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Bioss p21
P21, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+p21/P21+Polyclonal+Antibody%2C+AbBy+Fluor+555+Conjugated/10__3390_slash_ijms27083618-185-12-15
Average 94 stars, based on 1 article reviews

p21 - by Bioz Stars, 2026-10

94/100 stars

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Article Title: ML216 Prevents DNA Damage-Induced Senescence by Modulating DBC1–BLM Interaction
Article Snippet: The antibodies used included anti-DBC1 (Bethyl Labotatories, Montgomery, TX, USA, A300-434A), anti-V5 (Invitrogen, Waltham, MA, USA, R960-25), anti-Flag (Sigma, F7425), anti-BLM (Bethyl Labotatories, A300-110A), anti-GAPDH (Millipore, St. Louis, MO, USA, MAB374), anti-p21 (BD Biosciences, San Jose, CA, USA, 556430), anti-β Tubulin (Santa Cruz, Dallas, TX, USA, SC-166729), anti-p53 (Santa Cruz, SC-126), anti-Bcl-2 (Santa Cruz, SC-7382), anti-p16 (Santa Cruz, SC-56330), anti-phospho-H2A.X (Millipore, 07-164-25UG), anti-β-actin (Absin, Shanghai, China, ABS830031), anti-PARP1 (CST, Danvers, MA, USA, 9542S), anti-cleaved PARP1 (CST, 5625S), anti-BLM (Bioss, Beijing, China, bs-12872R) and anti-p21 (Bioss, bs-0741R).

Binding Assay:

Article Title: Irradiation Accelerates Plaque Formation and Cellular Senescence in Flow‐Altered Carotid Arteries of Apolipoprotein E Knock‐Out Mice
Article Snippet: Following incubation with horseradish peroxidaseconjugated secondary antibodies (ImmPRESS Horse Anti- Rabbit IgG Polymer Reagent; Vector Laboratories, Burlingame, CA) for 30 minutes, the sections were visualized using a 3,3ʹ- diaminobenzine Peroxidase Substrate Kit (Vector Laboratories) with hematoxylin counterstaining. .. The following antibodies were used: anti- alphasmooth muscle actin (19245, rabbit monoclonal, 1:200, Cell Signaling Technology, Danvers, MA), antivimentin (Alexa Fluor 488 conjugate, 9854, rabbit monoclonal, 1:200, Cell Signaling Technology), anti- Iba- 1 (013- 27691, rabbit polyclonal, 1:1000, Fujifilm Wako, Osaka, Japan), anti- gamma H2AX (05- 636- I, mouse monoclonal, 1:250, Millipore, Billerica, MA), anti- 53BP1 (p53 binding protein 1; NB100- 304, rabbit polyclonal, 1:1000 and Alexa Fluor 594 conjugate, NB100- 304AF594, rabbit polyclonal, 1:100, Novus Biologicals, Littleton, CO), anti- p16INK4a (10883- 1- AP, rabbit polyclonal, 1:300, Proteintech, Rosemont, IL), and anti- p21 (bs- 10129R, rabbit polyclonal, 1:100, Bioss, Woburn, MA). .. The slides were observed under a fluorescence microscope (BZ- X710; Keyence) and images were analyzed using a BZ- X analyzer (Keyence).

Article Title: Irradiation Accelerates Plaque Formation and Cellular Senescence in Flow‐Altered Carotid Arteries of Apolipoprotein E Knock‐Out Mice
Article Snippet: Following incubation with horseradish peroxidase‐conjugated secondary antibodies (ImmPRESS Horse Anti‐Rabbit IgG Polymer Reagent; Vector Laboratories, Burlingame, CA) for 30 minutes, the sections were visualized using a 3,3ʹ‐diaminobenzine Peroxidase Substrate Kit (Vector Laboratories) with hematoxylin counterstaining. .. The following antibodies were used: anti‐alpha‐smooth muscle actin (19245, rabbit monoclonal, 1:200, Cell Signaling Technology, Danvers, MA), antivimentin (Alexa Fluor 488 conjugate, 9854, rabbit monoclonal, 1:200, Cell Signaling Technology), anti‐Iba‐1 (013‐27691, rabbit polyclonal, 1:1000, Fujifilm Wako, Osaka, Japan), anti‐gamma H2AX (05‐636‐I, mouse monoclonal, 1:250, Millipore, Billerica, MA), anti‐53BP1 (p53 binding protein 1; NB100‐304, rabbit polyclonal, 1:1000 and Alexa Fluor 594 conjugate, NB100‐304AF594, rabbit polyclonal, 1:100, Novus Biologicals, Littleton, CO), anti‐p16INK4a (10883‐1‐AP, rabbit polyclonal, 1:300, Proteintech, Rosemont, IL), and anti‐p21 (bs‐10129R, rabbit polyclonal, 1:100, Bioss, Woburn, MA). .. The slides were observed under a fluorescence microscope (BZ‐X710; Keyence) and images were analyzed using a BZ‐X analyzer (Keyence).

Saline:

Article Title: Valproic Acid Enhances the Anticancer Effect of L-Ascorbic Acid by Upregulating Sodium-Dependent Vitamin C Transporter 2 in Colorectal Cancer.
Article Snippet: Protein concentrations were measured using a Bradford Protein Assay Plus Kit (P7200-050; GenDepot, Katy, TX, USA). .. The membranes were blocked with 5% skimmed milk in Tris-buffered saline with Tween 20 (TBST) at room temperature for 2 h. Subsequently, the membranes were incubated overnight at 4 ◦C with anti-SVCT2 (1:500) (A6740; ABclonal, Wuhan, China), anti-p21 (1:2500) (bs10129R; Bioss, Beijing, China), anti-caspase-3 (1:2500) (#9662S; Cell Signaling Technology, Danvers, MA, USA), and anti-beta-actin (1:2000) (NB600-501; Novus biologics, Centennial, CO, USA) antibodies. ..

Article Title: Valproic Acid Enhances the Anticancer Effect of L-Ascorbic Acid by Upregulating Sodium-Dependent Vitamin C Transporter 2 in Colorectal Cancer
Article Snippet: .. The membranes were blocked with 5% skimmed milk in Tris-buffered saline with Tween 20 (TBST) at room temperature for 2 h. Subsequently, the membranes were incubated overnight at 4 °C with anti-SVCT2 (1:500) (A6740; ABclonal, Wuhan, China), anti-p21 (1:2500) (bs-10129R; Bioss, Beijing, China), anti-caspase-3 (1:2500) (#9662S; Cell Signaling Technology, Danvers, MA, USA), and anti-beta-actin (1:2000) (NB600-501; Novus biologics, Centennial, CO, USA) antibodies. ..

Incubation:

Article Title: Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease
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). .. After washing, a poly-horseradish peroxidase (HRP)-conjugated anti-rabbit secondary antibody (CELNOVTE, SD5300) was applied according to the manufacturer’s instructions.

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GPEVs improve d UVB irradiation-induced senescence of HEKa cells in vitro. (A) The SA-β-gal staining of UVB-irradiated HEKa (6 mJ/cm 2 ) cells subjected to treatments with a range of GPEVs concentrations (1 × 10 8 , 2 × 10 8 , 4 × 10 8 particles/ml) and NAC (1 mM). Scale bar: 50 μm. (B) The Quantification of SA-β-gal staining in A. (C) Representative images of EdU staining in UVB-irradiated HEKa cells following treatment with NAC and varying concentrations of GPEVs. Scale bar: 50 μm. (D) Quantification of EdU-positive cells in C. (E) The protein levels of p16, p21 and p53 in HEKa cells exposed to UVB irradiation and GPEVs treatment were assessed using Western blot analysis. (F) The quantification of E was performed using Image J software. (G) The relative mRNA levels of the senescence-associated secretory phenotype in irradiated HEKa cells treated with or without GPEVs were measured by RT-qPCR. All the experiments were repeated at least three times. Data are represented as means ± SD. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc test. Not significant (ns), ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

Article Title: Gynostemma pentaphyllum -derived extracellular vesicles alleviate skin aging by destabilizing STING

doi: 10.1016/j.bioactmat.2026.03.010

Figure Lengend Snippet: GPEVs improve d UVB irradiation-induced senescence of HEKa cells in vitro. (A) The SA-β-gal staining of UVB-irradiated HEKa (6 mJ/cm 2 ) cells subjected to treatments with a range of GPEVs concentrations (1 × 10 8 , 2 × 10 8 , 4 × 10 8 particles/ml) and NAC (1 mM). Scale bar: 50 μm. (B) The Quantification of SA-β-gal staining in A. (C) Representative images of EdU staining in UVB-irradiated HEKa cells following treatment with NAC and varying concentrations of GPEVs. Scale bar: 50 μm. (D) Quantification of EdU-positive cells in C. (E) The protein levels of p16, p21 and p53 in HEKa cells exposed to UVB irradiation and GPEVs treatment were assessed using Western blot analysis. (F) The quantification of E was performed using Image J software. (G) The relative mRNA levels of the senescence-associated secretory phenotype in irradiated HEKa cells treated with or without GPEVs were measured by RT-qPCR. All the experiments were repeated at least three times. Data are represented as means ± SD. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc test. Not significant (ns), ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: The primary antibodies used included γ-H2AX and CTCF (1:1,000, Cell Signaling), p21 and STING (diluted 1:1,000, Cell Signaling).

Techniques: Irradiation, In Vitro, Staining, Western Blot, Software, Quantitative RT-PCR

The application of GPEVs effectively mitigate d UVB-induced skin aging in Balb/C mice. (A) Representative images of Masson's trichrome staining of mice skin from each group. Collagen fibers are stained blue. Scale bar: 200 μm. (B) Quantitative analysis of collagen fibers in Masson's trichrome stained skin tissue sections by Image J software. (C and D) The levels of p21 in mice skin were detected by immunofluorescent staining and quantified using Image J software. (E) The protein levels of aging-related proteins in skin tissues were determined by Western Blots. (F) The quantification of E was conducted using Image J software. (G) The mRNA levels of senescence-associated secretory phenotype in skin tissues were detected by RT-qPCR. Data are represented as means ± SD. Statistical analysis was performed using One-way ANOVA followed by Bonferroni post hoc test. Not significant (ns), ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

Article Title: Gynostemma pentaphyllum -derived extracellular vesicles alleviate skin aging by destabilizing STING

doi: 10.1016/j.bioactmat.2026.03.010

Figure Lengend Snippet: The application of GPEVs effectively mitigate d UVB-induced skin aging in Balb/C mice. (A) Representative images of Masson's trichrome staining of mice skin from each group. Collagen fibers are stained blue. Scale bar: 200 μm. (B) Quantitative analysis of collagen fibers in Masson's trichrome stained skin tissue sections by Image J software. (C and D) The levels of p21 in mice skin were detected by immunofluorescent staining and quantified using Image J software. (E) The protein levels of aging-related proteins in skin tissues were determined by Western Blots. (F) The quantification of E was conducted using Image J software. (G) The mRNA levels of senescence-associated secretory phenotype in skin tissues were detected by RT-qPCR. Data are represented as means ± SD. Statistical analysis was performed using One-way ANOVA followed by Bonferroni post hoc test. Not significant (ns), ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: The primary antibodies used included γ-H2AX and CTCF (1:1,000, Cell Signaling), p21 and STING (diluted 1:1,000, Cell Signaling).

Techniques: Staining, Software, Western Blot, Quantitative RT-PCR

Senescent Microenvironment-Educated Mesenchymal Stem Cells Release High-Affinity Senescent NPC Domesticated Extracellular Vesicles. (A) Schematic diagram of the experimental setup for educating MSCs with SASP-CM to generate D-EVs versus N-EVs. (B) Confocal microscopy images showing different EVs internalization by senescent NPCs after 12 h in vitro. (C) Flow cytometry and quantification analysis of different EVs uptake by senescent NPCs. (D) In vivo validation of the senescent niche. Representative fluorescence images following injection of senescence-tracer (Red). (E) In vivo PKH26-labeled D-EVs tracking. (F) Representative SA-β-Gal images and quantification of MSCs treated with SASP-CM or not. (G) Gene Ontology (GO) analysis confirming enrichment of external encapsulating structure organization and cytokine production in Biological Process (BP) categories. (H) Heatmap indicating gene expression associated with EVs biogenesis within D-MSCs and N-MSCs. (I) Heatmap indicating gene expression associated with cytokine production within D-MSCs and N-MSCs. (J and L) Gene Ontology (GO) analysis confirming enrichment of terms related to vesicle organization and transport in the Cellular Component (CC) categories. (K) Western blot analysis confirmed core senescence markers p16 and p21 and DNA damage marker γ-H2AX in N-MSC and D-MSC. (M) Western blot analysis confirmed the expression of CD9, CD63, TSG101, Calnexin, and GM130 in MSC-EVs, N-EVs, or D-EVs. (N) TEM images showing the morphology and size of MSC-derived EVs, N-EVs, and D-EVs. (O) NTA shows size distribution in MSC-EVs, N-EVs, or D-EVs. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

Article Title: Microenvironment-educated MSC-EVs loaded injectable smart hydrogel for targeting senescent nucleus pulposus cells and inhibiting ferroptosis against intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: Senescent Microenvironment-Educated Mesenchymal Stem Cells Release High-Affinity Senescent NPC Domesticated Extracellular Vesicles. (A) Schematic diagram of the experimental setup for educating MSCs with SASP-CM to generate D-EVs versus N-EVs. (B) Confocal microscopy images showing different EVs internalization by senescent NPCs after 12 h in vitro. (C) Flow cytometry and quantification analysis of different EVs uptake by senescent NPCs. (D) In vivo validation of the senescent niche. Representative fluorescence images following injection of senescence-tracer (Red). (E) In vivo PKH26-labeled D-EVs tracking. (F) Representative SA-β-Gal images and quantification of MSCs treated with SASP-CM or not. (G) Gene Ontology (GO) analysis confirming enrichment of external encapsulating structure organization and cytokine production in Biological Process (BP) categories. (H) Heatmap indicating gene expression associated with EVs biogenesis within D-MSCs and N-MSCs. (I) Heatmap indicating gene expression associated with cytokine production within D-MSCs and N-MSCs. (J and L) Gene Ontology (GO) analysis confirming enrichment of terms related to vesicle organization and transport in the Cellular Component (CC) categories. (K) Western blot analysis confirmed core senescence markers p16 and p21 and DNA damage marker γ-H2AX in N-MSC and D-MSC. (M) Western blot analysis confirmed the expression of CD9, CD63, TSG101, Calnexin, and GM130 in MSC-EVs, N-EVs, or D-EVs. (N) TEM images showing the morphology and size of MSC-derived EVs, N-EVs, and D-EVs. (O) NTA shows size distribution in MSC-EVs, N-EVs, or D-EVs. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: After blocked with 5% non-fat milk for 2 h at room temperature, the membranes were incubated with primary antibodies against GAPDH (1:5000, 104941-AP, Proteintech), TSG101 (1:1000, DF8427, Affinity), CD9 (1:1000, AF5139, Affinity), CD63 (1:2000, 25682-1-AP, Proteintech), Calnexin (1:5000, 10427-2-AP, Proteintech), GM130 (1:20000, 11308-1-AP, Proteintech), CXCR3 (1:5000, 26756-1-AP, Proteintech), CXCL10 (1:2000, 10937-1-AP, Proteintech), MMP3 (1:2000, 17873-1-AP, Proteintech), ADAMTS5 (DF13268, Affinity), P16 (AF5484, Affinity), P21 (10355-1-AP, Proteintech), GPX4 (1:1000, 381958, Zen-bio), SLC7A11 (1:1000, 26864-1-AP, Proteintech), ACSL4 (1:5000, 22401-1-AP, Proteintech) and Tubulin (1:10000, T40103 , Abmart) overnight at 4 °C.

Techniques: Confocal Microscopy, In Vitro, Flow Cytometry, In Vivo, Biomarker Discovery, Fluorescence, Injection, Labeling, Gene Expression, Western Blot, Marker, Expressing, Derivative Assay

D-EVs Alleviate Cellular Senescence and Restore ECM anabolic/catabolic metabolism in Senescent NPCs. (A) The CCK8 assay was used to determine D-EVs concentrations on cell viability. (B) Flow cytometry analysis of proliferative capacity in the above group, and (C) quantitative analysis. (D) Representative ROS images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869. (E) Representative SA-β-Gal images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869, and (F) quantitative analysis. (G) Confocal analysis of γ-H2A with IF staining depicting DNA damage in the control, TBHP, N-Evs, or D-EVs group. (H) WB analysis of ECM metabolism–related and aging-related proteins in NPCs following treatment with Control, TBHP, N-Evs, or D-EVs. (I) Western blot analysis of p53, p21, and p16 in senescent NPCs treated with D-EVs, D-CM, or D-CM EV-dep . (J) Confocal analysis of COL2 with IF staining in the control, TBHP, N-EVs, or D-EVs group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Alleviate Cellular Senescence and Restore ECM anabolic/catabolic metabolism in Senescent NPCs. (A) The CCK8 assay was used to determine D-EVs concentrations on cell viability. (B) Flow cytometry analysis of proliferative capacity in the above group, and (C) quantitative analysis. (D) Representative ROS images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869. (E) Representative SA-β-Gal images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869, and (F) quantitative analysis. (G) Confocal analysis of γ-H2A with IF staining depicting DNA damage in the control, TBHP, N-Evs, or D-EVs group. (H) WB analysis of ECM metabolism–related and aging-related proteins in NPCs following treatment with Control, TBHP, N-Evs, or D-EVs. (I) Western blot analysis of p53, p21, and p16 in senescent NPCs treated with D-EVs, D-CM, or D-CM EV-dep . (J) Confocal analysis of COL2 with IF staining in the control, TBHP, N-EVs, or D-EVs group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Techniques: CCK-8 Assay, Flow Cytometry, Staining, Control, Western Blot

D-EVs Counteract NPC Senescence by Suppressing Ferroptosis. (A) KEGG pathway analysis of DEGs in senescent NPCs following treatment with D-EVs or not. (B-C) GSEA plots showing significant enrichment of ferroptosis and cell cycle in senescent NPCs. (D-E) Heatmap quantification of key genes involved in ferroptosis and cell cycle. (F) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with different experimental conditions. (G) Representative images of C11-BODIPY 581/591 staining to detect lipid peroxidation (green) in the control, TBHP, Era, Era + Fer-1, or TBHP + Fer-1 groups. (H-I) Quantitative assessment of malondialdehyde (MDA) levels (H) and glutathione (GSH) levels (I) in the control, TBHP, N-EVs, D-EVs, or D-EVs + Era groups. (J) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with PBS, N-EVs, D-EVs, or D-EVs + Era. (K) Confocal analysis of GPX4 with IF staining in the control, TBHP, N-Evs, D-EVs, and D-EVs + Era group. (L) Flow cytometry analysis of cell cycle distribution in the above experimental conditions. Statistical comparisons were performed between the experimental group and the TBHP-induced group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Counteract NPC Senescence by Suppressing Ferroptosis. (A) KEGG pathway analysis of DEGs in senescent NPCs following treatment with D-EVs or not. (B-C) GSEA plots showing significant enrichment of ferroptosis and cell cycle in senescent NPCs. (D-E) Heatmap quantification of key genes involved in ferroptosis and cell cycle. (F) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with different experimental conditions. (G) Representative images of C11-BODIPY 581/591 staining to detect lipid peroxidation (green) in the control, TBHP, Era, Era + Fer-1, or TBHP + Fer-1 groups. (H-I) Quantitative assessment of malondialdehyde (MDA) levels (H) and glutathione (GSH) levels (I) in the control, TBHP, N-EVs, D-EVs, or D-EVs + Era groups. (J) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with PBS, N-EVs, D-EVs, or D-EVs + Era. (K) Confocal analysis of GPX4 with IF staining in the control, TBHP, N-Evs, D-EVs, and D-EVs + Era group. (L) Flow cytometry analysis of cell cycle distribution in the above experimental conditions. Statistical comparisons were performed between the experimental group and the TBHP-induced group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Techniques: Western Blot, Staining, Control, Flow Cytometry

D-EVs Deliver GPX4 to Inhibit Ferroptosis in Senescent NPCs. (A) Representative Senescent-Tracker images of NPCs treated with N-EVs, D-EVs, Era, and D-Evs sh-CXCL10 . (B) Volcano plot of transcriptomic data comparing D-MSC and N-MSC. (C) KEGG pathway analysis of DEGs in D-MSCs versus N-MSCs. (D) Volcano plot of proteomic data comparing D-EVs and N-EVs. (E) KEGG pathway analysis of transcriptomic and proteomic data integration. (F) A Venn diagram illustrating the intersection of genes from the D-MSC transcriptome, the D-EVs proteome, and the ferroptosis-related gene set. (G) Bar graph showing the relative expression levels of core overlapping genes identified in (F). (H) MS analysis revealed that GPX4 is enriched in the D-EVs proteome. (I) Western blot analysis confirming GPX4 protein in D-EVs and N-EVs. (J) Western blot analysis of key senescence (p21, P16) markers in NPCs following treatment with PBS or N-EVs with CXCL10 or GPX4 knockout. (K) Representative images of EdU depicting cell proliferation ability in the control, TBHP, D-EVs, D-EVs sh-CXCL10 , D-EVs sh-GPX4 , and D-EVs sh-CXCL10+GPX4 groups. (L-M) Confocal images showing GPX4 delivery from different EVs to senescent NPCs at 12h and 24h co-culture, and (N) colocalization analysis. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Deliver GPX4 to Inhibit Ferroptosis in Senescent NPCs. (A) Representative Senescent-Tracker images of NPCs treated with N-EVs, D-EVs, Era, and D-Evs sh-CXCL10 . (B) Volcano plot of transcriptomic data comparing D-MSC and N-MSC. (C) KEGG pathway analysis of DEGs in D-MSCs versus N-MSCs. (D) Volcano plot of proteomic data comparing D-EVs and N-EVs. (E) KEGG pathway analysis of transcriptomic and proteomic data integration. (F) A Venn diagram illustrating the intersection of genes from the D-MSC transcriptome, the D-EVs proteome, and the ferroptosis-related gene set. (G) Bar graph showing the relative expression levels of core overlapping genes identified in (F). (H) MS analysis revealed that GPX4 is enriched in the D-EVs proteome. (I) Western blot analysis confirming GPX4 protein in D-EVs and N-EVs. (J) Western blot analysis of key senescence (p21, P16) markers in NPCs following treatment with PBS or N-EVs with CXCL10 or GPX4 knockout. (K) Representative images of EdU depicting cell proliferation ability in the control, TBHP, D-EVs, D-EVs sh-CXCL10 , D-EVs sh-GPX4 , and D-EVs sh-CXCL10+GPX4 groups. (L-M) Confocal images showing GPX4 delivery from different EVs to senescent NPCs at 12h and 24h co-culture, and (N) colocalization analysis. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Techniques: Expressing, Western Blot, Knock-Out, Control, Co-Culture Assay

Influence of RB1–K900lac on the cell cycle pathway. ( A to C ) Cell cycle analysis by flow cytometry in A549 and PC-9 cell lines stably expressing RB1–WT or RB1–K900R via lentiviral vectors. ( D ) Representative immunofluorescence images showing the distribution of CDK1 in A549 and PC-9 cells. CDK1 protein was labeled with red fluorescent Cy3, and nuclei were counterstained with blue fluorescent DAPI. Images were acquired using a high-resolution confocal multiphoton microscopy system (NIKON AX RMP, Japan). ( E , F ) Western blot analysis of cell cycle-related CDK molecule expression. ( G , H ) Expression of cell cycle-related cyclin molecules. ( I , J ) Expression of P21 and Chk1 molecules. ( K ) Schematic diagram illustrating how LDHC4 promotes the cell cycle by inducing RB1 lactylation. ** p < 0.01, *** p < 0.001

Journal: Journal of Translational Medicine

Article Title: LDHC4 drives lung adenocarcinoma progression by inducing lactylation of RB1 at lysine 900 to disrupt the RB1–E2F1 complex

doi: 10.1186/s12967-026-08070-9

Figure Lengend Snippet: Influence of RB1–K900lac on the cell cycle pathway. ( A to C ) Cell cycle analysis by flow cytometry in A549 and PC-9 cell lines stably expressing RB1–WT or RB1–K900R via lentiviral vectors. ( D ) Representative immunofluorescence images showing the distribution of CDK1 in A549 and PC-9 cells. CDK1 protein was labeled with red fluorescent Cy3, and nuclei were counterstained with blue fluorescent DAPI. Images were acquired using a high-resolution confocal multiphoton microscopy system (NIKON AX RMP, Japan). ( E , F ) Western blot analysis of cell cycle-related CDK molecule expression. ( G , H ) Expression of cell cycle-related cyclin molecules. ( I , J ) Expression of P21 and Chk1 molecules. ( K ) Schematic diagram illustrating how LDHC4 promotes the cell cycle by inducing RB1 lactylation. ** p < 0.01, *** p < 0.001

Article Snippet: The following antibodies were used in this study: rabbit anti-human LDHC (subunit C) monoclonal antibody (mAb) (Proteintech Group, Inc., 1:1000), rabbit anti-human RB1 mAb (Proteintech Group, Inc., 1:2000), rabbit anti-human L-Lactyl Lysine mAb (PTM Bio, Inc., 1:1000), rabbit anti-human E2F1 mAb (APExBIO Technology, LLC, 1:500), rabbit anti-human Lamin B mAb (Beyotime Biotech, Inc., 1:1000), rabbit anti-human CDK1 mAb (Beyotime Biotech, Inc., 1:800), rabbit anti-human CDK2 mAb (Beyotime Biotech, Inc., 1:800), rabbit anti-human CDK4 mAb (Beyotime Biotech, Inc., 1:1000), rabbit anti-human CDK6 mAb (Beyotime Biotech, Inc., 1:1000), rabbit anti-human cyclin A2 mAb (Beyotime Biotech, Inc., 1:1000), rabbit anti-human cyclin B1 mAb (Beyotime Biotech, Inc., 1:1000), rabbit anti-human cyclin D1 mAb (Beyotime Biotech, Inc., 1:500), rabbit anti-human P21 mAb (Abmart Bio, Inc., 1:500), rabbit anti-human Chk1 mAb (Immunoway Bio, Inc., 1:2000), and rabbit anti-β-Actin monoclonal antibody (Beyotime Biotech, Inc., 1:1000). β-Actin and Lamin B served as loading controls, and protein band intensities were quantified using Image J software.

Techniques: Cell Cycle Assay, Flow Cytometry, Stable Transfection, Expressing, Immunofluorescence, Labeling, Microscopy, Western Blot

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