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Proteintech p21 polyclonal antibody

Expression and functional exploration of the key genes in single-cell sequencing data (A) The UMAP plot shows the total sample composition, tissue sources, and cell subtypes. (B) The stacked graph shows the proportion of each type of cell in the control group and the AILI group. (C) Bubble plots of marker gene expression demonstrating the accuracy of the cell annotations. (D) Bubble chart showing the expression of <t>Cdkn1a</t> and Pdk1 in various cells in the control group. (E) Bubble chart showing the expression of Cdkn1a and Pdk1 in various cells in the AILI group. (F) Circle plot and heatmap showing the cell communication weights and numbers of all cell subtypes. (G–J) Receptor‒ligand communication weights between AILI and control samples.

P21 Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1278 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1278 article reviews

p21 polyclonal antibody - by Bioz Stars, 2026-06

96/100 stars

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1) Product Images from "Identification and validation of key PANoptosis-related genes via integrative machine learning and single-cell sequencing in AILI"

Article Title: Identification and validation of key PANoptosis-related genes via integrative machine learning and single-cell sequencing in AILI

Journal: iScience

doi: 10.1016/j.isci.2026.115183

Figure Legend Snippet: Expression and functional exploration of the key genes in single-cell sequencing data (A) The UMAP plot shows the total sample composition, tissue sources, and cell subtypes. (B) The stacked graph shows the proportion of each type of cell in the control group and the AILI group. (C) Bubble plots of marker gene expression demonstrating the accuracy of the cell annotations. (D) Bubble chart showing the expression of Cdkn1a and Pdk1 in various cells in the control group. (E) Bubble chart showing the expression of Cdkn1a and Pdk1 in various cells in the AILI group. (F) Circle plot and heatmap showing the cell communication weights and numbers of all cell subtypes. (G–J) Receptor‒ligand communication weights between AILI and control samples.

Techniques Used: Expressing, Functional Assay, Single Cell, Sequencing, Control, Marker, Gene Expression

Validation of key PANoptosis-related genes in animal models (A) H&E staining of liver tissues from WT and AILI mice (scale bars, 100 μm; n = 5). (B) mRNA expression of Cdkn1a and Pdk1 by RT-qPCR. (C–F) Correlation analyses between hepatic Cdkn1a and Pdk1 mRNA levels and serum ALT and AST levels at 24 h after AILI. (G) Detection and statistical analysis of key PANoptosis-related gene and marker protein expression in liver tissues from WT and AILI mice. (H) Immunohistochemical staining for P21 and PDK1 in liver tissues from WT and AILI mice (scale bars, 50 μm; n = 5). All the data are presented as the means ± SDs. One-way ANOVA with Tukey’s test and a two-tailed Student’s t test were used for statistical analysis. Spearman’s rank correlation was used to assess the associations between relative mRNA expression levels of Cdkn1a and Pdk1 and serum ALT and AST levels. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Figure Legend Snippet: Validation of key PANoptosis-related genes in animal models (A) H&E staining of liver tissues from WT and AILI mice (scale bars, 100 μm; n = 5). (B) mRNA expression of Cdkn1a and Pdk1 by RT-qPCR. (C–F) Correlation analyses between hepatic Cdkn1a and Pdk1 mRNA levels and serum ALT and AST levels at 24 h after AILI. (G) Detection and statistical analysis of key PANoptosis-related gene and marker protein expression in liver tissues from WT and AILI mice. (H) Immunohistochemical staining for P21 and PDK1 in liver tissues from WT and AILI mice (scale bars, 50 μm; n = 5). All the data are presented as the means ± SDs. One-way ANOVA with Tukey’s test and a two-tailed Student’s t test were used for statistical analysis. Spearman’s rank correlation was used to assess the associations between relative mRNA expression levels of Cdkn1a and Pdk1 and serum ALT and AST levels. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Techniques Used: Biomarker Discovery, Staining, Expressing, Quantitative RT-PCR, Marker, Immunohistochemical staining, Two Tailed Test

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Journal: iScience

Article Title: Identification and validation of key PANoptosis-related genes via integrative machine learning and single-cell sequencing in AILI

doi: 10.1016/j.isci.2026.115183

Figure Lengend Snippet: Expression and functional exploration of the key genes in single-cell sequencing data (A) The UMAP plot shows the total sample composition, tissue sources, and cell subtypes. (B) The stacked graph shows the proportion of each type of cell in the control group and the AILI group. (C) Bubble plots of marker gene expression demonstrating the accuracy of the cell annotations. (D) Bubble chart showing the expression of Cdkn1a and Pdk1 in various cells in the control group. (E) Bubble chart showing the expression of Cdkn1a and Pdk1 in various cells in the AILI group. (F) Circle plot and heatmap showing the cell communication weights and numbers of all cell subtypes. (G–J) Receptor‒ligand communication weights between AILI and control samples.

Article Snippet: p21 Polyclonal antibody , Proteintech , Cat No.28248-1-AP; RRID: AB_2881097.

Techniques: Expressing, Functional Assay, Single Cell, Sequencing, Control, Marker, Gene Expression

Journal: iScience

Article Title: Identification and validation of key PANoptosis-related genes via integrative machine learning and single-cell sequencing in AILI

doi: 10.1016/j.isci.2026.115183

Figure Lengend Snippet: Validation of key PANoptosis-related genes in animal models (A) H&E staining of liver tissues from WT and AILI mice (scale bars, 100 μm; n = 5). (B) mRNA expression of Cdkn1a and Pdk1 by RT-qPCR. (C–F) Correlation analyses between hepatic Cdkn1a and Pdk1 mRNA levels and serum ALT and AST levels at 24 h after AILI. (G) Detection and statistical analysis of key PANoptosis-related gene and marker protein expression in liver tissues from WT and AILI mice. (H) Immunohistochemical staining for P21 and PDK1 in liver tissues from WT and AILI mice (scale bars, 50 μm; n = 5). All the data are presented as the means ± SDs. One-way ANOVA with Tukey’s test and a two-tailed Student’s t test were used for statistical analysis. Spearman’s rank correlation was used to assess the associations between relative mRNA expression levels of Cdkn1a and Pdk1 and serum ALT and AST levels. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: p21 Polyclonal antibody , Proteintech , Cat No.28248-1-AP; RRID: AB_2881097.

Techniques: Biomarker Discovery, Staining, Expressing, Quantitative RT-PCR, Marker, Immunohistochemical staining, Two Tailed Test

Formononetin intervention delays high glucose-induced senescence in MPC-5 cells. A: Heatmap of genes related to the p53 signaling pathway showing that formononetin (FN) intervention upregulates MDM2 and CCND1 expression and downregulates p21 expression; B: The molecular docking results of FN and MDM2; C: Western blot bands of proliferating cell nuclear antigen; D and E: Cell staining and cell supernatant β-galactosidase (β-GAL) activity assay demonstrating that FN intervention significantly reduces β-GAL activity in MPC-5 cells; F: Β-GAL indicator cell staining photography (100 ×); G: Western blot analysis revealing that FN intervention significantly decreases proliferating cell nuclear antigen protein levels. n = 3 per group. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups. NS: Not significant; FN: Formononetin; HG: High glucose; H-FN: High dose of formononetin; PCNA: Proliferating cell nuclear antigen.

Journal: World Journal of Diabetes

Article Title: Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

doi: 10.4239/wjd.v17.i2.112500

Figure Lengend Snippet: Formononetin intervention delays high glucose-induced senescence in MPC-5 cells. A: Heatmap of genes related to the p53 signaling pathway showing that formononetin (FN) intervention upregulates MDM2 and CCND1 expression and downregulates p21 expression; B: The molecular docking results of FN and MDM2; C: Western blot bands of proliferating cell nuclear antigen; D and E: Cell staining and cell supernatant β-galactosidase (β-GAL) activity assay demonstrating that FN intervention significantly reduces β-GAL activity in MPC-5 cells; F: Β-GAL indicator cell staining photography (100 ×); G: Western blot analysis revealing that FN intervention significantly decreases proliferating cell nuclear antigen protein levels. n = 3 per group. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups. NS: Not significant; FN: Formononetin; HG: High glucose; H-FN: High dose of formononetin; PCNA: Proliferating cell nuclear antigen.

Article Snippet: Sections were then incubated with the following rabbit-derived primary antibodies: Anti-nephrin (Affinity, DF7501; 1:100), anti-p21 (Bioss, bs-55160R; 1:50), anti-Ki67 (Proteintech, 28074-1-AP; 1:2000), and anti-α-smooth muscle actin (Proteintech, 14395-1-AP; 1:3000).

Techniques: Expressing, Western Blot, Staining, Activity Assay, Control

Formononetin intervention delays senescence of MPC-5 cells via p53 signaling pathway. A: Western blot bands of p53 signaling pathway; B: Dual-luciferase reporter gene assay demonstrating that formononetin (FN) intervention significantly reduces p53 transcriptional activity; C-F: Western blot analysis reveals that FN intervention significantly increases MDM2 and CCND1 protein levels and decreases p53 and p21 protein levels; G: Β-galactosidase (β-GAL) indicator cell staining photography (100 ×); H: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay showing that MDM2 silencing weakens the protective effects of FN on high glucose-induced MPC-5 cell viability; I and J: Cell staining and cell supernatant β-GAL activity assay showing that MDM2 silencing eliminates the reduction in β-GAL activity induced by FN. n = 3 per group. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups. NS: Not significant; FN: Formononetin; HG: High glucose; H-FN: High dose of formononetin; C: Control; shNC: Short hairpin negative control; shMDM2: Short hairpin RNA targeting MDM2.

Journal: World Journal of Diabetes

Article Title: Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

doi: 10.4239/wjd.v17.i2.112500

Figure Lengend Snippet: Formononetin intervention delays senescence of MPC-5 cells via p53 signaling pathway. A: Western blot bands of p53 signaling pathway; B: Dual-luciferase reporter gene assay demonstrating that formononetin (FN) intervention significantly reduces p53 transcriptional activity; C-F: Western blot analysis reveals that FN intervention significantly increases MDM2 and CCND1 protein levels and decreases p53 and p21 protein levels; G: Β-galactosidase (β-GAL) indicator cell staining photography (100 ×); H: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay showing that MDM2 silencing weakens the protective effects of FN on high glucose-induced MPC-5 cell viability; I and J: Cell staining and cell supernatant β-GAL activity assay showing that MDM2 silencing eliminates the reduction in β-GAL activity induced by FN. n = 3 per group. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups. NS: Not significant; FN: Formononetin; HG: High glucose; H-FN: High dose of formononetin; C: Control; shNC: Short hairpin negative control; shMDM2: Short hairpin RNA targeting MDM2.

Techniques: Western Blot, Luciferase, Reporter Gene Assay, Activity Assay, Staining, Control, Negative Control, shRNA

MDM2 silencing attenuates anti-senescence effects of formononetin. We silenced the MDM2 gene in MPC-5 cells to investigate whether formononetin (FN) exerts its anti-senescence effects through MDM2 ( n = 3 per group). A: Western blot bands of p53 signaling pathway; B: Dual-luciferase reporter gene assay demonstrating that MDM2 silencing attenuates inhibitory effects of FN on p53 transcriptional activity; C-G: Western blot analysis showing that MDM2 silencing abolishes regulatory effects of FN on MDM2, p53, p21, proliferating cell nuclear antigen and CCND1 protein expression; H-J: Silencing MDM2 abolishes inhibitory effects of FN on interleukin-1β, interleukin-6, and tumor necrosis factor α levels in the culture supernatant of high glucose-exposed MPC-5 cells. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups; e P < 0.05 vs short hairpin RNA targeting MDM2 group; f P < 0.01 vs short hairpin RNA targeting MDM2 groups. NS: Not significant; FN: Formononetin; HG: High glucose; C: Control; shNC: Short hairpin negative control; shMDM2: Short hairpin RNA targeting MDM2; PCNA: Proliferating cell nuclear antigen; IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor α.

Journal: World Journal of Diabetes

Article Title: Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

doi: 10.4239/wjd.v17.i2.112500

Figure Lengend Snippet: MDM2 silencing attenuates anti-senescence effects of formononetin. We silenced the MDM2 gene in MPC-5 cells to investigate whether formononetin (FN) exerts its anti-senescence effects through MDM2 ( n = 3 per group). A: Western blot bands of p53 signaling pathway; B: Dual-luciferase reporter gene assay demonstrating that MDM2 silencing attenuates inhibitory effects of FN on p53 transcriptional activity; C-G: Western blot analysis showing that MDM2 silencing abolishes regulatory effects of FN on MDM2, p53, p21, proliferating cell nuclear antigen and CCND1 protein expression; H-J: Silencing MDM2 abolishes inhibitory effects of FN on interleukin-1β, interleukin-6, and tumor necrosis factor α levels in the culture supernatant of high glucose-exposed MPC-5 cells. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups; e P < 0.05 vs short hairpin RNA targeting MDM2 group; f P < 0.01 vs short hairpin RNA targeting MDM2 groups. NS: Not significant; FN: Formononetin; HG: High glucose; C: Control; shNC: Short hairpin negative control; shMDM2: Short hairpin RNA targeting MDM2; PCNA: Proliferating cell nuclear antigen; IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor α.

Techniques: Western Blot, Luciferase, Reporter Gene Assay, Activity Assay, Expressing, Control, shRNA, Negative Control

Formononetin intervention ameliorates podocyte injury and cellular senescence in diabetic kidney disease mice. A: Immunofluorescence staining of podocyte-specific markers (nephrin, podocin, and CD2AP; bars = 50 μm); B: Immunofluorescence staining of fibrosis markers (α-smooth muscle actin; bars = 50 μm); C: Immunofluorescence staining of aging markers (p21; bars = 50 μm); D: Immunofluorescence staining of cellular proliferation dynamics markers (Ki67; bars = 50 μm). n = 4 per group. a P < 0.05 vs control groups; b P < 0.01 vs high glucose groups. NS: Not significant; IRB: Irbesartan; L-FN: Low dose of formononetin; M-FN: Medium dose of formononetin; H-FN: High dose of formononetin; α-SMA: Α-smooth muscle actin.

Journal: World Journal of Diabetes

Article Title: Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

doi: 10.4239/wjd.v17.i2.112500

Figure Lengend Snippet: Formononetin intervention ameliorates podocyte injury and cellular senescence in diabetic kidney disease mice. A: Immunofluorescence staining of podocyte-specific markers (nephrin, podocin, and CD2AP; bars = 50 μm); B: Immunofluorescence staining of fibrosis markers (α-smooth muscle actin; bars = 50 μm); C: Immunofluorescence staining of aging markers (p21; bars = 50 μm); D: Immunofluorescence staining of cellular proliferation dynamics markers (Ki67; bars = 50 μm). n = 4 per group. a P < 0.05 vs control groups; b P < 0.01 vs high glucose groups. NS: Not significant; IRB: Irbesartan; L-FN: Low dose of formononetin; M-FN: Medium dose of formononetin; H-FN: High dose of formononetin; α-SMA: Α-smooth muscle actin.

Techniques: Immunofluorescence, Staining, Control

Formononetin exhibits anti-senescence effects in diabetic kidney disease mice. A-C: Formononetin (FN) intervention significantly reduces levels of interleukin-1β, interleukin-6, and tumor necrosis factor α in renal tissues of diabetic kidney disease mice; D: FN intervention significantly decreases β-galactosidase activity in renal tissues; E-H: FN intervention significantly upregulates MDM2 and CCND1 gene expression and downregulates p53 and p21 gene expression; I: Western blot bands of p53 signaling pathway; J-M: FN intervention significantly increases MDM2 and CCND1 protein levels and decreases p53 and p21 protein levels. n = 10 for A-D, n = 3 for F. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups. H-FN: High dose of formononetin; IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor α.

Journal: World Journal of Diabetes

Article Title: Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

doi: 10.4239/wjd.v17.i2.112500

Figure Lengend Snippet: Formononetin exhibits anti-senescence effects in diabetic kidney disease mice. A-C: Formononetin (FN) intervention significantly reduces levels of interleukin-1β, interleukin-6, and tumor necrosis factor α in renal tissues of diabetic kidney disease mice; D: FN intervention significantly decreases β-galactosidase activity in renal tissues; E-H: FN intervention significantly upregulates MDM2 and CCND1 gene expression and downregulates p53 and p21 gene expression; I: Western blot bands of p53 signaling pathway; J-M: FN intervention significantly increases MDM2 and CCND1 protein levels and decreases p53 and p21 protein levels. n = 10 for A-D, n = 3 for F. a P < 0.05 vs control groups; b P < 0.01 vs control groups; c P < 0.05 vs high glucose groups; d P < 0.01 vs high glucose groups. H-FN: High dose of formononetin; IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor α.

Techniques: Activity Assay, Gene Expression, Western Blot, Control

Presence and distribution of senescent cells during OTM. ( A ) Representative p21 and p16 immunofluorescence staining images with DAPI. ( B ) Quantitative analysis of p21 + area in PDL. ( C ) Quantitative analysis of p16 + area in PDL. ( D , E ) Distribution of senescence marker–positive areas in the 60 g and 180 g groups. Scale bars: 100 µm (low magnification), 10 µm (high magnification). Data are mean ± SD (n = 4). * p < 0.05; *** p < 0.001; **** p < 0.0001; one-way ANOVA with Tukey’s test. PDL: periodontal ligament, AB: alveolar bone.

Journal: Biology

Article Title: Force-Dependent Presence of Senescent Cells Expressing Vascular Endothelial Growth Factor During Orthodontic Tooth Movement

doi: 10.3390/biology15020187

Figure Lengend Snippet: Presence and distribution of senescent cells during OTM. ( A ) Representative p21 and p16 immunofluorescence staining images with DAPI. ( B ) Quantitative analysis of p21 + area in PDL. ( C ) Quantitative analysis of p16 + area in PDL. ( D , E ) Distribution of senescence marker–positive areas in the 60 g and 180 g groups. Scale bars: 100 µm (low magnification), 10 µm (high magnification). Data are mean ± SD (n = 4). * p < 0.05; *** p < 0.001; **** p < 0.0001; one-way ANOVA with Tukey’s test. PDL: periodontal ligament, AB: alveolar bone.

Article Snippet: p21 , Senescence marker , Bioss Antibodies (Shanghai, China) , bs-10129R , AF555 , 1:100.

Techniques: Immunofluorescence, Staining, Marker

Cellular senescence of vascular endothelial cells (ECs) induced by OTM. ( A ) Representative p21 and CD31 immunofluorescence staining images. p21/CD31 staining without DAPI ( left ) and merged images with DAPI ( right ) are shown. ( B ) Quantitative analysis of p21 + CD31 + area in PDL. ( C ) Representative p16 and CD31 immunofluorescence staining images. p16/CD31 staining without DAPI ( left ) and merged images with DAPI ( right ) are shown. ( D ) Quantitative analysis of p16 + CD31 + area in PDL. Scale bars: 100 µm (low magnification), 10 µm (high magnification). Data are mean ± SD (n = 4). ns: not significant, * p < 0.05; ** p < 0.01; Kruskal–Wallis with Dunn’s post hoc test. PDL: periodontal ligament, AB: alveolar bone.

Journal: Biology

Article Title: Force-Dependent Presence of Senescent Cells Expressing Vascular Endothelial Growth Factor During Orthodontic Tooth Movement

doi: 10.3390/biology15020187

Figure Lengend Snippet: Cellular senescence of vascular endothelial cells (ECs) induced by OTM. ( A ) Representative p21 and CD31 immunofluorescence staining images. p21/CD31 staining without DAPI ( left ) and merged images with DAPI ( right ) are shown. ( B ) Quantitative analysis of p21 + CD31 + area in PDL. ( C ) Representative p16 and CD31 immunofluorescence staining images. p16/CD31 staining without DAPI ( left ) and merged images with DAPI ( right ) are shown. ( D ) Quantitative analysis of p16 + CD31 + area in PDL. Scale bars: 100 µm (low magnification), 10 µm (high magnification). Data are mean ± SD (n = 4). ns: not significant, * p < 0.05; ** p < 0.01; Kruskal–Wallis with Dunn’s post hoc test. PDL: periodontal ligament, AB: alveolar bone.

Article Snippet: p21 , Senescence marker , Bioss Antibodies (Shanghai, China) , bs-10129R , AF555 , 1:100.

Techniques: Immunofluorescence, Staining

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