Review

cdkn1a (Proteintech)

Proteintech is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Proteintech cdkn1a

miR-34a-5p directly targets <t>CDKN1A</t> to promotes ferroptosis of B cells. (A) The interaction between miR-34a-5p and CDKN1A was verified using a dual-luciferase reporter assay. (B, C) CDKN1A mRNA and protein levels were detected by qRT-PCR and western blot in IM-9 cells after miR-34a-5p inhibition. (D, E) qRT-PCR and western blot analysis CDKN1A knockdown efficiency in IM-9 cells. (F–H) The abilities of cell viability, LDH activity, and lipid peroxidation in IM-9 cells treated with miR-34a-5p inhibitor NC, miR-34a-5p inhibitor, or the combination of miR-34a-5p inhibitor and siCDKN1A. All experiments were conducted with n=3, except for the CCK-8 assay, which was conducted with n=6. The data are depicted as the mean ± standard deviation (SD). *, p<0.05; **, p<0.01.

Cdkn1a, supplied by Proteintech, used in various techniques. Bioz Stars score: 98/100, based on 9204 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdkn1a/pmc13007560-55-39-42?v=Proteintech
Average 98 stars, based on 9204 article reviews

cdkn1a - by Bioz Stars, 2026-07

98/100 stars

Images

1) Product Images from "B cell-derived exosomal miR-34a-5p mediates radiation-induced bystander effect through ferroptosis"

Article Title: B cell-derived exosomal miR-34a-5p mediates radiation-induced bystander effect through ferroptosis

Journal: Open Medicine

doi: 10.1515/med-2026-1375

miR-34a-5p directly targets CDKN1A to promotes ferroptosis of B cells. (A) The interaction between miR-34a-5p and CDKN1A was verified using a dual-luciferase reporter assay. (B, C) CDKN1A mRNA and protein levels were detected by qRT-PCR and western blot in IM-9 cells after miR-34a-5p inhibition. (D, E) qRT-PCR and western blot analysis CDKN1A knockdown efficiency in IM-9 cells. (F–H) The abilities of cell viability, LDH activity, and lipid peroxidation in IM-9 cells treated with miR-34a-5p inhibitor NC, miR-34a-5p inhibitor, or the combination of miR-34a-5p inhibitor and siCDKN1A. All experiments were conducted with n=3, except for the CCK-8 assay, which was conducted with n=6. The data are depicted as the mean ± standard deviation (SD). *, p<0.05; **, p<0.01.

Figure Legend Snippet: miR-34a-5p directly targets CDKN1A to promotes ferroptosis of B cells. (A) The interaction between miR-34a-5p and CDKN1A was verified using a dual-luciferase reporter assay. (B, C) CDKN1A mRNA and protein levels were detected by qRT-PCR and western blot in IM-9 cells after miR-34a-5p inhibition. (D, E) qRT-PCR and western blot analysis CDKN1A knockdown efficiency in IM-9 cells. (F–H) The abilities of cell viability, LDH activity, and lipid peroxidation in IM-9 cells treated with miR-34a-5p inhibitor NC, miR-34a-5p inhibitor, or the combination of miR-34a-5p inhibitor and siCDKN1A. All experiments were conducted with n=3, except for the CCK-8 assay, which was conducted with n=6. The data are depicted as the mean ± standard deviation (SD). *, p<0.05; **, p<0.01.

Techniques Used: Luciferase, Reporter Assay, Quantitative RT-PCR, Western Blot, Inhibition, Knockdown, Activity Assay, CCK-8 Assay, Standard Deviation

Image Search Results

RT-qPCR analysis of CDKN1A ( a, f, k ), KLF5 ( b, g, l ), KLF4 ( c, h, m ), BAX ( d, i, n ), and BCL2 ( e, j, o ) in HCT116, RKO and DLD-1 calculated as a fold change at 6, 24, 48 and 72 h after irradiation. HPRT1 was used as a housekeeping gene (control). RT-qPCR was performed as described in the “Materials and methods” section. Data points represent the average of three independent experiments, with the mean ±SD indicated. Significance was determined by the Student’s test followed by an analysis of the normal distribution (Tukey’s test), *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: bioRxiv

Article Title: Comparison studies between Cesium-137 and X-ray irradiators in epithelial injury using in vitro and in vivo models

doi: 10.64898/2026.04.17.719248

Figure Lengend Snippet: RT-qPCR analysis of CDKN1A ( a, f, k ), KLF5 ( b, g, l ), KLF4 ( c, h, m ), BAX ( d, i, n ), and BCL2 ( e, j, o ) in HCT116, RKO and DLD-1 calculated as a fold change at 6, 24, 48 and 72 h after irradiation. HPRT1 was used as a housekeeping gene (control). RT-qPCR was performed as described in the “Materials and methods” section. Data points represent the average of three independent experiments, with the mean ±SD indicated. Significance was determined by the Student’s test followed by an analysis of the normal distribution (Tukey’s test), *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Commercially available TaqMan primers detecting mouse ChgA (Mm00514341-FAM), Alpi1 (Mm01285814-FAM), Olfm4 (Mm01320260-FAM), Cdkn1a (Mm00432448-FAM), Lgr5 (Mm00438890-FAM), Mki67 (Mm01278617-FAM), Actb (Mm04394036-VIC) and human CDKN1A (Hs00355782-FAM), KLF4 (Hs00358836-FAM), KLF5 (Hs0000000-FAM), BCL2 (Hs01048932-FAM), BAX (Hs00180269-FAM) and HPRT1 (Hs02800695-VIC) transcripts were used.

Techniques: Quantitative RT-PCR, Irradiation, Control

Markers of cell injury (p21, γH2AX, TP53, and phospho-TP53), proliferation (KLF5), and pro-apoptotic (BAX) markers were analyzed using Western blot for HCT116 ( a ), RKO ( b ), and DLD-1( c ) at 6-, 24-, 48-, and 72 h post-irradiation. The figure displays representative images from N = 3 .

Journal: bioRxiv

Article Title: Comparison studies between Cesium-137 and X-ray irradiators in epithelial injury using in vitro and in vivo models

doi: 10.64898/2026.04.17.719248

Figure Lengend Snippet: Markers of cell injury (p21, γH2AX, TP53, and phospho-TP53), proliferation (KLF5), and pro-apoptotic (BAX) markers were analyzed using Western blot for HCT116 ( a ), RKO ( b ), and DLD-1( c ) at 6-, 24-, 48-, and 72 h post-irradiation. The figure displays representative images from N = 3 .

Techniques: Western Blot, Irradiation

RT-qPCR analysis of ( a ) Cdkn1a expression levels after 6Gy, ( b ) Cdkn1a expression levels after 8Gy, ( c ) Mki67 expression levels after 6Gy, ( d ) Mki67 expression levels after 8Gy, ( e ) Lgr5 expression levels after 6Gy, ( f ) Lgr5 expression levels after 8Gy, ( g ) Olfm4 expression levels after 6Gy, ( h ) Olfm4 expression levels after 8Gy, ( i ) Alpi1 expression levels after 6Gy, ( j ) Alpi1 expression levels after 8Gy, ( k ) Chga expression levels after 6Gy, and ( l ) Chga expression levels after 8Gy were calculated as a fold change at 6, 24, 48 and 72 h with either 137 Cs or X-ray irradiation. Actb was used as a housekeeping gene (control). Data points represent the average of three independent experiments, with the mean ±SD indicated. Significance was determined by the student’s test followed by an analysis of the normal distribution (Tukey’s test), *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: bioRxiv

Article Title: Comparison studies between Cesium-137 and X-ray irradiators in epithelial injury using in vitro and in vivo models

doi: 10.64898/2026.04.17.719248

Figure Lengend Snippet: RT-qPCR analysis of ( a ) Cdkn1a expression levels after 6Gy, ( b ) Cdkn1a expression levels after 8Gy, ( c ) Mki67 expression levels after 6Gy, ( d ) Mki67 expression levels after 8Gy, ( e ) Lgr5 expression levels after 6Gy, ( f ) Lgr5 expression levels after 8Gy, ( g ) Olfm4 expression levels after 6Gy, ( h ) Olfm4 expression levels after 8Gy, ( i ) Alpi1 expression levels after 6Gy, ( j ) Alpi1 expression levels after 8Gy, ( k ) Chga expression levels after 6Gy, and ( l ) Chga expression levels after 8Gy were calculated as a fold change at 6, 24, 48 and 72 h with either 137 Cs or X-ray irradiation. Actb was used as a housekeeping gene (control). Data points represent the average of three independent experiments, with the mean ±SD indicated. Significance was determined by the student’s test followed by an analysis of the normal distribution (Tukey’s test), *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Techniques: Quantitative RT-PCR, Expressing, Irradiation, Control

Representative images of immunofluorescence staining for P21, MUSHASHI-1 (MSI1), and nuclei marker (DAPI) in the duodenum of Bmi1-Cre ER mice exposed to 0 or 12 Gy TBI at 6-, 24-, 48-, and 96-h using 137 Cs ( a ), or X-ray irradiator ( b ), or 12Gy X-ray ABD irradiation ( c ). Scale bar = 100 µm.

Journal: bioRxiv

Article Title: Comparison studies between Cesium-137 and X-ray irradiators in epithelial injury using in vitro and in vivo models

doi: 10.64898/2026.04.17.719248

Figure Lengend Snippet: Representative images of immunofluorescence staining for P21, MUSHASHI-1 (MSI1), and nuclei marker (DAPI) in the duodenum of Bmi1-Cre ER mice exposed to 0 or 12 Gy TBI at 6-, 24-, 48-, and 96-h using 137 Cs ( a ), or X-ray irradiator ( b ), or 12Gy X-ray ABD irradiation ( c ). Scale bar = 100 µm.

Techniques: Immunofluorescence, Staining, Marker, Irradiation

a -Transcriptome analyses from P5 hyaloid bulk-RNA sequencing data from R.A. Lang group compared to P5 retina pseudo bulk single-cell RNA sequencing data from S. Blackshaw group. Enrichment analysis was performed on selected mouse gene sets by Gene Set Variation Analysis (GSVA) and coefficient comparison was performed using limma with the difference in GSVA enrichment score (contrast fit coefficient) displayed as bar plot. Blue arrows point senescence-related pathways. b- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) of SASP-related genes ( Tgf-β1, Il1β, Il6, Serpine1 ) comparing between hyaloids and retina at P0, P4 and P8. β-Actin was used as reference gene. Data are presented as fold change compared to retina at each developmental stage (n=3). Bar graphs are means ± SEM. Represented P values are **<0.01, ***<0.001 and **** < 0.0001 from two-tailed parametric unpaired t -test. c - Bar charts of qRT-PCR from SASP-related genes ( Tgf-β1, Il1β, Il6, Serpine1, Vegf-a ) and d- cell cycle arrest markers ( Cdkn1a, Tp53 ) in hyaloids at P0, P4 and P8. Lmnb1 is used as a negative control. β-Actin was used as a reference gene. Data are presented as fold change compared to P0 ( n ≥3-6). Bar graphs are represented as means ± SEM. Represented P values are *<0.05, **<0.01, ***<0.001 and ****<0.0001 from ordinary one-way ANOVA test followed by Dunnett’s multiple comparisons for Tgf-β1, Il1β, Il6, Serpine1, Vegf-a and Cdkn1a and Kruskal-Wallis test followed by Dunn’s multiple comparisons for Tp53 . e - Immunoblots of hyaloid cell lysates from P0, P4 and P8 for senescence markers (P21, TP53, PAI-1). β-ACTIN was used as a loading control (n = 3). f - Representative confocal immunofluorescence staining of P21 (green) and g - PAI-1 (green) of flat-mounted hyaloid vessels at P0, P4 and P8. Blood vessels were stained with IB4 (red). Scale bars, 100 µm. Non-significant (ns).

Journal: bioRxiv

Article Title: Developmental senescence orchestrates hyaloid vessel regression in the postnatal eye

doi: 10.64898/2026.05.12.724389

Figure Lengend Snippet: a -Transcriptome analyses from P5 hyaloid bulk-RNA sequencing data from R.A. Lang group compared to P5 retina pseudo bulk single-cell RNA sequencing data from S. Blackshaw group. Enrichment analysis was performed on selected mouse gene sets by Gene Set Variation Analysis (GSVA) and coefficient comparison was performed using limma with the difference in GSVA enrichment score (contrast fit coefficient) displayed as bar plot. Blue arrows point senescence-related pathways. b- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) of SASP-related genes ( Tgf-β1, Il1β, Il6, Serpine1 ) comparing between hyaloids and retina at P0, P4 and P8. β-Actin was used as reference gene. Data are presented as fold change compared to retina at each developmental stage (n=3). Bar graphs are means ± SEM. Represented P values are **<0.01, ***<0.001 and **** < 0.0001 from two-tailed parametric unpaired t -test. c - Bar charts of qRT-PCR from SASP-related genes ( Tgf-β1, Il1β, Il6, Serpine1, Vegf-a ) and d- cell cycle arrest markers ( Cdkn1a, Tp53 ) in hyaloids at P0, P4 and P8. Lmnb1 is used as a negative control. β-Actin was used as a reference gene. Data are presented as fold change compared to P0 ( n ≥3-6). Bar graphs are represented as means ± SEM. Represented P values are *<0.05, **<0.01, ***<0.001 and ****<0.0001 from ordinary one-way ANOVA test followed by Dunnett’s multiple comparisons for Tgf-β1, Il1β, Il6, Serpine1, Vegf-a and Cdkn1a and Kruskal-Wallis test followed by Dunn’s multiple comparisons for Tp53 . e - Immunoblots of hyaloid cell lysates from P0, P4 and P8 for senescence markers (P21, TP53, PAI-1). β-ACTIN was used as a loading control (n = 3). f - Representative confocal immunofluorescence staining of P21 (green) and g - PAI-1 (green) of flat-mounted hyaloid vessels at P0, P4 and P8. Blood vessels were stained with IB4 (red). Scale bars, 100 µm. Non-significant (ns).

Article Snippet: C57BL/6 wild-type and Cdkn1a (p21) ( Cdkn1a tm1Led /J, no. 016565) knock-out ( Cdkn1a -/- ) [ ] mice lines were obtained from The Jackson Laboratory.

Techniques: RNA Sequencing, Single Cell, Comparison, Reverse Transcription, Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test, Negative Control, Western Blot, Control, Immunofluorescence, Staining

a- Uniform manifold approximation and projection (UMAP) of single-cell RNA sequencing from P4 hyaloid vessels representing the 9 hyaloid cell types identified by graph-based clustering of normalized RNA count. b- Heat map displaying log2 FC of VISION calculated enrichment scores across the 9 hyaloid cell populations for selected senescence- and c - SASP-related gene sets, show enrichment in immune, VSMCs and endothelial cell clusters. d - Dot plot illustrating the expression levels of SenMayo-related genes across the 9 hyaloid cell clusters. e- UMAP feature plot representation of Cdkn1a expression across the 9 hyaloid cell populations. f - Relative mRNA levels of Cdkn1a in P8 hyaloid vessels Cdkn1a +/+ versus Cdkn1a -/- measured by qRT-PCR (n = 3). β-Actin was used as reference gene. g- Representative IB4 and h- SA-β-Gal staining of flat-mounted P8 hyaloid vessels Cdkn1a +/+ (control) and Cdkn1a -/- (lacking Cdkn1a). Higher magnifications of vessels are shown. i - Quantification of total vessel length of P8 flat-mounted hyaloids Cdkn1a +/+ control versus Cdkn1a -/- . Each dot represents a flat-mounted hyaloid sample (n = 8-11). j- Quantification of SA-β-Gal staining per 100 µm of vessels (in percentage) of P8 Cdkn1a +/+ versus Cdkn1a -/- flat-mounted hyaloid. k- Representative IB4 staining of P8 retinal flat-mount Cdkn1a +/+ and Cdkn1a -/- and l - quantification of radial outgrowth of retinal vascular plexus (n = 3), showing delayed expansion of the superficial vascular plexus in Cdkn1a -/- mice. Data are presented as fold change normalized to Cdkn1a +/+ control ( f, j, l ) or as Arbitrary Unit (A.U.) ( i ). Data are represented as means ± SEM ( f, j, l ) or as individual values ( i ). Represented P values are * * < 0.01, *** < 0.001 and **** < 0.0001 from two-tailed parametric unpaired t -test. Scale bars, 500 µm ( g, h ) and 100 µm ( k ) [for higher magnification in g, h ].

Journal: bioRxiv

Article Title: Developmental senescence orchestrates hyaloid vessel regression in the postnatal eye

doi: 10.64898/2026.05.12.724389

Figure Lengend Snippet: a- Uniform manifold approximation and projection (UMAP) of single-cell RNA sequencing from P4 hyaloid vessels representing the 9 hyaloid cell types identified by graph-based clustering of normalized RNA count. b- Heat map displaying log2 FC of VISION calculated enrichment scores across the 9 hyaloid cell populations for selected senescence- and c - SASP-related gene sets, show enrichment in immune, VSMCs and endothelial cell clusters. d - Dot plot illustrating the expression levels of SenMayo-related genes across the 9 hyaloid cell clusters. e- UMAP feature plot representation of Cdkn1a expression across the 9 hyaloid cell populations. f - Relative mRNA levels of Cdkn1a in P8 hyaloid vessels Cdkn1a +/+ versus Cdkn1a -/- measured by qRT-PCR (n = 3). β-Actin was used as reference gene. g- Representative IB4 and h- SA-β-Gal staining of flat-mounted P8 hyaloid vessels Cdkn1a +/+ (control) and Cdkn1a -/- (lacking Cdkn1a). Higher magnifications of vessels are shown. i - Quantification of total vessel length of P8 flat-mounted hyaloids Cdkn1a +/+ control versus Cdkn1a -/- . Each dot represents a flat-mounted hyaloid sample (n = 8-11). j- Quantification of SA-β-Gal staining per 100 µm of vessels (in percentage) of P8 Cdkn1a +/+ versus Cdkn1a -/- flat-mounted hyaloid. k- Representative IB4 staining of P8 retinal flat-mount Cdkn1a +/+ and Cdkn1a -/- and l - quantification of radial outgrowth of retinal vascular plexus (n = 3), showing delayed expansion of the superficial vascular plexus in Cdkn1a -/- mice. Data are presented as fold change normalized to Cdkn1a +/+ control ( f, j, l ) or as Arbitrary Unit (A.U.) ( i ). Data are represented as means ± SEM ( f, j, l ) or as individual values ( i ). Represented P values are * * < 0.01, *** < 0.001 and **** < 0.0001 from two-tailed parametric unpaired t -test. Scale bars, 500 µm ( g, h ) and 100 µm ( k ) [for higher magnification in g, h ].

Article Snippet: C57BL/6 wild-type and Cdkn1a (p21) ( Cdkn1a tm1Led /J, no. 016565) knock-out ( Cdkn1a -/- ) [ ] mice lines were obtained from The Jackson Laboratory.

Techniques: Single Cell, RNA Sequencing, Expressing, Quantitative RT-PCR, Staining, Control, Two Tailed Test

Effects of ENR exposure on intestinal barrier integrity in zebrafish. (A) Experimental design illustrating the exposure protocol. (B, C) Representative immunofluorescence images of Cdkn1a and quantification. (D, E) Representative immunofluorescence images of Cdkn2a and quantification. (F, G) Zebrafish intestinal permeability assessment using Smurf assay ( n = 10). (H) Hematoxylin and eosin staining of zebrafish intestinal tissues. (I) Quantification of goblet cells in zebrafish intestinal tissues. (J, K) Representative Periodic Acid‐Schiff (PAS) staining and quantification of mucus production in zebrafish intestinal tissue. (L–R) Representative immunofluorescence images of intestinal tight junction proteins (Occludin, Mucin‐2, Zo‐1, Claudin) and quantification. (S, T) Representative immunofluorescence images of intestinal CD3‐positive T cells and quantification. Data are presented as the mean ± standard error of the mean. Statistical significance was assessed using Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Aging Cell

Article Title: Environmental Enrofloxacin Exposure as a Modifiable Driver of Mitochondria‐Mediated Intestinal Aging and Barrier Dysfunction

doi: 10.1111/acel.70526

Figure Lengend Snippet: Effects of ENR exposure on intestinal barrier integrity in zebrafish. (A) Experimental design illustrating the exposure protocol. (B, C) Representative immunofluorescence images of Cdkn1a and quantification. (D, E) Representative immunofluorescence images of Cdkn2a and quantification. (F, G) Zebrafish intestinal permeability assessment using Smurf assay ( n = 10). (H) Hematoxylin and eosin staining of zebrafish intestinal tissues. (I) Quantification of goblet cells in zebrafish intestinal tissues. (J, K) Representative Periodic Acid‐Schiff (PAS) staining and quantification of mucus production in zebrafish intestinal tissue. (L–R) Representative immunofluorescence images of intestinal tight junction proteins (Occludin, Mucin‐2, Zo‐1, Claudin) and quantification. (S, T) Representative immunofluorescence images of intestinal CD3‐positive T cells and quantification. Data are presented as the mean ± standard error of the mean. Statistical significance was assessed using Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Intestinal tissues were fixed (4% paraformaldehyde, 15 min), blocked (10% goat serum albumin, 0.4% Triton X‐100), and incubated with primary antibodies from Servicebio: Cdkn1a (GB11153, 1:300), Cdkn2a ( GB151143 , 1:300), Tomm20 ( GB151481 , 1:1000), Grp75 ( GB112273 , 1:650), Cox5a ( GB111676 , 1:500), Hsp60 ( GB112464 , 1:800), Cox4 (GB11250, 1:200), CD3 (GB13014, 1:100), Mucin‐2 (GB11344, 1:500), Occludin ( GB111401 , 1:750), Zo‐1 ( GB115686 , 1:1000), and Claudin‐1 ( GB112543 , 1:1000).

Techniques: Immunofluorescence, Permeability, Staining

Effects of PQQ treatment on ENR‐induced intestinal barrier damage. (A, B) Representative immunofluorescence images of Cdkn1a and quantification. (C, D) Representative immunofluorescence images of Cdkn2a and quantification. (E, F) Periodic Acid–Schiff (PAS) staining of zebrafish intestinal tissues and quantitative analysis. (G, H) Zebrafish intestinal barrier integrity assessed using the Smurf assay. (I–O) Representative immunofluorescence images of intestinal tight junction proteins (Mucin‐2, Occludin, ZO‐1, Claudin) and quantification. (P, Q) Western blot analysis and quantification of intestinal TNF‐α protein levels. Data are presented as the mean ± standard error of the mean. Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Aging Cell

Article Title: Environmental Enrofloxacin Exposure as a Modifiable Driver of Mitochondria‐Mediated Intestinal Aging and Barrier Dysfunction

doi: 10.1111/acel.70526

Figure Lengend Snippet: Effects of PQQ treatment on ENR‐induced intestinal barrier damage. (A, B) Representative immunofluorescence images of Cdkn1a and quantification. (C, D) Representative immunofluorescence images of Cdkn2a and quantification. (E, F) Periodic Acid–Schiff (PAS) staining of zebrafish intestinal tissues and quantitative analysis. (G, H) Zebrafish intestinal barrier integrity assessed using the Smurf assay. (I–O) Representative immunofluorescence images of intestinal tight junction proteins (Mucin‐2, Occludin, ZO‐1, Claudin) and quantification. (P, Q) Western blot analysis and quantification of intestinal TNF‐α protein levels. Data are presented as the mean ± standard error of the mean. Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Immunofluorescence, Staining, Western Blot, Control

CDKN1A is enriched in PGCCs. (A) DEGs were identified using RNA-seq experiments. (B) Volcano plot showing the log 2 FC vs. −log 10 (P value) of differential mRNA expression. (C) KEGG enrichment top 20 were shown. (D) DEGs were used to screen out the top 14 genes with significantly differentially expressed genes, and the (E) Venn diagram analysis intersected with genes involved in signaling pathways such as cell senescence, cell cycle, P53 signaling pathway, and oxidative stress. (F) TCGA analysis of the relationship between CDKN1A and patient survival. (G) Real-time qPCR and Western blot were used to detect the expression level of CDKN1A. DEGs, differentially expressed genes; FC, fold change; KEGG, Kyoto Encyclopedia of Genes and Genomes; PGCC, polyploid giant cancer cell; qPCR, quantitative polymerase chain reaction; TCGA, The Cancer Genome Atlas.

Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: CDKN1A is enriched in PGCCs. (A) DEGs were identified using RNA-seq experiments. (B) Volcano plot showing the log 2 FC vs. −log 10 (P value) of differential mRNA expression. (C) KEGG enrichment top 20 were shown. (D) DEGs were used to screen out the top 14 genes with significantly differentially expressed genes, and the (E) Venn diagram analysis intersected with genes involved in signaling pathways such as cell senescence, cell cycle, P53 signaling pathway, and oxidative stress. (F) TCGA analysis of the relationship between CDKN1A and patient survival. (G) Real-time qPCR and Western blot were used to detect the expression level of CDKN1A. DEGs, differentially expressed genes; FC, fold change; KEGG, Kyoto Encyclopedia of Genes and Genomes; PGCC, polyploid giant cancer cell; qPCR, quantitative polymerase chain reaction; TCGA, The Cancer Genome Atlas.

Article Snippet: The shRNA oligos of CDKN1A gene ( Table S1 ) were designed and synthesized by Sangon Biotech (Shanghai) Co., Ltd. to construct the pLKO.1 shRNA plasmid.

Techniques: RNA Sequencing, Expressing, Protein-Protein interactions, Western Blot, Real-time Polymerase Chain Reaction

CDKN1A mediates the formation of PGCCs induced by paclitaxel. (A,B) Interference efficiency of CDKN1A was detected by qPCR and Western blot in A549 (A) and H1299 (B). (C) The ratios of PGCCs were statistically shown. Each bar represents the mean ± SD of three independent experiments. Student’s t -test was used to determine statistical significance. (D) Western blot was used to detect the expression changes of CDKN1A under different concentrations of UC2288 inhibitor treatment. (E) Quantification of PGCCs number after UC2288 treatment. (F) The morphological changes induced by PTX in lung cancer cell PGCCs and daughter cells at different time points after treatment with UC2288 were observed by phase contrast microscope. (G) The morphological changes induced by PTX in PGCCs and daughter cells of lung cancer cells were observed under laser confocal microscopy after treatment with UC2288 at different time points. Scale bar, 10 μm. (H) Quantification analysis of tumor cell surface area following PTX and UC2288 treatment over time. **, P<0.01; ***, P<0.001. DAPI, 4',6-diamidino-2-phenylindole; PGCC, polyploid giant cancer cell; PTX, paclitaxel; qPCR, quantitative polymerase chain reaction; SD, standard deviation.

Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: CDKN1A mediates the formation of PGCCs induced by paclitaxel. (A,B) Interference efficiency of CDKN1A was detected by qPCR and Western blot in A549 (A) and H1299 (B). (C) The ratios of PGCCs were statistically shown. Each bar represents the mean ± SD of three independent experiments. Student’s t -test was used to determine statistical significance. (D) Western blot was used to detect the expression changes of CDKN1A under different concentrations of UC2288 inhibitor treatment. (E) Quantification of PGCCs number after UC2288 treatment. (F) The morphological changes induced by PTX in lung cancer cell PGCCs and daughter cells at different time points after treatment with UC2288 were observed by phase contrast microscope. (G) The morphological changes induced by PTX in PGCCs and daughter cells of lung cancer cells were observed under laser confocal microscopy after treatment with UC2288 at different time points. Scale bar, 10 μm. (H) Quantification analysis of tumor cell surface area following PTX and UC2288 treatment over time. **, P<0.01; ***, P<0.001. DAPI, 4',6-diamidino-2-phenylindole; PGCC, polyploid giant cancer cell; PTX, paclitaxel; qPCR, quantitative polymerase chain reaction; SD, standard deviation.

Article Snippet: The shRNA oligos of CDKN1A gene ( Table S1 ) were designed and synthesized by Sangon Biotech (Shanghai) Co., Ltd. to construct the pLKO.1 shRNA plasmid.

Techniques: Western Blot, Expressing, Microscopy, Confocal Microscopy, Real-time Polymerase Chain Reaction, Standard Deviation

CDKN1A is associated with AKT, ERK, autophagy, stemness and EMT markers during the formation of PGCCs induced by paclitaxel and neosis. (A-D) Western blot analysis of protein expression in pLKO and CDKN1A-interfered A549 cells. p-AKT and p-ERK (A), LC3 (B), P-STAT3 and PCNA (C), p-histone H2AX and CD133, VIMENTIN (D). (E) Gray value analysis of Western blot. All data represent the mean ± SD of at least three independent experiments. P values were calculated using t -tests. **, P<0.01; ***, P<0.001; ns, not significant. (F) β-gal detection of cells at different time points. PGCC, polyploid giant cancer cell; SD, standard deviation.

Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: CDKN1A is associated with AKT, ERK, autophagy, stemness and EMT markers during the formation of PGCCs induced by paclitaxel and neosis. (A-D) Western blot analysis of protein expression in pLKO and CDKN1A-interfered A549 cells. p-AKT and p-ERK (A), LC3 (B), P-STAT3 and PCNA (C), p-histone H2AX and CD133, VIMENTIN (D). (E) Gray value analysis of Western blot. All data represent the mean ± SD of at least three independent experiments. P values were calculated using t -tests. **, P<0.01; ***, P<0.001; ns, not significant. (F) β-gal detection of cells at different time points. PGCC, polyploid giant cancer cell; SD, standard deviation.

Article Snippet: The shRNA oligos of CDKN1A gene ( Table S1 ) were designed and synthesized by Sangon Biotech (Shanghai) Co., Ltd. to construct the pLKO.1 shRNA plasmid.

Techniques: Western Blot, Expressing, Standard Deviation

CDKN1A mediated tumor formation in mice. (A) The size of tumors formed by inoculating mice (n=5) with tumor cells, PGCCs, daughter cells. (B) Statistical analysis of tumor volumes. All data represent the mean ± SD of at least three independent experiments. A two-way repeated-measures ANOVA followed by Sidak’s test was employed for the statistical analysis of the animal experiment data. *, P<0.05; **, P<0.01. (C) H&E staining of mice tumor tissues. Scale bar, 50 μm. The green arrows indicate PGCCs. (D) Immunohistochemical detection of p-ERK in mice tumor tissues. Scale bar, 50 μm. ANOVA, analysis of variance; H&E, hematoxylin and eosin; PGCC, polyploid giant cancer cell; SD, standard deviation.

Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: CDKN1A mediated tumor formation in mice. (A) The size of tumors formed by inoculating mice (n=5) with tumor cells, PGCCs, daughter cells. (B) Statistical analysis of tumor volumes. All data represent the mean ± SD of at least three independent experiments. A two-way repeated-measures ANOVA followed by Sidak’s test was employed for the statistical analysis of the animal experiment data. *, P<0.05; **, P<0.01. (C) H&E staining of mice tumor tissues. Scale bar, 50 μm. The green arrows indicate PGCCs. (D) Immunohistochemical detection of p-ERK in mice tumor tissues. Scale bar, 50 μm. ANOVA, analysis of variance; H&E, hematoxylin and eosin; PGCC, polyploid giant cancer cell; SD, standard deviation.

Article Snippet: The shRNA oligos of CDKN1A gene ( Table S1 ) were designed and synthesized by Sangon Biotech (Shanghai) Co., Ltd. to construct the pLKO.1 shRNA plasmid.

Techniques: Staining, Immunohistochemical staining, Standard Deviation

Clinical correlation of CDKN1A and PGCCs content. (A) H&E staining of clinical samples from NSCLC patients with low or high levels of PGCC. The black arrows indicate PGCCs. (B) Immunohistochemical detection of CDKN1A expression in human tissues from NSCLC patients with different PGCCs content. Scale bar, 50 μm. H&E, hematoxylin and eosin; NSCLC, non-small cell lung cancer; PGCC, polyploid giant cancer cell.

Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: Clinical correlation of CDKN1A and PGCCs content. (A) H&E staining of clinical samples from NSCLC patients with low or high levels of PGCC. The black arrows indicate PGCCs. (B) Immunohistochemical detection of CDKN1A expression in human tissues from NSCLC patients with different PGCCs content. Scale bar, 50 μm. H&E, hematoxylin and eosin; NSCLC, non-small cell lung cancer; PGCC, polyploid giant cancer cell.

Article Snippet: The shRNA oligos of CDKN1A gene ( Table S1 ) were designed and synthesized by Sangon Biotech (Shanghai) Co., Ltd. to construct the pLKO.1 shRNA plasmid.

Techniques: Staining, Immunohistochemical staining, Expressing

Journal: Open Medicine

Article Title: B cell-derived exosomal miR-34a-5p mediates radiation-induced bystander effect through ferroptosis

doi: 10.1515/med-2026-1375

Figure Lengend Snippet: miR-34a-5p directly targets CDKN1A to promotes ferroptosis of B cells. (A) The interaction between miR-34a-5p and CDKN1A was verified using a dual-luciferase reporter assay. (B, C) CDKN1A mRNA and protein levels were detected by qRT-PCR and western blot in IM-9 cells after miR-34a-5p inhibition. (D, E) qRT-PCR and western blot analysis CDKN1A knockdown efficiency in IM-9 cells. (F–H) The abilities of cell viability, LDH activity, and lipid peroxidation in IM-9 cells treated with miR-34a-5p inhibitor NC, miR-34a-5p inhibitor, or the combination of miR-34a-5p inhibitor and siCDKN1A. All experiments were conducted with n=3, except for the CCK-8 assay, which was conducted with n=6. The data are depicted as the mean ± standard deviation (SD). *, p<0.05; **, p<0.01.

Article Snippet: Following a 1-h blocking step with 5 % non-fat milk, the membranes were incubated with primary antibodies against TSG101 (1:5,000, ab125011, Abcam), ALIX (1:10,000, 12422-1-AP, Proteintech), SLC7A11 (1:2,000, 26864-1-AP, Proteintech), GPX4 (1:1,000, sc-166570, Santa cruz), FTH1 (1:5,000, 11682-1-AP, Proteintech), CDKN1A (1:20,00, 82669-2-RR, Proteintech), and GAPDH (1:15,000, 60004-1-Ig, Proteintech) overnight at 4 °C.

Techniques: Luciferase, Reporter Assay, Quantitative RT-PCR, Western Blot, Inhibition, Knockdown, Activity Assay, CCK-8 Assay, Standard Deviation

(A-D) The analysis of male 19 months WT or Gzmk -/- mice (male). (A) Staining of SA-β-gal in liver and hippocampus. (B) H&E staining in liver, lung and kidney. (C) SA-β-gal staining for WAT from indicated mice. (D) Western blot analysis of the expression of p16, p21 and p53 in liver. (E) The bioluminescence imaging of indicated mice (15 months, female) by injecting luciferase substrates. (F-G) CD8 T cells (4 x10 6 ) from old or old Gzmk -/- mice were adoptively transferred into young p16 Ink4a -luciferase reporter mice, one month later, the luciferase activity was measured (F), and the expression of the p16 -driven luciferase reporter in indicated tissues were measured by RT-qPCR.

Journal: bioRxiv

Article Title: A feed-forward loop between niche adenosine and Gzmk⁺ CD8 T cells propagates systemic inflammaging

doi: 10.64898/2026.03.18.712515

Figure Lengend Snippet: (A-D) The analysis of male 19 months WT or Gzmk -/- mice (male). (A) Staining of SA-β-gal in liver and hippocampus. (B) H&E staining in liver, lung and kidney. (C) SA-β-gal staining for WAT from indicated mice. (D) Western blot analysis of the expression of p16, p21 and p53 in liver. (E) The bioluminescence imaging of indicated mice (15 months, female) by injecting luciferase substrates. (F-G) CD8 T cells (4 x10 6 ) from old or old Gzmk -/- mice were adoptively transferred into young p16 Ink4a -luciferase reporter mice, one month later, the luciferase activity was measured (F), and the expression of the p16 -driven luciferase reporter in indicated tissues were measured by RT-qPCR.

Article Snippet: Primary antibodies used in this study: Mouse anti-CDKN2A/p16 (Santa Cruz Biotechnology, cat# sc-1661, 1:1000) Mouse anti-CDKN1A p21 (Santa Cruz Biotechnology, cat# sc-6246, 1:1000) Mouse anti-p53 (Santa Cruz Biotechnology, cat# sc-98, 1:1000) Mouse anti-GAPDH (Absin, abs830030,1:10000) Rabbit anti-γH2A.X (Cell Signaling Technology, cat# 9718S, 1:1000)

Techniques: Staining, Western Blot, Expressing, Imaging, Luciferase, Activity Assay, Quantitative RT-PCR

(A, B) Primary human bladder fibroblasts were isolated from surgical excision from bladder cancer patients and subjected to GZMK treatment. (A) HBFs were treated with 100nM GZMK for 5 days, and SA-β-gal staining were performed. (B) HBFs were treated with 100nM GZMK in medium without FBS for one day, IL-6 and TNFα in supernatant were measured by ELISA. (C, D) MEFs were isolated and subjected to GZMK treatment as same with . (E-H) BMDMs were subjected to Gzmk or indicated inhibitors treatment. (E) BMDMs were stimulated with Gzmk for 30 minutes and phosphorylated ERK and p38 were determined by flow cytometry. (F) BMDMs were cultured with Gzmk or combined with indicated inhibitors for three days, SA-β-gal staining were performed. BMDMs were cultured with Gzmk or combined with indicated inhibitors for one day, expression of P16 (G) and P21 (H) were analyzed by flow cytometry, IL-6 and TNFα (I) in supernatant were measured by ELISA.

Journal: bioRxiv

Article Title: A feed-forward loop between niche adenosine and Gzmk⁺ CD8 T cells propagates systemic inflammaging

doi: 10.64898/2026.03.18.712515

Figure Lengend Snippet: (A, B) Primary human bladder fibroblasts were isolated from surgical excision from bladder cancer patients and subjected to GZMK treatment. (A) HBFs were treated with 100nM GZMK for 5 days, and SA-β-gal staining were performed. (B) HBFs were treated with 100nM GZMK in medium without FBS for one day, IL-6 and TNFα in supernatant were measured by ELISA. (C, D) MEFs were isolated and subjected to GZMK treatment as same with . (E-H) BMDMs were subjected to Gzmk or indicated inhibitors treatment. (E) BMDMs were stimulated with Gzmk for 30 minutes and phosphorylated ERK and p38 were determined by flow cytometry. (F) BMDMs were cultured with Gzmk or combined with indicated inhibitors for three days, SA-β-gal staining were performed. BMDMs were cultured with Gzmk or combined with indicated inhibitors for one day, expression of P16 (G) and P21 (H) were analyzed by flow cytometry, IL-6 and TNFα (I) in supernatant were measured by ELISA.

Techniques: Isolation, Staining, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Cell Culture, Expressing

Old mice (19 months) were administrated with SCH or PPACK for one-month. The level of IL-6 and TNFα (A), ALT and AST (B) in plasma from indicated mice were determined by ELSIA. (C) Staining of SA-β-gal in liver. (D) H&E staining of lungs from indicated mice. (E) Staining of SA-β-gal in hippocampus from indicated mice. (F-G) Western blot analysis of P16, P21 and P53 at liver and brain from indicated mice.

Journal: bioRxiv

Article Title: A feed-forward loop between niche adenosine and Gzmk⁺ CD8 T cells propagates systemic inflammaging

doi: 10.64898/2026.03.18.712515

Figure Lengend Snippet: Old mice (19 months) were administrated with SCH or PPACK for one-month. The level of IL-6 and TNFα (A), ALT and AST (B) in plasma from indicated mice were determined by ELSIA. (C) Staining of SA-β-gal in liver. (D) H&E staining of lungs from indicated mice. (E) Staining of SA-β-gal in hippocampus from indicated mice. (F-G) Western blot analysis of P16, P21 and P53 at liver and brain from indicated mice.

Techniques: Clinical Proteomics, Staining, Western Blot

Review

Structured Review

Images

1) Product Images from "B cell-derived exosomal miR-34a-5p mediates radiation-induced bystander effect through ferroptosis"

Similar Products

Image Search Results