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Santa Cruz Biotechnology p53

Matrin‐3 silencing alters the proteome in Human Umbilical Vein Endothelial Cells. (A) Schematic depicting the workflow of quantitative proteomics by TMT10 plex labeling followed by mass spectrometry and analysis. (B) Principal component analysis. (C) A volcano plot showing the differentially expressed proteins by quantitative proteomics in HUVECs. (D) Top Hallmark terms and KEGG pathways identified by Enrichr analysis. Gene symbols of the identified proteins were used for analysis. (E) Matrin‐3, <t>p53,</t> p21, and p16 protein expression by Western blot analysis.

P53, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 15836 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p53/p53+Antibody/pmc13675935-183-12-13
Average 96 stars, based on 15836 article reviews

p53 - by Bioz Stars, 2026-11

96/100 stars

Images

1) Product Images from "Endothelial Matrin‐3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis"

Article Title: Endothelial Matrin‐3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis

Journal: The FASEB Journal

doi: 10.1096/fj.202602809RR

Figure Legend Snippet: Matrin‐3 silencing alters the proteome in Human Umbilical Vein Endothelial Cells. (A) Schematic depicting the workflow of quantitative proteomics by TMT10 plex labeling followed by mass spectrometry and analysis. (B) Principal component analysis. (C) A volcano plot showing the differentially expressed proteins by quantitative proteomics in HUVECs. (D) Top Hallmark terms and KEGG pathways identified by Enrichr analysis. Gene symbols of the identified proteins were used for analysis. (E) Matrin‐3, p53, p21, and p16 protein expression by Western blot analysis.

Techniques Used: Quantitative Proteomics, Labeling, Mass Spectrometry, Analysis, Expressing, Western Blot, shRNA, Significance Assay

Matrin‐3 silencing alters the transcriptome in Human Coronary Artery Endothelial Cells. (A) Schematic depicting the workflow. (B) Principal component analysis showing the data variation among samples and a MA plot showing the differentially expressed genes identified by bulk RNA‐seq. (C) Top Hallmark terms and KEGG pathways identified by Enrichr analysis. 3136 differential genes ( p adj < 0.05) were used for analysis. (D) Gene symbols of differential proteins were overlapped with the differentially expressed genes identified by bulk RNA‐seq. Common differential genes were used for Enrichr analysis to identify enriched Hallmark terms and KEGG pathways.

Figure Legend Snippet: Matrin‐3 silencing alters the transcriptome in Human Coronary Artery Endothelial Cells. (A) Schematic depicting the workflow. (B) Principal component analysis showing the data variation among samples and a MA plot showing the differentially expressed genes identified by bulk RNA‐seq. (C) Top Hallmark terms and KEGG pathways identified by Enrichr analysis. 3136 differential genes ( p adj < 0.05) were used for analysis. (D) Gene symbols of differential proteins were overlapped with the differentially expressed genes identified by bulk RNA‐seq. Common differential genes were used for Enrichr analysis to identify enriched Hallmark terms and KEGG pathways.

Techniques Used: Analysis, RNA Sequencing, shRNA, Significance Assay

Western Blot:

Article Title: Loss of human SMC5/6 induces spindle multipolarity and genome stress exacerbated by BLM helicase deficiency
Article Snippet: .. Primary antibodies used for Western blotting or Immunofluorescence in this study include: HA (CST, Cat #3724S, 1:500), β-Actin (Santa Cruz, Cat #sc-69879, 1:2000), phospho-CHK1 (p-CHK1 (S345), CST, Cat #2348, 1:1000), CHK1 (Santa Cruz, Cat #sc-8408, 1:1000), RPA2 (Abcam, Cat #ab2175, 1:500), p53 (Santa Cruz, Cat #sc-126, 1:1000), p21 (Santa Cruz, Cat #sc-397, 1:100), γ-H2AX (Sigma-Aldrich, Cat #ZMS05636, 1:1000), phospho-PLK1 (p-PLK1 (T210), CST, Cat #9062, 1:1000), Vinculin (Sigma-Aldrich, Cat #V9264, 1:4000), Flag (Sigma-Aldrich, Cat #F3165, 1:2000), MUS81 (Santa Cruz, Cat #sc-53382, 1:1000), PrimPol (Proteintech, Cat #29824-1-AP, 1:1000) BLM (Bethyl, Cat #A300-110A, 1:1000), γ‐tubulin (Sigma, Cat #T3320, 1:500), α-tubulin (Sigma, Cat #T5168, 1:1000) and GAPDH (Santa Cruz, Cat #sc-32233, 1:1000). ..

Article Title: Context‐Dependent TP53 Mutation Gain‐of‐Function Is Correlated With Its Contribution to Genomic Instability
Article Snippet: .. Whole‐cell lysates harvested from the cultured cell lines were subjected to Western blot analysis with primary antibodies against p110α (Cell Signaling; 4249), phospho‐AKT S473 (Cell Signaling; 4051), p53 (Santa Cruz Technologies; sc‐126), and β‐actin (Sigma‐Aldrich; A5316) as described previously [ ]. .. Six‐well plates (Corning) were used for 3D cultures.

Immunofluorescence:

Hemagglutination Assay:

Cell-Signaling:

Article Title: Endothelial Matrin‐3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis
Article Snippet: .. The following primary antibodies were used: anti‐Matrin‐3 (Bethyl Laboratories #A300‐591A; 1:1000 dilution), p53 (Santa Cruz Biotechnology, cat# sc‐126×; 1:5000 dilution), p21 (Cell Signaling Technology, cat# 2947S; 1:1000 dilution), p16 (Abcam, cat# ab108349; 1:1000 dilution), and anti‐GAPDH (Cell Signaling Technology, cat# 2118S; 1:10000 dilution). .. Protein bands were visualized using ECL Plus Western Blotting Detection Reagents (GE Healthcare, cat# RPN2236).

Article Title: TP53 mutations orchestrate partial EMT states in oral squamous cell carcinoma: spatially resolved and in vitro preliminary insights into tumour plasticity.
Article Snippet: Images were acquired using the IX83 Inverted Fluorescence Microscope (Evident Corporation, Tokyo, Japan) with three predefined regions of interest (ROIs) per section. .. Multiplex staining was performed using the Cell DIVE platform (Leica Biosystems, Wetzlar, Germany) with directly conjugated antibodies to vimentin-AF555 (D21H3; Cat. No. 9855S; Cell Signaling Technology; dilution 1:250), CD44-AF750 (156-3C11; Cat. No. NBP2-34520AF750; Novus Biologicals, Centennial, CO, USA; dilution 1:100), and PCK-AF488 (AE1/AE3; Cat. No. 53-9,003-82; Invitrogen; dilution 1:100), while p53 (DO-1, Santa Cruz Biotechnology) was conjugated in the lab using the Mix-n-Stain CF647 Antibody Labelling Kit (Cat. No. 92274; Sigma-Aldrich, St. Louis, MO, USA; dilution 1:200) following the manufacturer’s protocols. ..

Article Title: Mitofusin 2 orchestrates mitochondrial metabolic homeostasis and suppresses cutaneous squamous cell carcinoma by stabilizing ER-mitochondria contacts.
Article Snippet: Extended author information available on the last page of the article Abstract This study aimed to elucidate the biological role of Mitofusin 2 (Mfn2) in cutaneous squamous cell carcinoma (cSCC) and evaluate how its regulation of mitochondria-associated membranes (MAMs) may suppress tumor progression by reshaping mitochondrial metabolic homeostasis and apoptosis.. We compared Mfn2 expression between normal keratinocytes (HaCaT) and cSCC cells (A431), establishing a stable Mfn2-overexpressing (Mfn2-OE) A431 model.. Structural impacts on ER-mitochondrial contacts and MAMs were evaluated using immunofluorescence, STED super-resolution microscopy, TEM, and subcellular fractionation (VDAC1/IP3R/Grp75).

Immunohistochemistry:

Article Title: Distinct Rb expression pattern in HPV-associated neuroendocrine carcinomas of the uterine cervix.
Article Snippet: .. IHC was performed with p16 (E6H4, prediluted, CIN Histology Kit; Roche, Heidelberg, Germany), Rb (G3-245, dilution 1/50; BD Pharmingen, Franklin Lakes, NJ, USA), synaptophysin (27G12, dilution 1/50; Leica Biosystems, Newcastle upon Tyne, UK), chromogranin A (LK2H10, dilution 1/ 800; Thermo Fisher Scientific, Waltham, MA, USA), CD56 (CD564, dilution 1/20; Leica Biosystems, Newcastle upon Tyne, UK), insulinoma-associated protein 1 (INSM1) (A-8, dilution 1/3000; Santa Cruz Biotechnology, Dallas, TX, USA), p40 (BC28, ready-to-use; Nichirei Biosciences, Tokyo, Japan), p53 (Pab1801, dilution 1/ 2000; Santa Cruz Biotechnology, Dallas, TX, USA), cyclin D1 (SP4, dilution 1/75; Abcam, Cambridge, UK) using an autostainer (Bond III automated stainer; Leica Biosystems, Melbourne, Australia), following the manufacturer’s protocol. ..

Histology:

Automated:

Multiplex Assay:

Staining:

Translocation Assay:

Membrane:

Cell Culture:

Analysis:

Incubation:

Article Title: Tributyl phosphate induces liver aging via fumarate-mediated mitochondrial DNA escape triggered FPR2 activation.
Article Snippet: .. Membranes were blocked with 5% non-fat milk in PBS-Tween-20 for 2 h, followed by incubation with primary antibodies against HP1 (Santa Cruz, USA), Lamin B1 (Santa Cruz, USA), Di/Tri-Methyl-Histone H3 (Lys9) (Santa Cruz, USA), p53 (Santa Cruz, USA), γ-H2A.X (Santa Cruz, USA), FPR2 (Proteintech, USA) GAPDH (Proteintech, USA), β-actin (Proteintech, USA), and α-tubulin (Proteintech, USA) overnight at 4◦C. .. After three washes with Tris-buffered saline containing Tween 20, membranes were incubated with corresponding secondary antibodies (Proteintech, USA).

Image Search Results

Effects of tRF5‐GlyTCC on tumor growth and response to 5‐FU. (A–B) CCK‐8‐based 5‐FU dose–response assays in HCT116 and DLD1 cells transfected with NC mimic or tRF5‐GlyTCC mimic and treated with increasing concentrations of 5‐FU in the presence or absence of chloroquine (CQ). (C) CCK‐8‐based 5‐FU dose‐response assay in SW1116 cells transfected with NC mimic or tRF5‐GlyTCC mimic. (D–G) Tumor growth curves and tumor weights in HCT116 xenograft models treated with agomir NC + PBS, tRF5‐GlyTCC agomir + PBS, agomir NC + 5‐FU, or tRF5‐GlyTCC agomir + 5‐FU. (H) Representative H&E staining and immunohistochemical staining for Ki‐67, PCNA, p53, and RPL23 in tumor tissue sections from each treatment group. Ki‐67 and PCNA show nuclear localization, with changes consistent with differences in tumor cell proliferation among the treatment groups. (I) RT‐qPCR analysis of tRF5‐GlyTCC abundance in xenograft tumor tissues following agomir treatment. Data are presented as mean ± SD. Statistical significance for the 5‐FU dose–response and CQ experiments was determined using two‐way ANOVA followed by Šídák's multiple‐comparisons test. P < 0.05, * P < 0.01, ** P < 0.001, *** P < 0.0001.

Journal: Advanced Science

Article Title: NSUN3‐Associated m5C Modification of tRF5‐GlyTCC Suppresses Colorectal Cancer Progression via RPL23‐Linked Nucleolar Stress and p53‐Associated Autophagy and Enhances 5‐FU Sensitivity

doi: 10.1002/advs.78345

Figure Lengend Snippet: Effects of tRF5‐GlyTCC on tumor growth and response to 5‐FU. (A–B) CCK‐8‐based 5‐FU dose–response assays in HCT116 and DLD1 cells transfected with NC mimic or tRF5‐GlyTCC mimic and treated with increasing concentrations of 5‐FU in the presence or absence of chloroquine (CQ). (C) CCK‐8‐based 5‐FU dose‐response assay in SW1116 cells transfected with NC mimic or tRF5‐GlyTCC mimic. (D–G) Tumor growth curves and tumor weights in HCT116 xenograft models treated with agomir NC + PBS, tRF5‐GlyTCC agomir + PBS, agomir NC + 5‐FU, or tRF5‐GlyTCC agomir + 5‐FU. (H) Representative H&E staining and immunohistochemical staining for Ki‐67, PCNA, p53, and RPL23 in tumor tissue sections from each treatment group. Ki‐67 and PCNA show nuclear localization, with changes consistent with differences in tumor cell proliferation among the treatment groups. (I) RT‐qPCR analysis of tRF5‐GlyTCC abundance in xenograft tumor tissues following agomir treatment. Data are presented as mean ± SD. Statistical significance for the 5‐FU dose–response and CQ experiments was determined using two‐way ANOVA followed by Šídák's multiple‐comparisons test. P < 0.05, * P < 0.01, ** P < 0.001, *** P < 0.0001.

Article Snippet: Antibodies against GAPDH, RPL23, and p53 were obtained from Proteintech (China).

Techniques: CCK-8 Assay, Transfection, Xenograft Assay, Staining, Immunohistochemical staining, Tissue, Quantitative RT-PCR, Analysis

Identification of RPL23 as a downstream target of tRF5‐GlyTCC. (A–B) Schematic overview of the transcriptomic analysis performed in tRF5‐GlyTCC‐overexpressing cells. (C) Venn diagram showing the overlap of candidate target genes identified by integrated bioinformatic analyses. (D) RT‐qPCR analysis of candidate genes following tRF5‐GlyTCC overexpression. (E) Schematic representation of the wild‐type (WT) and mutant (MUT) RPL23 3′UTR luciferase reporter constructs. (F–G) Dual‐luciferase reporter assays in SW1116 and HEK‐293T cells co‐transfected with tRF5‐GlyTCC mimic and WT or MUT RPL23 3′UTR reporters. (H) Western blotting analysis of RPL23 protein levels following tRF5‐GlyTCC overexpression or inhibition. (I) RPL23 expression levels in CRC tissues and matched adjacent non‐tumor tissues. (J) Pearson correlation analysis of tRF5‐GlyTCC and RPL23 expression in 97 paired CRC tissue samples. (K) Pathway enrichment analysis associated with RPL23 expression. P < 0.05, * P < 0.01, ** P < 0.001, *** P < 0.0001.

Journal: Advanced Science

doi: 10.1002/advs.78345

Figure Lengend Snippet: Identification of RPL23 as a downstream target of tRF5‐GlyTCC. (A–B) Schematic overview of the transcriptomic analysis performed in tRF5‐GlyTCC‐overexpressing cells. (C) Venn diagram showing the overlap of candidate target genes identified by integrated bioinformatic analyses. (D) RT‐qPCR analysis of candidate genes following tRF5‐GlyTCC overexpression. (E) Schematic representation of the wild‐type (WT) and mutant (MUT) RPL23 3′UTR luciferase reporter constructs. (F–G) Dual‐luciferase reporter assays in SW1116 and HEK‐293T cells co‐transfected with tRF5‐GlyTCC mimic and WT or MUT RPL23 3′UTR reporters. (H) Western blotting analysis of RPL23 protein levels following tRF5‐GlyTCC overexpression or inhibition. (I) RPL23 expression levels in CRC tissues and matched adjacent non‐tumor tissues. (J) Pearson correlation analysis of tRF5‐GlyTCC and RPL23 expression in 97 paired CRC tissue samples. (K) Pathway enrichment analysis associated with RPL23 expression. P < 0.05, * P < 0.01, ** P < 0.001, *** P < 0.0001.

Article Snippet: Antibodies against GAPDH, RPL23, and p53 were obtained from Proteintech (China).

Techniques: Analysis, Quantitative RT-PCR, Over Expression, Mutagenesis, Luciferase, Construct, Transfection, Western Blot, Inhibition, Expressing, Tissue, Gene Expression

Regulation of p53 signaling and autophagy‐associated responses by tRF5‐GlyTCC. (A–B) Gene set enrichment analysis (GSEA) showing enrichment of p53 signaling and autophagy‐related pathways in tRF5‐GlyTCC‐overexpressing cells. (C) Western blotting analysis of p53 and autophagy‐associated proteins following modulation of tRF5‐GlyTCC expression. (D) Representative Western blotting analysis of LC3‐II, p62, RPL23, and p53 in DLD1 and HCT116 cells transfected with a negative control (NC) mimic or tRF5‐GlyTCC mimic (tRF5‐M), with or without chloroquine (CQ) treatment. (E) Quantification of LC3‐II and p62 protein levels normalized to GAPDH. Data are presented as mean ± SD from independent experiments. Statistical significance was determined using one‐way ANOVA followed by Šídák's multiple‐comparisons test. (F) Representative transmission electron microscopy images showing autophagosome formation in CRC cells following gain‐ or loss‐of‐function of tRF5‐GlyTCC. (G–H) Western blotting analysis of p53 protein levels following RPL23 silencing. P < 0.05, * P < 0.01, ** P < 0.001.

Journal: Advanced Science

doi: 10.1002/advs.78345

Figure Lengend Snippet: Regulation of p53 signaling and autophagy‐associated responses by tRF5‐GlyTCC. (A–B) Gene set enrichment analysis (GSEA) showing enrichment of p53 signaling and autophagy‐related pathways in tRF5‐GlyTCC‐overexpressing cells. (C) Western blotting analysis of p53 and autophagy‐associated proteins following modulation of tRF5‐GlyTCC expression. (D) Representative Western blotting analysis of LC3‐II, p62, RPL23, and p53 in DLD1 and HCT116 cells transfected with a negative control (NC) mimic or tRF5‐GlyTCC mimic (tRF5‐M), with or without chloroquine (CQ) treatment. (E) Quantification of LC3‐II and p62 protein levels normalized to GAPDH. Data are presented as mean ± SD from independent experiments. Statistical significance was determined using one‐way ANOVA followed by Šídák's multiple‐comparisons test. (F) Representative transmission electron microscopy images showing autophagosome formation in CRC cells following gain‐ or loss‐of‐function of tRF5‐GlyTCC. (G–H) Western blotting analysis of p53 protein levels following RPL23 silencing. P < 0.05, * P < 0.01, ** P < 0.001.

Article Snippet: Antibodies against GAPDH, RPL23, and p53 were obtained from Proteintech (China).

Techniques: Analysis, Western Blot, Expressing, Transfection, Negative Control, Transmission Assay, Electron Microscopy

Further mechanistic insights into RPL23‐associated nucleolar stress and p53 signaling in CRC cells. (A)Immunofluorescence analysis of nucleophosmin (NPM1) in DLD1 and HCT116 cells transfected with NC, tRF5‐GlyTCC inhibitor, siRPL23, or siRPL23 + tRF5‐GlyTCC inhibitor. Scale bars: 10 µm. (B) Western blotting analysis of RPL23 and p53 in DLD1 and HCT116 cells following the indicated genetic manipulations. (C) SUnSET assay assessing global protein synthesis in DLD1 cells transfected with tRF5‐GlyTCC mimic or NC mimic. Puromycin incorporation indicates nascent protein synthesis. (D) Representative images of p53‐GFP reporter fluorescence in DLD1 cells following tRF5‐GlyTCC overexpression. (E–F) Quantification of puromycin incorporation (E) and p53‐GFP fluorescence intensity (F). (G–H) Western blotting analysis of RPL23, p53, LC3II, and p62/SQSTM1 expression in HCT116 cells following tRF5‐GlyTCC overexpression (G) or RPL23 knockdown (H). (I) Quantification of RPL23 and p53 protein levels shown in (B). Data are presented as mean ± SEM. ns, not significant; P < 0.05, * P < 0.01, ** P < 0.001.

Journal: Advanced Science

doi: 10.1002/advs.78345

Figure Lengend Snippet: Further mechanistic insights into RPL23‐associated nucleolar stress and p53 signaling in CRC cells. (A)Immunofluorescence analysis of nucleophosmin (NPM1) in DLD1 and HCT116 cells transfected with NC, tRF5‐GlyTCC inhibitor, siRPL23, or siRPL23 + tRF5‐GlyTCC inhibitor. Scale bars: 10 µm. (B) Western blotting analysis of RPL23 and p53 in DLD1 and HCT116 cells following the indicated genetic manipulations. (C) SUnSET assay assessing global protein synthesis in DLD1 cells transfected with tRF5‐GlyTCC mimic or NC mimic. Puromycin incorporation indicates nascent protein synthesis. (D) Representative images of p53‐GFP reporter fluorescence in DLD1 cells following tRF5‐GlyTCC overexpression. (E–F) Quantification of puromycin incorporation (E) and p53‐GFP fluorescence intensity (F). (G–H) Western blotting analysis of RPL23, p53, LC3II, and p62/SQSTM1 expression in HCT116 cells following tRF5‐GlyTCC overexpression (G) or RPL23 knockdown (H). (I) Quantification of RPL23 and p53 protein levels shown in (B). Data are presented as mean ± SEM. ns, not significant; P < 0.05, * P < 0.01, ** P < 0.001.

Article Snippet: Antibodies against GAPDH, RPL23, and p53 were obtained from Proteintech (China).

Techniques: Immunofluorescence, Analysis, Transfection, Western Blot, Fluorescence, Over Expression, Expressing, Knockdown

NSUN3‐associated m5C modification contributes to the stability of tRF5‐GlyTCC. (A–B) Prediction and MeRIP‐qPCR validation of m5C modification in the annotated precursor tRNA‐Gly‐TCC region encompassing the predicted C66 site. (C–D) NSUN3 expression in CRC tissues ( n = 97) and CRC cell lines. (E) Knockdown efficiency of NSUN3 siRNA in CRC cells. (F) Effects of NSUN3 silencing on tRF5‐GlyTCC expression. (G) Effects of NSUN3 silencing on the abundance of the annotated precursor tRNA‐Gly‐TCC. (H) MeRIP‐qPCR analysis of m5C enrichment in the precursor tRNA‐Gly‐TCC region encompassing C66 following NSUN3 knockdown. (I) Pearson correlation analysis between NSUN3 and tRF5‐GlyTCC expression in 97 paired CRC tissue samples ( n = 97). (J–K) Actinomycin D chase assays showing tRF5‐GlyTCC decay in DLD1 and HCT116 cells following NSUN3 knockdown. tRF5‐GlyTCC levels were measured by RT‐qPCR at 0, 2, 4, and 8 h after Actinomycin D treatment and normalized to the corresponding 0 h level. Decay curves were fitted by nonlinear regression, and statistical significance was determined using two‐way ANOVA followed by Šídák's multiple‐comparisons test. (L–M) Kaplan–Meier survival analysis of the prognostic relevance of NSUN3 stratified by TP53 mutation status using the Kaplan–Meier Plotter platform. (L) TP53‐mutant; (M) TP53‐wild‐type. (N) Western blotting analysis showing that NSUN3 knockdown increases RPL23 expression and is accompanied by decreased p53 and LC3II levels and increased p62/SQSTM1 levels. (O) Gene set enrichment analysis (GSEA) showing positive associations between NSUN3 expression and p53‐related signaling pathways. P < 0.05, * P < 0.01, ** P < 0.001, *** P < 0.0001.

Journal: Advanced Science

doi: 10.1002/advs.78345

Figure Lengend Snippet: NSUN3‐associated m5C modification contributes to the stability of tRF5‐GlyTCC. (A–B) Prediction and MeRIP‐qPCR validation of m5C modification in the annotated precursor tRNA‐Gly‐TCC region encompassing the predicted C66 site. (C–D) NSUN3 expression in CRC tissues ( n = 97) and CRC cell lines. (E) Knockdown efficiency of NSUN3 siRNA in CRC cells. (F) Effects of NSUN3 silencing on tRF5‐GlyTCC expression. (G) Effects of NSUN3 silencing on the abundance of the annotated precursor tRNA‐Gly‐TCC. (H) MeRIP‐qPCR analysis of m5C enrichment in the precursor tRNA‐Gly‐TCC region encompassing C66 following NSUN3 knockdown. (I) Pearson correlation analysis between NSUN3 and tRF5‐GlyTCC expression in 97 paired CRC tissue samples ( n = 97). (J–K) Actinomycin D chase assays showing tRF5‐GlyTCC decay in DLD1 and HCT116 cells following NSUN3 knockdown. tRF5‐GlyTCC levels were measured by RT‐qPCR at 0, 2, 4, and 8 h after Actinomycin D treatment and normalized to the corresponding 0 h level. Decay curves were fitted by nonlinear regression, and statistical significance was determined using two‐way ANOVA followed by Šídák's multiple‐comparisons test. (L–M) Kaplan–Meier survival analysis of the prognostic relevance of NSUN3 stratified by TP53 mutation status using the Kaplan–Meier Plotter platform. (L) TP53‐mutant; (M) TP53‐wild‐type. (N) Western blotting analysis showing that NSUN3 knockdown increases RPL23 expression and is accompanied by decreased p53 and LC3II levels and increased p62/SQSTM1 levels. (O) Gene set enrichment analysis (GSEA) showing positive associations between NSUN3 expression and p53‐related signaling pathways. P < 0.05, * P < 0.01, ** P < 0.001, *** P < 0.0001.

Article Snippet: Antibodies against GAPDH, RPL23, and p53 were obtained from Proteintech (China).

Techniques: Modification, Stability, Biomarker Discovery, Expressing, Knockdown, Analysis, Tissue, Quantitative RT-PCR, Mutagenesis, Western Blot, Protein-Protein interactions, Gene Expression

Proposed working model of NSUN3‐associated regulation of tRF5‐GlyTCC in colorectal cancer. The proposed model summarizes the relationships supported by the present study. NSUN3‐associated m5C modification in the annotated precursor tRNA‐Gly‐TCC region, encompassing C66, is associated with maintenance of tRF5‐GlyTCC stability. Increased tRF5‐GlyTCC expression is associated with reduced RPL23 expression, which is accompanied by NPM1 redistribution and a nucleolar stress phenotype, together with increased p53 signaling and autophagy‐associated responses. These changes are associated with tumor‐suppressive effects and enhanced sensitivity to 5‐fluorouracil (5‐FU). The model is intended to represent the experimentally supported relationships and does not imply a strictly linear causal pathway.

Journal: Advanced Science

doi: 10.1002/advs.78345

Figure Lengend Snippet: Proposed working model of NSUN3‐associated regulation of tRF5‐GlyTCC in colorectal cancer. The proposed model summarizes the relationships supported by the present study. NSUN3‐associated m5C modification in the annotated precursor tRNA‐Gly‐TCC region, encompassing C66, is associated with maintenance of tRF5‐GlyTCC stability. Increased tRF5‐GlyTCC expression is associated with reduced RPL23 expression, which is accompanied by NPM1 redistribution and a nucleolar stress phenotype, together with increased p53 signaling and autophagy‐associated responses. These changes are associated with tumor‐suppressive effects and enhanced sensitivity to 5‐fluorouracil (5‐FU). The model is intended to represent the experimentally supported relationships and does not imply a strictly linear causal pathway.

Article Snippet: Antibodies against GAPDH, RPL23, and p53 were obtained from Proteintech (China).

Techniques: Modification, Stability, Expressing, Sensitivity

Journal: The FASEB Journal

Article Title: Endothelial Matrin‐3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis

doi: 10.1096/fj.202602809RR

Figure Lengend Snippet: Matrin‐3 silencing alters the proteome in Human Umbilical Vein Endothelial Cells. (A) Schematic depicting the workflow of quantitative proteomics by TMT10 plex labeling followed by mass spectrometry and analysis. (B) Principal component analysis. (C) A volcano plot showing the differentially expressed proteins by quantitative proteomics in HUVECs. (D) Top Hallmark terms and KEGG pathways identified by Enrichr analysis. Gene symbols of the identified proteins were used for analysis. (E) Matrin‐3, p53, p21, and p16 protein expression by Western blot analysis.

Article Snippet: The following primary antibodies were used: anti‐Matrin‐3 (Bethyl Laboratories #A300‐591A; 1:1000 dilution), p53 (Santa Cruz Biotechnology, cat# sc‐126×; 1:5000 dilution), p21 (Cell Signaling Technology, cat# 2947S; 1:1000 dilution), p16 (Abcam, cat# ab108349; 1:1000 dilution), and anti‐GAPDH (Cell Signaling Technology, cat# 2118S; 1:10000 dilution).

Techniques: Quantitative Proteomics, Labeling, Mass Spectrometry, Analysis, Expressing, Western Blot, shRNA, Significance Assay

Journal: The FASEB Journal

Article Title: Endothelial Matrin‐3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis

doi: 10.1096/fj.202602809RR

Figure Lengend Snippet: Matrin‐3 silencing alters the transcriptome in Human Coronary Artery Endothelial Cells. (A) Schematic depicting the workflow. (B) Principal component analysis showing the data variation among samples and a MA plot showing the differentially expressed genes identified by bulk RNA‐seq. (C) Top Hallmark terms and KEGG pathways identified by Enrichr analysis. 3136 differential genes ( p adj < 0.05) were used for analysis. (D) Gene symbols of differential proteins were overlapped with the differentially expressed genes identified by bulk RNA‐seq. Common differential genes were used for Enrichr analysis to identify enriched Hallmark terms and KEGG pathways.

Techniques: Analysis, RNA Sequencing, shRNA, Significance Assay

Dynamic changes in p53/p63 and regulators, ASPP2 and iASPP in 13del-MCDS mice hypertrophic chondrocytes. a Immunohistochemistry staining of p53 on the 10-day-old proximal tibia growth plate. Specific regions of the hypertrophic zone (HZ) in +/+ and M/M mice are shown in higher magnification, illustrating very low staining in +/+ in regions 1, 2, and 3. Whereas in M/M mice, there are varying low (L1, L2, and L3) and high (H1, H2, and H3) p53-expressing regions. b Co-immunofluorescence staining of p53 and DAPI showing p53 in +/+ HCs is cytoplasmic, whereas in M/M mice, p53 is primarily localized to the nucleus (yellow arrowheads). c Immunohistochemistry staining of Tap63 showed an upregulation in M/M HCs (black arrowheads). d Immunohistochemistry staining of ΔNp63 showed a downregulation in M/M HCs. e Immunofluorescence staining of ASPP2 and f iASPP proteins on 10-day-old proximal tibia growth plates, showing a differential and dynamic down- and up-regulation in HCs of M/M mice, respectively. Scale bar = 50 μm

Journal: Bone Research

Article Title: Integrated stress signaling pathways promote adaptive reprogramming for chondrocyte survival in Metaphyseal Chondrodysplasia Type Schmid

doi: 10.1038/s41413-026-00587-5

Figure Lengend Snippet: Dynamic changes in p53/p63 and regulators, ASPP2 and iASPP in 13del-MCDS mice hypertrophic chondrocytes. a Immunohistochemistry staining of p53 on the 10-day-old proximal tibia growth plate. Specific regions of the hypertrophic zone (HZ) in +/+ and M/M mice are shown in higher magnification, illustrating very low staining in +/+ in regions 1, 2, and 3. Whereas in M/M mice, there are varying low (L1, L2, and L3) and high (H1, H2, and H3) p53-expressing regions. b Co-immunofluorescence staining of p53 and DAPI showing p53 in +/+ HCs is cytoplasmic, whereas in M/M mice, p53 is primarily localized to the nucleus (yellow arrowheads). c Immunohistochemistry staining of Tap63 showed an upregulation in M/M HCs (black arrowheads). d Immunohistochemistry staining of ΔNp63 showed a downregulation in M/M HCs. e Immunofluorescence staining of ASPP2 and f iASPP proteins on 10-day-old proximal tibia growth plates, showing a differential and dynamic down- and up-regulation in HCs of M/M mice, respectively. Scale bar = 50 μm

Article Snippet: It was subsequently probed with an appropriately diluted primary antibody overnight at 4 o C. The next step was incubation with a horseradish peroxidase-conjugated secondary antibody (which recognized the primary antibody) for 30 min. Immunohistochemistry and immunofluorescence staining were performed using antibodies specific for Collagen X and 13del mutant Collagen X (Generated by our lab ), Cyclin D1 (Santa Cruz, Cat#sc-753), Xbp1s (BioLegend, Cat# 647502), CD31 (Abcam, Cat# ab28364), HIF1a (SANTA CRUZ BIOTECH, Cat# sc-10790), HIF2a (SANTA CRUZ BIOTECH, Cat# sc-28706), p53 (E-19) (SANTA CRUZ BIOTECH, Cat# sc-1315), Tap63 (NOVUS BIOLOGICALS, Cat# NBP3-11703), ΔNp63 (BioLegend, Cat# 619001), EDEM (Provided by Kumamoto University, Japan), iASPP (Sigma, Cat# A4605), ASPP2 (Provided by Dr. Xin Lu from University of Oxford), ATF4 (SANTA CRUZ BIOTECH, Cat# sc-200), p57Kip2 (SANTA CRUZ BIOTECH, Cat# sc-56341), EF5-Cy3 regular stain antibody and EF5-competed stain antibody (Provided by Dr. Cameron Koch from University of Pennsylvania Department of Radiation Oncology), Map-LC3B (MBL life science, Cat# PM036), CHOP (SANTA CRUZ BIOTECH, Cat# sc-166682), GADD34 (SANTA CRUZ BIOTECH, Cat# sc-794), ATF3 (SANTA CRUZ BIOTECH, Cat# sc-81189), 488 Goat Anti-Rabbit IgG (Life technologies, Cat# A-11008) were used.

Techniques: Immunohistochemistry, Staining, Expressing, Immunofluorescence

Protein clearance is correlated with the hypertrophic chondrocyte differentiation status. a Immunohistochemistry staining of Collagen type X on paraffin sections of the tibia proximal growth plate from 4-week-old M/M mice. Scale bar = 50 μm. b Immunohistochemistry staining of p53 on paraffin sections of the tibia proximal growth plate from 4-week-old M/M mice. Scale bar = 50 μm. c Immunohistochemistry staining of Edem on paraffin sections of the tibia proximal growth plate from P10 M/M mice. d Immunofluorescence staining of Map1-lc3b on paraffin sections of the tibia proximal growth plate from 4-week-old M/M mice and their littermate controls. Boxed regions are the amplified dotted area. e Chloroquine was administered to M/M mice to monitor the dynamics of autophagy activity by blocking the fusion of autophagosomes with lysosomes. Immunofluorescence staining and quantification of LC3 puncta cells demonstrated an increase in LC3 puncta-positive cells in the UHZ and LHZ of MCDS mice after the chloroquine administration. UHZ (1, 1’): the upper hypertrophic zone; MHZ (2, 2’): the middle hypertrophic zone; LHZ (3, 3’): the lower hypertrophic zone

Journal: Bone Research

Article Title: Integrated stress signaling pathways promote adaptive reprogramming for chondrocyte survival in Metaphyseal Chondrodysplasia Type Schmid

doi: 10.1038/s41413-026-00587-5

Figure Lengend Snippet: Protein clearance is correlated with the hypertrophic chondrocyte differentiation status. a Immunohistochemistry staining of Collagen type X on paraffin sections of the tibia proximal growth plate from 4-week-old M/M mice. Scale bar = 50 μm. b Immunohistochemistry staining of p53 on paraffin sections of the tibia proximal growth plate from 4-week-old M/M mice. Scale bar = 50 μm. c Immunohistochemistry staining of Edem on paraffin sections of the tibia proximal growth plate from P10 M/M mice. d Immunofluorescence staining of Map1-lc3b on paraffin sections of the tibia proximal growth plate from 4-week-old M/M mice and their littermate controls. Boxed regions are the amplified dotted area. e Chloroquine was administered to M/M mice to monitor the dynamics of autophagy activity by blocking the fusion of autophagosomes with lysosomes. Immunofluorescence staining and quantification of LC3 puncta cells demonstrated an increase in LC3 puncta-positive cells in the UHZ and LHZ of MCDS mice after the chloroquine administration. UHZ (1, 1’): the upper hypertrophic zone; MHZ (2, 2’): the middle hypertrophic zone; LHZ (3, 3’): the lower hypertrophic zone

Techniques: Immunohistochemistry, Staining, Immunofluorescence, Amplification, Activity Assay, Blocking Assay

Proposed mechanism linking ER stress to integrated survival signaling in 13del-MCDS hypertrophic chondrocytes. A 13-bp deletion in Col10a1 leads to production of misfolded collagen X and its accumulation within the endoplasmic reticulum (ER) of HCs, triggering ER stress. ER stress activates ATF4 and hypoxia/HIF signaling as an intrinsic adaptive response. In parallel, p53 signaling and autophagy are engaged. Autophagy facilitates the clearance of accumulated misfolded proteins, thereby reducing proteotoxic stress. Collectively, HIF, ATF4, p53, and autophagy form an integrated survival network that promotes HC survival, supports metabolic adaptation, and enables cell-cycle re-entry. This coordinated response enables partial adaptation to ER stress and contributes to the growth plate phenotype observed in 13del-MCDS mice

Journal: Bone Research

Article Title: Integrated stress signaling pathways promote adaptive reprogramming for chondrocyte survival in Metaphyseal Chondrodysplasia Type Schmid

doi: 10.1038/s41413-026-00587-5

Figure Lengend Snippet: Proposed mechanism linking ER stress to integrated survival signaling in 13del-MCDS hypertrophic chondrocytes. A 13-bp deletion in Col10a1 leads to production of misfolded collagen X and its accumulation within the endoplasmic reticulum (ER) of HCs, triggering ER stress. ER stress activates ATF4 and hypoxia/HIF signaling as an intrinsic adaptive response. In parallel, p53 signaling and autophagy are engaged. Autophagy facilitates the clearance of accumulated misfolded proteins, thereby reducing proteotoxic stress. Collectively, HIF, ATF4, p53, and autophagy form an integrated survival network that promotes HC survival, supports metabolic adaptation, and enables cell-cycle re-entry. This coordinated response enables partial adaptation to ER stress and contributes to the growth plate phenotype observed in 13del-MCDS mice

Techniques:

Review

p53 (Santa Cruz Biotechnology)

Structured Review

Images

1) Product Images from "Endothelial Matrin‐3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis"

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