM3 and MHCC97-H cells. (G – H) Flow cytometry was applied to test the apoptosis of HCC cells transfected with si-ARPC5 #1 in HCC-LM3 and MHCC 97-H cells. All data are presented as the M ± SD of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001. ns, no significance.

Techniques: Knockdown, Western Blot, Expressing, CCK-8 Assay, Flow Cytometry, Transfection

Role of ARPC5 inhibition on migration, invasion, and epithelial–mesenchymal transition (EMT) of HCC cells. (A–D) Migration ability was assessed by scratch wound healing assay, representative images (A, B) were shown (original magnification, ×200; scale bars, 50 µm), and wound healing areas were calculated (C, D) . (E , F) Transwell assay was applied to examine the invasion ability, representative images (F) were shown (original magnification, ×200; scale bars, 50 µm), and the histogram showed the number of invasion cells (E) . (G) Western blot showed the changes of EMT proteins in HCC-LM3 and MHCC97-H cells transfected with si-ARPC5#1. *p < 0.05; **p < 0.01; ***p < 0.001.

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet: Role of ARPC5 inhibition on migration, invasion, and epithelial–mesenchymal transition (EMT) of HCC cells. (A–D) Migration ability was assessed by scratch wound healing assay, representative images (A, B) were shown (original magnification, ×200; scale bars, 50 µm), and wound healing areas were calculated (C, D) . (E , F) Transwell assay was applied to examine the invasion ability, representative images (F) were shown (original magnification, ×200; scale bars, 50 µm), and the histogram showed the number of invasion cells (E) . (G) Western blot showed the changes of EMT proteins in HCC-LM3 and MHCC97-H cells transfected with si-ARPC5#1. *p < 0.05; **p < 0.01; ***p < 0.001.

Techniques: Inhibition, Migration, Wound Healing Assay, Transwell Assay, Western Blot, Transfection

Journal: Frontiers in Immunology

Article Title: A comprehensively prognostic and immunological analysis of actin-related protein 2/3 complex subunit 5 in pan-cancer and identification in hepatocellular carcinoma

doi: 10.3389/fimmu.2022.944898

Figure Lengend Snippet:

Techniques: Expressing, Mutagenesis, Real-time Polymerase Chain Reaction, Small Interfering RNA

Review

rabbit anti arpc5 (Novus Biologicals)

Structured Review

Images

Related Articles

Electrophoresis:

Saline:

Similar Products

Image Search Results