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Novus Biologicals anti tap73
Anti Tap73, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 85/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+p73/p73+Antibody+(5B1288)+-+Azide+Free/pmc12866144-474-11-12
Average 85 stars, based on 3 article reviews

anti tap73 - by Bioz Stars, 2026-10

85/100 stars

Images

Immunoprecipitation:

Article Title: TAp73 opposes tumor angiogenesis by promoting hypoxia-inducible factor 1α degradation
Article Snippet: Tubular structures were examined using a phase contrast microscope (Axiovert 200M, Zeiss) and photographed. .. Immunoprecipitation of endogenous or overexpressed proteins have been performed by incubating overnight (ON) at 4 °C with anti-p73 (Imgenex) and then 1 h at 4 °C with Protein G-Agarose (Roche) or ON at 4 °C with Ez view Red anti-HA affinity gel (E6779, Sigma) or Myc-Tag Sepharose beads (3400S, Cell Signaling). ..

Staining:

Article Title: Ubiquitin-dependent Degradation of p73 Is Inhibited by PML
Article Snippet: MEFs were transiently transfected with an expression vector for human GFP-p73α in the absence or in the presence of full-length PML or PML-RARα for 24 h. Cells were washed and fixed in 4% paraformaldehyde solution for 10 min at room temperature and permeabilized with 0.1% Triton X-100. .. For p73 and PML staining, cells were incubated with anti-p73 (clone 5B429; Imgenex) and a rabbit polyclonal anti-PML antibody in PBS and 10% goat serum. ..

Incubation:

other:

Article Title: 1,25D 3 potentiates cisplatin antitumor activity by p73 induction in a squamous cell carcinoma model
Article Snippet: Anti-p73 (IMG-246, clone 5B429) was from Imgenex (San Diago, CA).

Article Title: 1,25D 3 enhances antitumor activity of gemcitabine and cisplatin in human bladder cancer models
Article Snippet: Anti-p73 (IMG-246, clone 5B429) was from Imgenex (San Diago, CA).

Image Search Results

(A,B) RNA-Seq data retrieved from Protein Atlas were stratified by FDXR expression (≥75 nTPM = Mid-high_FDXR, <75 nTPM = Mid-low_FDXR). Differential transcription factor (TF) activity between groups was inferred using VIPER , based on regulatory networks constructed with DoRothEA and ARACNe. The bubble plot in (B) ranks TFs based on their differential activity in the two groups. The colour of the dots reflects relative TF activity, while the size of the dots represent -Log10 adjusted p values (FDR) calculated with the limma package. (C–F) Expression of TAp63 mRNA (C), p63α protein (D), TAp73 mRNA (E) and p73 protein (F) in HTLV-1 + , ATL, and uninfected cell lines and primary cells. Relative mRNA expression was quantified by qPCR; protein expression was assessed by western blot. In panels (C,E), each dot represents an independent qPCR assay (n = 3), and data are presented as mean ± SD. Relative mRNA levels were calculated by ΔΔCq using TBP expression as reference. Data were analyzed by non-parametric Wilcoxon rank-sum test. (G,H) Relative expression of TAp63 (G) and TAp73 (H) mRNA in primary CD4 T cells from PLHTLV stratified by disease condition and healthy controls. Relative mRNA expression was quantified by qPCR using the ΔΔCq method and TBP expression as reference. Each dot represents a donor and data are depicted as median ± IQR. Data were analyzed by non-parametric Kruskal–Wallis test followed by Dunn’s post hoc test with Benjamini–Hochberg correction for multiple comparisons. (I,N) Effect of TP63 and TP73 knockout on FDXR expression. The HTLV-1–infected MT-4 cell line (I-K) and the ATL-derived ATL-55T cell line (L-N) were stably transfected with Cas9 and subsequently transduced with lentiviruses expressing either a non-targeting (NT) sgRNA or sgRNAs targeting TP63 or TP73. Stable knockout cell lines were lysed and used to assess protein expression by Western blot. Panels I, L show p63 and FDXR expression in MT-4 and ATL-55T cells, respectively. Panels J, M show p73 and FDXR expression in MT-4 and ATL-55T cells, respectively. Wild-type and non-transduced Cas9-expressing cells served as additional controls. Panels K, N show relative FDXR protein levels normalized using actin as a loading control and the NT sgRNA condition as reference level. Barplots in K, N show mean ± SD for each condition. N = 2. **** p <0.0001; ** p <0.01; *p <0.05.

Journal: bioRxiv

Article Title: FDXR Upregulation by p63/p73 is a Prognostic and Therapeutic Marker of HTLV-1-Associated Adult T Cell Leukemia/Lymphoma

doi: 10.64898/2026.02.25.707207

Figure Lengend Snippet: (A,B) RNA-Seq data retrieved from Protein Atlas were stratified by FDXR expression (≥75 nTPM = Mid-high_FDXR, <75 nTPM = Mid-low_FDXR). Differential transcription factor (TF) activity between groups was inferred using VIPER , based on regulatory networks constructed with DoRothEA and ARACNe. The bubble plot in (B) ranks TFs based on their differential activity in the two groups. The colour of the dots reflects relative TF activity, while the size of the dots represent -Log10 adjusted p values (FDR) calculated with the limma package. (C–F) Expression of TAp63 mRNA (C), p63α protein (D), TAp73 mRNA (E) and p73 protein (F) in HTLV-1 + , ATL, and uninfected cell lines and primary cells. Relative mRNA expression was quantified by qPCR; protein expression was assessed by western blot. In panels (C,E), each dot represents an independent qPCR assay (n = 3), and data are presented as mean ± SD. Relative mRNA levels were calculated by ΔΔCq using TBP expression as reference. Data were analyzed by non-parametric Wilcoxon rank-sum test. (G,H) Relative expression of TAp63 (G) and TAp73 (H) mRNA in primary CD4 T cells from PLHTLV stratified by disease condition and healthy controls. Relative mRNA expression was quantified by qPCR using the ΔΔCq method and TBP expression as reference. Each dot represents a donor and data are depicted as median ± IQR. Data were analyzed by non-parametric Kruskal–Wallis test followed by Dunn’s post hoc test with Benjamini–Hochberg correction for multiple comparisons. (I,N) Effect of TP63 and TP73 knockout on FDXR expression. The HTLV-1–infected MT-4 cell line (I-K) and the ATL-derived ATL-55T cell line (L-N) were stably transfected with Cas9 and subsequently transduced with lentiviruses expressing either a non-targeting (NT) sgRNA or sgRNAs targeting TP63 or TP73. Stable knockout cell lines were lysed and used to assess protein expression by Western blot. Panels I, L show p63 and FDXR expression in MT-4 and ATL-55T cells, respectively. Panels J, M show p73 and FDXR expression in MT-4 and ATL-55T cells, respectively. Wild-type and non-transduced Cas9-expressing cells served as additional controls. Panels K, N show relative FDXR protein levels normalized using actin as a loading control and the NT sgRNA condition as reference level. Barplots in K, N show mean ± SD for each condition. N = 2. **** p <0.0001; ** p <0.01; *p <0.05.

Article Snippet: The primary antibodies used included anti-FDXR (1:1000, Rabbit, Proteintech #15584-1-AP), anti-p53 (Rabbit, Cell Signaling #2527), anti-p63α (1:1000, Rabbit, Cell Signaling #13109), anti-p73 (1:1000, Rabbit, Cell Signalling #14620), anti-S. pyogenes-Cas9 (1:1000, Mouse, Cell Signalling #14697) anti-VDAC (1:500, Rabbit, Invitrogen #MA5-33205), anti-Tax (1:250, Mouse, Merck #MABF3063), anti-HTLV-1-p24 (1:250, Mouse, Santa-Cruz #sc-53891), anti-HTLV-1-gp46 (1:250, Mouse #sc-53890), anti-alpha Tubulin (1:15000, Rabbit, GeneTex #GTX112141), anti-beta Actin (1:15000, Mouse, Cell Signaling #3700).

Techniques: RNA Sequencing, Expressing, Activity Assay, Construct, Western Blot, Knock-Out, Infection, Derivative Assay, Stable Transfection, Transfection, Transduction, Control

(A) Ai9 is seen in the cortical hem and its derivatives in an E12.5 control and Lmx1aCre; β-Catenin GOF brain. (B) Reelin staining in the same section as (A). (C) TRP73 staining at E14.5 co-localizes with Ai9 in the control but is undetectable in the β-Catenin GOF brain. (D) Genes enriched in CR cells are downregulated in midline tissue β-Catenin GOF brains at E14.5. (E, F) Reelin, βIII-Tubulin and NEUN staining is seen in Ai9+ cells in control brains (arrowheads). In β-catenin GOF brains there is no detectable Reelin (open arrowheads) (E) but βIII-TUBULIN and NEUN staining is seen in Ai9+ cells. (G, J) UMAPs representing tdTomato+ cells from E14.5 control and β-catenin GOF midline, color-coded by cell type (G); by age (H); by genotype (I); showing the expression of Wnt3a, Reln and tdTomato (J). (H) Heatmap of scaled expression of top 10 differentially expressed genes in control and β-Catenin GOF neurons. (I) Dot plots showing scaled expression levels of CR cell enriched genes in control and β-Catenin GOF neurons. Scatterplot in (D) displays Mean ± SEM. Statistical test(D): Multiple Mann-Whitney Tests; p < 0.0001; *p < 0.05; **p < 0.01; ***p < 0.001; ns if p value > 0.05. For (A-C, E-F), N ≥ 3 brains (biologically independent replicates); for (D) N=6 (control), 7 (GOF) biologically independent replicates. Scale bars: 100 μm (all images in A, B, C, E and F).

Journal: bioRxiv

Article Title: Cajal-Retzius fate specification is disrupted by constitutive activation of β-Catenin in hem progenitors

doi: 10.64898/2026.02.09.704731

Figure Lengend Snippet: (A) Ai9 is seen in the cortical hem and its derivatives in an E12.5 control and Lmx1aCre; β-Catenin GOF brain. (B) Reelin staining in the same section as (A). (C) TRP73 staining at E14.5 co-localizes with Ai9 in the control but is undetectable in the β-Catenin GOF brain. (D) Genes enriched in CR cells are downregulated in midline tissue β-Catenin GOF brains at E14.5. (E, F) Reelin, βIII-Tubulin and NEUN staining is seen in Ai9+ cells in control brains (arrowheads). In β-catenin GOF brains there is no detectable Reelin (open arrowheads) (E) but βIII-TUBULIN and NEUN staining is seen in Ai9+ cells. (G, J) UMAPs representing tdTomato+ cells from E14.5 control and β-catenin GOF midline, color-coded by cell type (G); by age (H); by genotype (I); showing the expression of Wnt3a, Reln and tdTomato (J). (H) Heatmap of scaled expression of top 10 differentially expressed genes in control and β-Catenin GOF neurons. (I) Dot plots showing scaled expression levels of CR cell enriched genes in control and β-Catenin GOF neurons. Scatterplot in (D) displays Mean ± SEM. Statistical test(D): Multiple Mann-Whitney Tests; p < 0.0001; *p < 0.05; **p < 0.01; ***p < 0.001; ns if p value > 0.05. For (A-C, E-F), N ≥ 3 brains (biologically independent replicates); for (D) N=6 (control), 7 (GOF) biologically independent replicates. Scale bars: 100 μm (all images in A, B, C, E and F).

Article Snippet: Primary antibodies used: Lef1(rabbit, 1:200, CST catalogue #C12A5), β-CATENIN (Mouse, 1:200, BDbiosciences catalogue #610153), β-CATENIN (Rabbit, 1:50, CST catalogue # 8814), RFP (rabbit, 1:200, Abcam catalogue #ab62341), RFP (Mouse, 1:200, Invitrogen catalogue #MA5-15257), β-III TUBULIN (mouse, 1:100, Promega catalogue #G7128), TRP73 (Rabbit, 1:200, CST catalogue #14620S), REELIN (Mouse, 1:200, Millipore catalogue #MAb5364), NEUN (Rabbit, 1:200, invitrogen catalogue #702022).

Techniques: Control, Staining, Expressing, MANN-WHITNEY, IF-P

(A) UMAPs from representing tdTomato+ cells from control and β-Catenin GOF, color-coded by cell type; by genotype; and by pseudo-differentiation trajectory derived from Monocle3. (B) Normalized mRNA expression of Pax6, Eomes/Tbr1, Neurog2, Neurod2, Dcx and Tbr1 across the pseudo-differentiation axis for control (blue) and β-Catenin GOF (red). Thick lines represent Loess smoothed curves. (C) TBR2 staining is seen in Ai9+ cells in controls (arrowheads) but not in β-Catenin GOF brains. Dashed lines mark the ROIs in which TBR2+Ai9+ cells were quantified. (D) The Eomes and Foxj1 expression trajectory along the pseudo-differentiation axis in control neurons (E) Ai9 reporter expression at E12.5 comparing Lmx1a Cre and Foxj1 Cre activity. Foxj1 Cre is not active in hem progenitors but is seen in CR cells and the choroid plexus epithelium. (F) Genes enriched in CR cells are unchanged in midline tissue of Foxj1Cre; β-Catenin GOF brains at E14.5. (G) TRP73 and REELIN staining co-localizes with Ai9+ cells in the hippocampal fissure in both control and Foxj1Cre ; β-Catenin GOF brains at E16.5 and E18.5. Scatterplots in (C) and (F) display Mean ± SEM. Statistical test (C): Shapiro-Wilk normality test, followed by Welch’s two sample t-test, (F) Multiple Mann-Whitney Tests; p < 0.0001; *p < 0.05; **p < 0.01; ***p < 0.001; ns if p value > 0.05. For (C), N=3 (biologically independent replicates), (E), N=5 (biologically independent replicates), (F), N=6 (biologically independent replicates), (G), N=3 (biologically independent replicates). Scale bars: 100 μm (all images in C, E and G).

Journal: bioRxiv

Article Title: Cajal-Retzius fate specification is disrupted by constitutive activation of β-Catenin in hem progenitors

doi: 10.64898/2026.02.09.704731

Figure Lengend Snippet: (A) UMAPs from representing tdTomato+ cells from control and β-Catenin GOF, color-coded by cell type; by genotype; and by pseudo-differentiation trajectory derived from Monocle3. (B) Normalized mRNA expression of Pax6, Eomes/Tbr1, Neurog2, Neurod2, Dcx and Tbr1 across the pseudo-differentiation axis for control (blue) and β-Catenin GOF (red). Thick lines represent Loess smoothed curves. (C) TBR2 staining is seen in Ai9+ cells in controls (arrowheads) but not in β-Catenin GOF brains. Dashed lines mark the ROIs in which TBR2+Ai9+ cells were quantified. (D) The Eomes and Foxj1 expression trajectory along the pseudo-differentiation axis in control neurons (E) Ai9 reporter expression at E12.5 comparing Lmx1a Cre and Foxj1 Cre activity. Foxj1 Cre is not active in hem progenitors but is seen in CR cells and the choroid plexus epithelium. (F) Genes enriched in CR cells are unchanged in midline tissue of Foxj1Cre; β-Catenin GOF brains at E14.5. (G) TRP73 and REELIN staining co-localizes with Ai9+ cells in the hippocampal fissure in both control and Foxj1Cre ; β-Catenin GOF brains at E16.5 and E18.5. Scatterplots in (C) and (F) display Mean ± SEM. Statistical test (C): Shapiro-Wilk normality test, followed by Welch’s two sample t-test, (F) Multiple Mann-Whitney Tests; p < 0.0001; *p < 0.05; **p < 0.01; ***p < 0.001; ns if p value > 0.05. For (C), N=3 (biologically independent replicates), (E), N=5 (biologically independent replicates), (F), N=6 (biologically independent replicates), (G), N=3 (biologically independent replicates). Scale bars: 100 μm (all images in C, E and G).

Techniques: Control, Derivative Assay, Expressing, Staining, Activity Assay, MANN-WHITNEY, IF-P

Enrichment analysis for genes associated with TP53 signaling identifies an AML subgroup with TP53 mut-like (A) General workflow of the differential gene expression analysis comparing patient with TP53 mut vs. TP53 wt included in the TCGA cohort ( n = 157) and BeatAML cohort ( n = 447). The top 20% differentially expressed genes, upregulated in TP53 mut AMLs from both datasets (157 genes), were used to create a TP53 AML signature. (B) Heatmap depicting the ssGSEA projection of TCGA dataset for 173 AML samples on the collection of 65 gene sets associated with the TP53 signaling pathway and normal and malignant hematopoiesis (MSigDB v.7.1), defining a cluster of AML samples enriched for the TP53 AML signature. AML samples are annotated with the enrichment scores (ESs) for the ssGSEAs for each individual dataset. Data are clustered according to the hierarchical clustering for Spearman rank correlation. Top-scoring gene sets within the cluster with strong positive (in red) and negative (in blue) enrichment for the TP53 mut signature are listed next to the heatmap, with their respective statistical analysis. (C) Violin plots displaying the ES for the TP53 AML signature and the LSC_17 signature for AML patients included in the TCGA cohort ( n = 173) and HOVON ( n = 530) cohort. , Patients were categorized according to the TP53 mutational status into TP53 wt, TP53 mut-like, and TP53 mut. (D) Principal-component analysis (PCA) of 173 patients with AML from the TCGA cohort based on the composition of their cellular hierarchy. Right: the levels of TP53 AML signature per patient. (E) Oncoprint displaying the baseline mutations of the patients with TP53 wt, TP53 mut-like, and TP53 mut AMLs in the TCGA cohort. Annotations regarding their cytogenetics are displayed at the bottom row. Genes in bold are the ones significantly different. (F–H) Violin plots displaying the methylation levels for TP73 gene (F), the TAp73 gene expression (G), and the ratio of expression between the ΔNp73 / TAp73 isoforms (H) for AML patients included in the TCGA cohort ( n = 173). (I) Violin plot displaying the ES for the SCIAN_ΔNp73_targets_UP signature for AML patients included in the HOVON cohort. Patients were categorized according to the TP53 mutational status into TP53 wt and TP53 mut-like ( n = 517). (J) Gene Ontology (GO) and gene set enrichment analysis (GSEA) of ΔNp73 low and ΔNp73 high patients ( n = 8) analyzed on the proteome of CD34 + -sorted AML cells. NES, normalized enrichment score; FDR, false discovery rate. (K) The probability of overall survival (OS) in AML patients treated with 3 + 7-based protocols according to the ΔNp73 levels (high versus low), compared to TP53 mut patients. OS curves were estimated using the Kaplan-Meier method, and the log rank test was used for comparison. (L and M) Violin plots displaying the drug sensitivity to AraC ( n = 33) and venetoclax (VEN, n = 36) (L) and the drug-induced apoptosis of VEN (100 nM) + 5-azacytidine (5′ Aza, 1.5 μM) ( n = 8) (M) in ex vivo -treated primary AML samples (72 h). In (L), values are displayed as area under the curve (AUC), where high levels indicate resistance to therapy. Patients were dichotomized based on ΔNp73 expression. The p values are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Journal: Cell Reports Medicine

Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

doi: 10.1016/j.xcrm.2025.102540

Figure Lengend Snippet: Enrichment analysis for genes associated with TP53 signaling identifies an AML subgroup with TP53 mut-like (A) General workflow of the differential gene expression analysis comparing patient with TP53 mut vs. TP53 wt included in the TCGA cohort ( n = 157) and BeatAML cohort ( n = 447). The top 20% differentially expressed genes, upregulated in TP53 mut AMLs from both datasets (157 genes), were used to create a TP53 AML signature. (B) Heatmap depicting the ssGSEA projection of TCGA dataset for 173 AML samples on the collection of 65 gene sets associated with the TP53 signaling pathway and normal and malignant hematopoiesis (MSigDB v.7.1), defining a cluster of AML samples enriched for the TP53 AML signature. AML samples are annotated with the enrichment scores (ESs) for the ssGSEAs for each individual dataset. Data are clustered according to the hierarchical clustering for Spearman rank correlation. Top-scoring gene sets within the cluster with strong positive (in red) and negative (in blue) enrichment for the TP53 mut signature are listed next to the heatmap, with their respective statistical analysis. (C) Violin plots displaying the ES for the TP53 AML signature and the LSC_17 signature for AML patients included in the TCGA cohort ( n = 173) and HOVON ( n = 530) cohort. , Patients were categorized according to the TP53 mutational status into TP53 wt, TP53 mut-like, and TP53 mut. (D) Principal-component analysis (PCA) of 173 patients with AML from the TCGA cohort based on the composition of their cellular hierarchy. Right: the levels of TP53 AML signature per patient. (E) Oncoprint displaying the baseline mutations of the patients with TP53 wt, TP53 mut-like, and TP53 mut AMLs in the TCGA cohort. Annotations regarding their cytogenetics are displayed at the bottom row. Genes in bold are the ones significantly different. (F–H) Violin plots displaying the methylation levels for TP73 gene (F), the TAp73 gene expression (G), and the ratio of expression between the ΔNp73 / TAp73 isoforms (H) for AML patients included in the TCGA cohort ( n = 173). (I) Violin plot displaying the ES for the SCIAN_ΔNp73_targets_UP signature for AML patients included in the HOVON cohort. Patients were categorized according to the TP53 mutational status into TP53 wt and TP53 mut-like ( n = 517). (J) Gene Ontology (GO) and gene set enrichment analysis (GSEA) of ΔNp73 low and ΔNp73 high patients ( n = 8) analyzed on the proteome of CD34 + -sorted AML cells. NES, normalized enrichment score; FDR, false discovery rate. (K) The probability of overall survival (OS) in AML patients treated with 3 + 7-based protocols according to the ΔNp73 levels (high versus low), compared to TP53 mut patients. OS curves were estimated using the Kaplan-Meier method, and the log rank test was used for comparison. (L and M) Violin plots displaying the drug sensitivity to AraC ( n = 33) and venetoclax (VEN, n = 36) (L) and the drug-induced apoptosis of VEN (100 nM) + 5-azacytidine (5′ Aza, 1.5 μM) ( n = 8) (M) in ex vivo -treated primary AML samples (72 h). In (L), values are displayed as area under the curve (AUC), where high levels indicate resistance to therapy. Patients were dichotomized based on ΔNp73 expression. The p values are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Article Snippet: Antibodies against ΔNp73 (sc-70966), anti-TP73 (5B1288), TP53 (sc-126), CEBPA (sc-365318) and β-actin (sc-47778) were obtained from Santa Cruz Biotechnology (San Jose, CA).

Techniques: Gene Expression, Methylation, Expressing, Comparison, Ex Vivo

ΔNp73 overexpression is associated with downregulation of the TP53 signaling pathway in TP53 wt AMLs (A) Western blot analysis for ΔNp73 and total TP73 in total cell extracts from MOLM13 cells transduced with lentivirus containing the EV (pMEG) or the ΔNp73α or ΔNp73β cDNA. (B) Volcano plot displaying the differentially expressed genes in MOLM13 cells with ΔNp73-OE versus EV control ( n = 2). (C) Expression of CD14 and CD117 in MOLM13 EV (pMEG) and ΔNp73α-OE cells ( n = 3). (D) GSEA analysis using the fold change values from the analysis depicted in (A). False discovery rate (FDR)-q values are indicated. (E) ChIP-seq data on MOLM13 cells used in (A) using antibodies against TP53 or GFP (for the GFP-ΔNp73 fusion), and TAp73. Heatmaps with signals ± 5 kb from the transcription start site (TSS) are shown. (F) Representative screenshots of TP53, TAp73, and ΔNp73 antibody binding at four TP53 target loci. (G) Venn diagram depicting overlapping peaks detected for the TP53 ChIP-seq in MOLM13 EV control cells and the GFP-ΔNp73 in MOLM13-ΔNp73 OE cells. Lower: GO analysis for the overlapping peaks (51 targets). (H and I) Cumulative cell count of MOLM13 ( TP53 wt, H) and TF1 ( TP53 mut, I) cells transduced with ΔNp73α, ΔNp73β, and EV control, cultured for 9 days ( n = 4). (J) Western blot analysis for TP53 and total TP73 in total cell extracts from MOLM13 cells transduced with EV (pMEG) or the shRNA targeting the TP53 gene (shTP53). Cumulative cell count of MOLM13 TP53 KD cells (sh TP53 ) transduced with ΔNp73α, ΔNp73β, and EV control, cultured for 9 days, is shown in the right ( n = 4). Data are reported as mean ± SEM for (H) and (I). The p values and cell lines are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Journal: Cell Reports Medicine

Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

doi: 10.1016/j.xcrm.2025.102540

Figure Lengend Snippet: ΔNp73 overexpression is associated with downregulation of the TP53 signaling pathway in TP53 wt AMLs (A) Western blot analysis for ΔNp73 and total TP73 in total cell extracts from MOLM13 cells transduced with lentivirus containing the EV (pMEG) or the ΔNp73α or ΔNp73β cDNA. (B) Volcano plot displaying the differentially expressed genes in MOLM13 cells with ΔNp73-OE versus EV control ( n = 2). (C) Expression of CD14 and CD117 in MOLM13 EV (pMEG) and ΔNp73α-OE cells ( n = 3). (D) GSEA analysis using the fold change values from the analysis depicted in (A). False discovery rate (FDR)-q values are indicated. (E) ChIP-seq data on MOLM13 cells used in (A) using antibodies against TP53 or GFP (for the GFP-ΔNp73 fusion), and TAp73. Heatmaps with signals ± 5 kb from the transcription start site (TSS) are shown. (F) Representative screenshots of TP53, TAp73, and ΔNp73 antibody binding at four TP53 target loci. (G) Venn diagram depicting overlapping peaks detected for the TP53 ChIP-seq in MOLM13 EV control cells and the GFP-ΔNp73 in MOLM13-ΔNp73 OE cells. Lower: GO analysis for the overlapping peaks (51 targets). (H and I) Cumulative cell count of MOLM13 ( TP53 wt, H) and TF1 ( TP53 mut, I) cells transduced with ΔNp73α, ΔNp73β, and EV control, cultured for 9 days ( n = 4). (J) Western blot analysis for TP53 and total TP73 in total cell extracts from MOLM13 cells transduced with EV (pMEG) or the shRNA targeting the TP53 gene (shTP53). Cumulative cell count of MOLM13 TP53 KD cells (sh TP53 ) transduced with ΔNp73α, ΔNp73β, and EV control, cultured for 9 days, is shown in the right ( n = 4). Data are reported as mean ± SEM for (H) and (I). The p values and cell lines are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Article Snippet: Antibodies against ΔNp73 (sc-70966), anti-TP73 (5B1288), TP53 (sc-126), CEBPA (sc-365318) and β-actin (sc-47778) were obtained from Santa Cruz Biotechnology (San Jose, CA).

Techniques: Over Expression, Western Blot, Transduction, Control, Expressing, ChIP-sequencing, Binding Assay, Cell Characterization, Cell Culture, shRNA

ΔNp73 expression is associated with drug resistance and is regulated by an intragenic region in the TP73 gene (A) MOLM13 cells (ΔNp73-OE and EV control) were treated with FLT3 inhibitors quizartinib (AC220) and midostaurin (PKC) and AML-related drugs venetoclax (VEN) and cytarabine (AraC) for 72 h. Apoptosis and viable cell numbers were assessed by flow cytometry. Experiments were performed in quadruplicates. Results are expressed as the mean ± standard error of the mean (SEM). ED 50 , half maximal effective concentration ( n = 4). (B and C) Drug-induced apoptosis in TF1 cells (ΔNp73-OE and EV control) (B) and MOLM13 cells (transduced with shTP53 and ΔNp73-OE, as depicted in the figure) (C) treated with AML-related drugs (AraC and VEN; concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D) DNAseI gene tracks in six AML samples from the BLUEPRINT consortium. The red arrows denote highly accessible sites (+24 kb from the TSS) in the TP73 gene. The blue arrow denotes the TA promoter, and the green arrow denotes the ΔN promoter of the TP73 gene locus. (E) Relative mRNA expression levels of Δ Np73 after Cas9-mediated TP73 enhancer excision in MOLM13 cells (MOLM13-KO) at baseline and upon AraC treatment (1 μM, 48 h) ( n = 4). (F) GSEA analysis using the fold change values from the RNA-seq analysis comparing MOLM13-KO versus MOLM13-SCR cells ( n = 2). (G) TP53 (+0.2) and CDKN1A (−0.8) ChIP-qPCRs with error bars representing SEM based on three independent experiments. (H) Cumulative cell count of Cas9-mediated excision of TP73 intragenic enhancer region in MOLM13 and HL60 cells (KO versus SCR control) cultured for 9 days ( n = 4). (I and J) Drug-induced apoptosis (I) and viable cell counts (J) in MOLM13-KO cells treated with AML-related drugs (drugs and concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (K) Genome browser screenshots of DNA hypersensitivity sites (DHSs) and digital footprints of the TP73 intragenic enhancer region in the TP73 loci, revealing the two regions of the intragenic enhancer. Results from motif analysis are displayed at the bottom. (L) Relative mRNA expression levels of Δ Np73 after Cas9-mediated TP73 enhancer excision of the separate regions 1 and 2 in MOLM13 cells (MOLM13-KO included as a control) at baseline and upon AraC treatment (1 μM, 48 h) ( n = 4). (M) Drug-induced apoptosis in region 2 KO MOLM13 cells treated with AML-related drugs (drugs and concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (N) Representative screenshots of CEBPA antibody binding at the TP73 enhancer region in primary AML samples. Data are reported as mean ± SEM for (A)–(C), (E), (H)–(J), (L), and (M). The p values and cell lines are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Journal: Cell Reports Medicine

Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

doi: 10.1016/j.xcrm.2025.102540

Figure Lengend Snippet: ΔNp73 expression is associated with drug resistance and is regulated by an intragenic region in the TP73 gene (A) MOLM13 cells (ΔNp73-OE and EV control) were treated with FLT3 inhibitors quizartinib (AC220) and midostaurin (PKC) and AML-related drugs venetoclax (VEN) and cytarabine (AraC) for 72 h. Apoptosis and viable cell numbers were assessed by flow cytometry. Experiments were performed in quadruplicates. Results are expressed as the mean ± standard error of the mean (SEM). ED 50 , half maximal effective concentration ( n = 4). (B and C) Drug-induced apoptosis in TF1 cells (ΔNp73-OE and EV control) (B) and MOLM13 cells (transduced with shTP53 and ΔNp73-OE, as depicted in the figure) (C) treated with AML-related drugs (AraC and VEN; concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D) DNAseI gene tracks in six AML samples from the BLUEPRINT consortium. The red arrows denote highly accessible sites (+24 kb from the TSS) in the TP73 gene. The blue arrow denotes the TA promoter, and the green arrow denotes the ΔN promoter of the TP73 gene locus. (E) Relative mRNA expression levels of Δ Np73 after Cas9-mediated TP73 enhancer excision in MOLM13 cells (MOLM13-KO) at baseline and upon AraC treatment (1 μM, 48 h) ( n = 4). (F) GSEA analysis using the fold change values from the RNA-seq analysis comparing MOLM13-KO versus MOLM13-SCR cells ( n = 2). (G) TP53 (+0.2) and CDKN1A (−0.8) ChIP-qPCRs with error bars representing SEM based on three independent experiments. (H) Cumulative cell count of Cas9-mediated excision of TP73 intragenic enhancer region in MOLM13 and HL60 cells (KO versus SCR control) cultured for 9 days ( n = 4). (I and J) Drug-induced apoptosis (I) and viable cell counts (J) in MOLM13-KO cells treated with AML-related drugs (drugs and concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (K) Genome browser screenshots of DNA hypersensitivity sites (DHSs) and digital footprints of the TP73 intragenic enhancer region in the TP73 loci, revealing the two regions of the intragenic enhancer. Results from motif analysis are displayed at the bottom. (L) Relative mRNA expression levels of Δ Np73 after Cas9-mediated TP73 enhancer excision of the separate regions 1 and 2 in MOLM13 cells (MOLM13-KO included as a control) at baseline and upon AraC treatment (1 μM, 48 h) ( n = 4). (M) Drug-induced apoptosis in region 2 KO MOLM13 cells treated with AML-related drugs (drugs and concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (N) Representative screenshots of CEBPA antibody binding at the TP73 enhancer region in primary AML samples. Data are reported as mean ± SEM for (A)–(C), (E), (H)–(J), (L), and (M). The p values and cell lines are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Article Snippet: Antibodies against ΔNp73 (sc-70966), anti-TP73 (5B1288), TP53 (sc-126), CEBPA (sc-365318) and β-actin (sc-47778) were obtained from Santa Cruz Biotechnology (San Jose, CA).

Techniques: Expressing, Control, Flow Cytometry, Concentration Assay, Transduction, RNA Sequencing, Cell Characterization, Cell Culture, Binding Assay

CEBPA controls ΔNp73 expression in AML cells (A) Spearman correlations between the TP53 AML signature and the ex vivo drug screening in the BeatAML cohort (122 drugs). . Red and blue dots indicate resistance and sensitivity to drug-induced cell death in TP53 mut-like AMLs, respectively. (B) Violin plots displaying the ES for the HALMOS_CEBPA_TARGETS_UP signature for AML patients included in the TCGA cohort ( n = 173). Patients were categorized according to the TP53 mutational status into TP53 wt, TP53 mut-like, and TP53 mut. (C) Simplified schematic and Venn diagram analysis for drug repurposing discovery via cMAP analysis integrating the significant gene sets associated with TP53 mut-like AMLs. (D and E) Relative mRNA expression levels of Δ Np73 (D) and TAp73 (E) at baseline and upon guanfacine (GFC) treatment (30 and 60 μM) in a panel of AML cell lines (48 h). (F) Relative mRNA expression levels of TAp73 , ΔNp73 , and CEBPA at baseline and upon guanfacine (GFC) treatment (30 and 60 μM) in MOLM13 SCR controls and KO cells (48 h) ( n = 4). (G) Relative mRNA expression levels of TP73 isoforms and CEBPA/CEBPB and its related targets ( HMGCS1 and DHCR7 ) at baseline and upon GFC treatment (30 and 60 μM) in MOLM13 cells (48 h) ( n = 4). (H) Western blot analysis for CEBPA and ΔNp73 in total cell extracts from MOLM13 cells treated with GFC (60 μM, 48 h). (I) Relative mRNA expression levels of TP73 isoforms and CEBPA/CEBPB and ex vivo -treated primary AML patients at baseline and upon GFC treatment ( TP53 mut/mut-like, 30 μM, 72 h) ( n = 10). (J) Relative mRNA expression levels of the same targets as described in (G) in MOLM13 cells transduced with shRNA targeting the CEBPA gene and the scrambled control ( n = 4). (K) Western blot analysis for CEBPA, ΔNp73, and total TP73 in total cell extracts from MOLM13 cells transduced with shScr (control) or the shRNA targeting the CEBPA gene (shCEBPA). Data are reported as mean ± SEM for (D)–(G), (I), and (J). The p values and cell lines are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Journal: Cell Reports Medicine

Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

doi: 10.1016/j.xcrm.2025.102540

Figure Lengend Snippet: CEBPA controls ΔNp73 expression in AML cells (A) Spearman correlations between the TP53 AML signature and the ex vivo drug screening in the BeatAML cohort (122 drugs). . Red and blue dots indicate resistance and sensitivity to drug-induced cell death in TP53 mut-like AMLs, respectively. (B) Violin plots displaying the ES for the HALMOS_CEBPA_TARGETS_UP signature for AML patients included in the TCGA cohort ( n = 173). Patients were categorized according to the TP53 mutational status into TP53 wt, TP53 mut-like, and TP53 mut. (C) Simplified schematic and Venn diagram analysis for drug repurposing discovery via cMAP analysis integrating the significant gene sets associated with TP53 mut-like AMLs. (D and E) Relative mRNA expression levels of Δ Np73 (D) and TAp73 (E) at baseline and upon guanfacine (GFC) treatment (30 and 60 μM) in a panel of AML cell lines (48 h). (F) Relative mRNA expression levels of TAp73 , ΔNp73 , and CEBPA at baseline and upon guanfacine (GFC) treatment (30 and 60 μM) in MOLM13 SCR controls and KO cells (48 h) ( n = 4). (G) Relative mRNA expression levels of TP73 isoforms and CEBPA/CEBPB and its related targets ( HMGCS1 and DHCR7 ) at baseline and upon GFC treatment (30 and 60 μM) in MOLM13 cells (48 h) ( n = 4). (H) Western blot analysis for CEBPA and ΔNp73 in total cell extracts from MOLM13 cells treated with GFC (60 μM, 48 h). (I) Relative mRNA expression levels of TP73 isoforms and CEBPA/CEBPB and ex vivo -treated primary AML patients at baseline and upon GFC treatment ( TP53 mut/mut-like, 30 μM, 72 h) ( n = 10). (J) Relative mRNA expression levels of the same targets as described in (G) in MOLM13 cells transduced with shRNA targeting the CEBPA gene and the scrambled control ( n = 4). (K) Western blot analysis for CEBPA, ΔNp73, and total TP73 in total cell extracts from MOLM13 cells transduced with shScr (control) or the shRNA targeting the CEBPA gene (shCEBPA). Data are reported as mean ± SEM for (D)–(G), (I), and (J). The p values and cell lines are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Article Snippet: Antibodies against ΔNp73 (sc-70966), anti-TP73 (5B1288), TP53 (sc-126), CEBPA (sc-365318) and β-actin (sc-47778) were obtained from Santa Cruz Biotechnology (San Jose, CA).

Techniques: Expressing, Ex Vivo, Drug discovery, Western Blot, Transduction, shRNA, Control

TP53 mut/mut-like AMLs are associated with increased susceptibility to ferroptosis-induced cell death (A) Violin plots displaying the ES for the REACTOME_ACTIVATION_GENE_EXPRESSION_BY_SREBF_SREBP (left side) and the gene expression levels (transcripts per million, TPM) for the SREBP-related genes ( SCD and HMGCS1 ) for AML patients included in the TCGA cohort ( n = 173). Patients were categorized according to the TP53 mutational status into TP53 wt, TP53 mut-like, and TP53 mut. (B and C) Relative mRNA expression levels of Δ Np73 , CEBPA/CEBPB , and its related targets at baseline and upon dipyridamole (DP) treatment (10 μM) in MOLM13 ΔNp73-OE/EV (pMEG) cells (48 h) (B) and at baseline in MOLM13-KO/Scr control cells (C) ( n = 4). (D) Drug-induced apoptosis in MOLM13 and MV4-11 cells (ΔNp73-OE and EV control) treated with ferroptosis-related drugs KPT-9274 (NAMPT inhibitor ) and DP alone or in combination with VEN (concentrations indicated in the plots, 72 h) detected by flow cytometry. (E and F) Drug-induced apoptosis (E) and total ROS levels (F) in MOLM13 cells (ΔNp73-OE and EV control) treated with the GPX4 inhibitors RSL3 and ML210 (concentrations indicated in the plots, 72 h) detected by flow cytometry. (G) Viable cell counts of MOLM13 cells (ΔNp73-OE and EV control) treated with the SCD inhibitor MK-8245 (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Journal: Cell Reports Medicine

Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

doi: 10.1016/j.xcrm.2025.102540

Figure Lengend Snippet: TP53 mut/mut-like AMLs are associated with increased susceptibility to ferroptosis-induced cell death (A) Violin plots displaying the ES for the REACTOME_ACTIVATION_GENE_EXPRESSION_BY_SREBF_SREBP (left side) and the gene expression levels (transcripts per million, TPM) for the SREBP-related genes ( SCD and HMGCS1 ) for AML patients included in the TCGA cohort ( n = 173). Patients were categorized according to the TP53 mutational status into TP53 wt, TP53 mut-like, and TP53 mut. (B and C) Relative mRNA expression levels of Δ Np73 , CEBPA/CEBPB , and its related targets at baseline and upon dipyridamole (DP) treatment (10 μM) in MOLM13 ΔNp73-OE/EV (pMEG) cells (48 h) (B) and at baseline in MOLM13-KO/Scr control cells (C) ( n = 4). (D) Drug-induced apoptosis in MOLM13 and MV4-11 cells (ΔNp73-OE and EV control) treated with ferroptosis-related drugs KPT-9274 (NAMPT inhibitor ) and DP alone or in combination with VEN (concentrations indicated in the plots, 72 h) detected by flow cytometry. (E and F) Drug-induced apoptosis (E) and total ROS levels (F) in MOLM13 cells (ΔNp73-OE and EV control) treated with the GPX4 inhibitors RSL3 and ML210 (concentrations indicated in the plots, 72 h) detected by flow cytometry. (G) Viable cell counts of MOLM13 cells (ΔNp73-OE and EV control) treated with the SCD inhibitor MK-8245 (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Article Snippet: Antibodies against ΔNp73 (sc-70966), anti-TP73 (5B1288), TP53 (sc-126), CEBPA (sc-365318) and β-actin (sc-47778) were obtained from Santa Cruz Biotechnology (San Jose, CA).

Techniques: Activation Assay, Gene Expression, Expressing, Control, Flow Cytometry

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