Journal: PLoS ONE

Article Title: Dysregulated ΔNp63α Inhibits Expression of Ink4a/arf, Blocks Senescence, and Promotes Malignant Conversion of Keratinocytes

doi: 10.1371/journal.pone.0021877

Figure Lengend Snippet: A, Primary mouse keratinocytes were infected with lentivirus encoding GFP, and infection efficiency was assessed by FACS analysis at day 5 post-infection. Y-axis indicates the intensity of GFP, X-axis represents forward angle light scatter. B, Primary keratinocytes were infected with lentivirus encoding GFP or ΔNp63α and whole cell protein was collected at day 5 and 14 and analyzed for p63 expression by western blot. C, Primary keratinocyte cultures expressing lenti-GFP or lenti-ΔNp63α were fixed at 14 days post-lentiviral transduction and incubated with anti-p63 antibody, followed by a secondary antibody conjugated with Alexa-488. The cells were then stained with DAPI to visualize the cell nuclei.

Article Snippet: For HP1γ detection, culture dishes were fixed with methanol at −20°C and incubated with antibody directed to HP1γ (MAB3450, Chemicon International, Billerica, MA), and p63 (4A4, Santa Cruz Biotechnology, Santa Cruz, CA).

Techniques: Infection, Expressing, Western Blot, Transduction, Incubation, Staining

Journal: PLoS ONE

Article Title: Dysregulated ΔNp63α Inhibits Expression of Ink4a/arf, Blocks Senescence, and Promotes Malignant Conversion of Keratinocytes

doi: 10.1371/journal.pone.0021877

Figure Lengend Snippet: A, Phase morphology of lenti-GFP- and lenti-ΔNp63α expressing keratinocytes cultured for 1 and 14 days post-infection. Results shown are representative of three independent experiments. B, Quantification of BrdU positive cells in lenti-GFP or lenti-ΔNp63α cultures at timepoints noted following lentiviral gene transduction. Data shown represent the means ± S.E. of three independent experiments. * indicates a statistically significant difference between lenti-GFP and lenti-ΔNp63α infected cells at p <0.05. C, Primary keratinocytes expressing lenti-GFP (left panel) or lenti-ΔNp63α (right panel) were fixed at 14 days post-lentiviral transduction. The cell senescence status was assessed by the presence of HP-1γ nuclear foci (red). The cells were double stained with p63 antibodies (green). Matched arrows indicate the same cell stained with both different antibodies. The image presented is representative of three independent experiments.

Article Snippet: For HP1γ detection, culture dishes were fixed with methanol at −20°C and incubated with antibody directed to HP1γ (MAB3450, Chemicon International, Billerica, MA), and p63 (4A4, Santa Cruz Biotechnology, Santa Cruz, CA).

Techniques: Expressing, Cell Culture, Infection, Transduction, Staining

Journal: PLoS ONE

Article Title: Dysregulated ΔNp63α Inhibits Expression of Ink4a/arf, Blocks Senescence, and Promotes Malignant Conversion of Keratinocytes

doi: 10.1371/journal.pone.0021877

Figure Lengend Snippet: A, Whole cell protein was collected from primary keratinocytes expressing lenti-GFP or lenti-ΔNp63α at timepoints indicated following lentiviral gene transduction. Expression levels of p16 ink4a , p19 arf , E2F1 and p63 were detected by western blot. Equal protein loading was confirmed by immunoblotting for β-actin. B, Primary keratinocytes were infected with lentivirus encoding ΔNp63α or GFP at day 3 after plating. Total RNA was harvested at day 3, 5, 7 and 10 post-infection and reverse transcribed. Expression of p16 ink4a and p19 arf was determined by PCR amplification. PCR amplification of GAPDH was used as a loading control. C, Primary keratinocytes were cultured for 7 days after plating and then infected with adenovirus encoding ΔNp63α or LacZ. Whole cell lysates were collected at day 2, 3, 6 and 8 post-adenovirus infection (equivalent to day 9, 10, 13 and 15 post-plating). The expression levels of p16 ink4a , p19 arf and p63 were detected by western blot. Equivalent protein loading was confirmed by immunoblotting for actin.

Article Snippet: For HP1γ detection, culture dishes were fixed with methanol at −20°C and incubated with antibody directed to HP1γ (MAB3450, Chemicon International, Billerica, MA), and p63 (4A4, Santa Cruz Biotechnology, Santa Cruz, CA).

Techniques: Expressing, Transduction, Western Blot, Infection, Reverse Transcription, Amplification, Control, Cell Culture

Journal: PLoS ONE

Article Title: Dysregulated ΔNp63α Inhibits Expression of Ink4a/arf, Blocks Senescence, and Promotes Malignant Conversion of Keratinocytes

doi: 10.1371/journal.pone.0021877

Figure Lengend Snippet: A, Primary keratinocytes were infected sequentially with retrovirus encoding oncogenic v-ras Ha , followed by lentivirus encoding GFP or ΔNp63α. Oncogene-induced senescence was assessed 14 days post-lentivirus infection by immunofluorescent analysis of nuclear foci of HP-1γ (upper panel), or enzymatic activity of SA-β-gal (lower panel). The images shown are representative of three independent experiments. B, Whole cell protein was collected from keratinocytes infected sequentially with retrovirus encoding oncogenic v-ras Ha followed by lentivirus encoding GFP or ΔNp63α at timepoints indicated following lentiviral gene transduction. The levels of phosphorylated AKT, total AKT, p19 arf and p63 were detected by western blot (upper panels). p16 ink4a and E2F1 levels with corresponding p63 expression are presented in the lower panels. Equal protein loading was confirmed by immunoblotting for β-actin.

Article Snippet: For HP1γ detection, culture dishes were fixed with methanol at −20°C and incubated with antibody directed to HP1γ (MAB3450, Chemicon International, Billerica, MA), and p63 (4A4, Santa Cruz Biotechnology, Santa Cruz, CA).

Techniques: Infection, Activity Assay, Transduction, Western Blot, Expressing

Journal: FEBS letters

Article Title: ING1b decreases cell proliferation through p53-dependent and -independent mechanisms.

doi: 10.1016/s0014-5793(03)01024-x

Figure Lengend Snippet: Fig. 7. ING1b can activate p53-related proteins. A: Activation of the transcriptional activities of p53-related proteins by ING1b. H1299 cells were transfected with plasmids expressing an MDM2 promoter-luciferase reporter and L-galactosidase. Control reactions without cotransfection of other plasmids are shown in experiment 1. Plasmids expressing p73K, p63K, and p53 were cotransfected with control plasmids (experiment 2) or ING1b (experiment 3) as indicated. Cell extracts were prepared, and the luciferase and L-galactosidase activities were determined. The lu- ciferase activities were normalized with the L-galactosidase activities to correct for transcriptional e⁄ciencies and plotted as a percentage of p53/p63K/p73K alone. The means and standard deviation of three independent experiments are shown. B: Puri¢cation of recombinant GST- ING1b. GST-ING1b was expressed in E. coli and puri¢ed as described in Section 2. The puri¢ed protein was applied onto SDS^PAGE and de- tected by Coomassie blue staining. The positions of molecular mass standards (in kDa) are indicated. C: ING1b can interact with p53 and p73K. Reticulocyte lysate-expressed p53 and p73K were incubated with either puri¢ed GST or GST-ING1b. The GST fusion proteins were cap- tured with GSH-agarose and unbound proteins were washed o¡. The coprecipitated p53 and p73K were detected by SDS^PAGE and Phos- phorImagery. D: ING1b can interact with p53 and p63K. H1299 cells were transfected with plasmids encoding p53 (lanes 1, 2, 5 and 6) or p63K (lanes 3, 4, 7 and 8) with control vector (odd-numbered lanes) or FLAG-ING1b (even-numbered lanes). Cell-free extracts were prepared at 24 h after transfection and 100 Wg was subjected to immunoprecipitation with anti-FLAG immune serum. The retained proteins were de- tected by immunoblotting using antibodies against p53 and p63.

Article Snippet: Goat antibodies raised against a C-terminal peptide derived from ING1 (sc-7566), polyclonal antibodies against p21CIP1=WAF1 (sc-397), monoclonal antibodies 4A4 against p63 (sc8431), and monoclonal antibodies DO-1 against p53 (sc-126) were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Activation Assay, Transfection, Expressing, Luciferase, Control, Cotransfection, Standard Deviation, Recombinant, SDS Page, Staining, Incubation, Plasmid Preparation, Immunoprecipitation, Western Blot

Journal: Histopathology

Article Title: Primary cutaneous NUT adnexal carcinoma: morphologic, genetic and methylation analysis of seven new cases with comparison to extracutaneous NUT carcinoma and NUTM1 ‐rearranged porocarcinoma

doi: 10.1111/his.15444

Figure Lengend Snippet: Immunohistochemical features of BRD4::NUTM1 adnexal carcinoma. Immunohistochemistry of the case showed diffuse positivity for EMA and SOX10. CEA confirmed the presence of ducts. P63 and p40 confined to the periphery of the tumour nests. Diffuse nuclear expression of NUT was demonstrated. YAP1 (C‐terminal) expression was preserved.

Article Snippet: Immunohistochemical staining for EMA (clone E29; Dako, Glostrup, Denmark), p40 (clone BC28; Eurobio, Les Ulis, France), p63 (clone 4A4; Biocare Medical, Pacheco, CA, USA), SOX10 (clone SP267; Cell Marque, Rocklin, CA, USA), CEA (clone CEA 31; Cell Marque), EpCAM (Clone BerEP4; Dako), NUT (clone C52B1; Cell Signalling Technology, Danvers, MA, USA), YAP1 (clone D8H1\u00D7; Cell Signalling Technology) was performed using a BenchMark XT Platform (Roche Diagnostics GmbH, Penzberg, Germany).

Techniques: Immunohistochemical staining, Immunohistochemistry, Expressing

Journal: NAR Cancer

Article Title: An integrated genomic approach identifies follistatin as a target of the p63-epidermal growth factor receptor oncogenic network in head and neck squamous cell carcinoma

doi: 10.1093/narcan/zcad038

Figure Lengend Snippet: Protein interaction network involving EGFR and TGF-β signaling pathways embedded in the p63 signature network. ( A ) Venn diagram showing the 291 genes that overlap between the p63 targets and p63 consensus signature. ( B ) The 291 genes were used as input to perform an interaction network analysis on the STRING database . ( C ) Approximately 21% of the 291 targets used as input in the STRING database were part of an interconnected network of protein–protein interactions that link the TGF-β1 signaling and EGFR signaling. The bubbles are color coded to reflect the corresponding log 2 fold change values.

Article Snippet: Proteins were then electro-transferred to Immunoblot polyvinylidene difluoride membranes (Bio-Rad), which were incubated with the following antibodies: p63 4A4, FST (sc-365003 [Santa Cruz Biotechnology] or EPR10903 [Abcam]), pAKT ser-473 (66444-I-Ig; Proteintech), pAKT Thr-308 (29163-1-AP; Proteintech), pSTAT3 (Epitomics), STAT3 (2281-1; Epitomics), AKT1 (10176-2-AP; Proteintech), pERK1/2 (sc-7883; Santa Cruz Biotechnology), ERK1/2 (sc-66192-1-Ig [Proteintech] or sc-514302 [Santa Cruz Biotechnology]), GAPDH (MAB374; EMD Millipore), pSMAD2 (GTX13364; GeneTex), SMAD2 (GTX111075; GeneTex), pSMAD1/5 (41D10; Cell Signaling), and SMAD1 (D49D7; Cell Signaling).

Techniques: Protein-Protein interactions

Journal: NAR Cancer

Article Title: An integrated genomic approach identifies follistatin as a target of the p63-epidermal growth factor receptor oncogenic network in head and neck squamous cell carcinoma

doi: 10.1093/narcan/zcad038

Figure Lengend Snippet: p63-driven gene signature. ( A ) Western blot showing robust depletion of p63 in A253 and SCC25 cells treated with p63-targeting shRNA constructs. ( B ) Schematic showing the analysis of the RNA-seq data generated from the p63 knockdown experiments. ( C ) Venn diagram showing the numbers of p63-regulated DEGs in both A253 and SCC25 cells. 555 genes (red) were upregulated, and 795 genes (blue) were downregulated in both cells. 140 genes (black) were not consistently upregulated or downregulated in both cells. ( D ) WikiPathway analyses of the genes that were upregulated following p63 ( E ) WikiPathway analyses of the genes that were downregulated after p63 depletion. ( F ) (Top) Schematic showing how both TCGA-HNSCC patient data and in vitro knockdown data were combined to generate the consensus signature. (Bottom left) Heat map showing the expression profile in the 430-gene consensus signature in the TCGA data set. (Bottom right) The pattern of expression of this signature is conserved in an independent preclinical HNSCC data set reported by Huang et al. . ( G ) Biological processes enriched in the 430-gene consensus signature, including Rho and ERK1/2 signaling cascades, cell migration and cellular response to drugs.

Article Snippet: Proteins were then electro-transferred to Immunoblot polyvinylidene difluoride membranes (Bio-Rad), which were incubated with the following antibodies: p63 4A4, FST (sc-365003 [Santa Cruz Biotechnology] or EPR10903 [Abcam]), pAKT ser-473 (66444-I-Ig; Proteintech), pAKT Thr-308 (29163-1-AP; Proteintech), pSTAT3 (Epitomics), STAT3 (2281-1; Epitomics), AKT1 (10176-2-AP; Proteintech), pERK1/2 (sc-7883; Santa Cruz Biotechnology), ERK1/2 (sc-66192-1-Ig [Proteintech] or sc-514302 [Santa Cruz Biotechnology]), GAPDH (MAB374; EMD Millipore), pSMAD2 (GTX13364; GeneTex), SMAD2 (GTX111075; GeneTex), pSMAD1/5 (41D10; Cell Signaling), and SMAD1 (D49D7; Cell Signaling).

Techniques: Western Blot, shRNA, Construct, RNA Sequencing, Generated, Knockdown, In Vitro, Expressing, Migration

Journal: NAR Cancer

Article Title: An integrated genomic approach identifies follistatin as a target of the p63-epidermal growth factor receptor oncogenic network in head and neck squamous cell carcinoma

doi: 10.1093/narcan/zcad038

Figure Lengend Snippet: Overview of the super enhancer landscape in A253 and SCC25 cells. ( A ) Super enhancer profiles of A253 and SCC25 cells according to H3K27Ac with gene assignment. ( B ) Pie charts detailing the distribution of p63 binding in regular enhancer versus super enhancer regions. ( C ) Common super enhancer-associated genes in A253 and SCC25 cells. ( D ) Genomic maps showing the super enhancers associated with TP63, FOSL1 and EGFR in both A253 and SCC25 cells.

Article Snippet: Proteins were then electro-transferred to Immunoblot polyvinylidene difluoride membranes (Bio-Rad), which were incubated with the following antibodies: p63 4A4, FST (sc-365003 [Santa Cruz Biotechnology] or EPR10903 [Abcam]), pAKT ser-473 (66444-I-Ig; Proteintech), pAKT Thr-308 (29163-1-AP; Proteintech), pSTAT3 (Epitomics), STAT3 (2281-1; Epitomics), AKT1 (10176-2-AP; Proteintech), pERK1/2 (sc-7883; Santa Cruz Biotechnology), ERK1/2 (sc-66192-1-Ig [Proteintech] or sc-514302 [Santa Cruz Biotechnology]), GAPDH (MAB374; EMD Millipore), pSMAD2 (GTX13364; GeneTex), SMAD2 (GTX111075; GeneTex), pSMAD1/5 (41D10; Cell Signaling), and SMAD1 (D49D7; Cell Signaling).

Techniques: Binding Assay

Journal: NAR Cancer

Article Title: An integrated genomic approach identifies follistatin as a target of the p63-epidermal growth factor receptor oncogenic network in head and neck squamous cell carcinoma

doi: 10.1093/narcan/zcad038

Figure Lengend Snippet: EGF signaling drives FST expression via ERK signaling in HNSCC. ( A ) Western blots showing the effects of 4-h stimulation of SCC25 (left) and A253 (right) cells with 50ng of indicated growth factors. Although the downstream signaling cascades of these growth factors were activated in both cell lines, only EGF treatment upregulated FST expression. ( B ) Treatment of A253 and SCC25 cells with 30 ng EGF for 4 h resulted in activation of ERK1/2 but not AKT or STAT3. ( C ) Depletion of p63 prevented EGF-mediated FST expression in A253 and SCC25 cells. ( D ) Inhibition of ERK phosphorylation via Selumetinib (ADZ6244) reduced basal levels of FST expression. ( E ) Inhibition of ERK activation by ADZ6244 blocks the EGF-mediated increase in FST expression in both A253 and SCC25 cells.

Article Snippet: Proteins were then electro-transferred to Immunoblot polyvinylidene difluoride membranes (Bio-Rad), which were incubated with the following antibodies: p63 4A4, FST (sc-365003 [Santa Cruz Biotechnology] or EPR10903 [Abcam]), pAKT ser-473 (66444-I-Ig; Proteintech), pAKT Thr-308 (29163-1-AP; Proteintech), pSTAT3 (Epitomics), STAT3 (2281-1; Epitomics), AKT1 (10176-2-AP; Proteintech), pERK1/2 (sc-7883; Santa Cruz Biotechnology), ERK1/2 (sc-66192-1-Ig [Proteintech] or sc-514302 [Santa Cruz Biotechnology]), GAPDH (MAB374; EMD Millipore), pSMAD2 (GTX13364; GeneTex), SMAD2 (GTX111075; GeneTex), pSMAD1/5 (41D10; Cell Signaling), and SMAD1 (D49D7; Cell Signaling).

Techniques: Expressing, Western Blot, Activation Assay, Inhibition, Phospho-proteomics

Journal: NAR Cancer

Article Title: An integrated genomic approach identifies follistatin as a target of the p63-epidermal growth factor receptor oncogenic network in head and neck squamous cell carcinoma

doi: 10.1093/narcan/zcad038

Figure Lengend Snippet: Epithelial cells are the primary producers of FST in the tumor microenvironment. ( A ) UMAP plot showing the identities of the various cellular clusters identified in the HNSCC single-cell RNA-seq data reported by Puram et al. . ( B ) Expression of FST by cells in the different clusters showing predominantly epithelial cell-specific expression. ( C ) UMAP plot showing that expression of TP63 is predominantly in epithelial cells. ( D ) EGFR expression in the different cellular clusters.

Article Snippet: Proteins were then electro-transferred to Immunoblot polyvinylidene difluoride membranes (Bio-Rad), which were incubated with the following antibodies: p63 4A4, FST (sc-365003 [Santa Cruz Biotechnology] or EPR10903 [Abcam]), pAKT ser-473 (66444-I-Ig; Proteintech), pAKT Thr-308 (29163-1-AP; Proteintech), pSTAT3 (Epitomics), STAT3 (2281-1; Epitomics), AKT1 (10176-2-AP; Proteintech), pERK1/2 (sc-7883; Santa Cruz Biotechnology), ERK1/2 (sc-66192-1-Ig [Proteintech] or sc-514302 [Santa Cruz Biotechnology]), GAPDH (MAB374; EMD Millipore), pSMAD2 (GTX13364; GeneTex), SMAD2 (GTX111075; GeneTex), pSMAD1/5 (41D10; Cell Signaling), and SMAD1 (D49D7; Cell Signaling).

Techniques: RNA Sequencing, Expressing

Journal: NAR Cancer

Article Title: An integrated genomic approach identifies follistatin as a target of the p63-epidermal growth factor receptor oncogenic network in head and neck squamous cell carcinoma

doi: 10.1093/narcan/zcad038

Figure Lengend Snippet: FST , EGFR and TP63 expression correlates with immune cell infiltration. FST , EGFR and TP63 expression correlated negatively with tumor suppressive T-lymphocyte infiltration ( A ) and positively with tumor-promoting myeloid suppressor cells ( B ) in HNSCC tissues. ( C ) Kaplan–Meier plot showing overall survival of cohorts of patients with high and low FST expression levels.

Article Snippet: Proteins were then electro-transferred to Immunoblot polyvinylidene difluoride membranes (Bio-Rad), which were incubated with the following antibodies: p63 4A4, FST (sc-365003 [Santa Cruz Biotechnology] or EPR10903 [Abcam]), pAKT ser-473 (66444-I-Ig; Proteintech), pAKT Thr-308 (29163-1-AP; Proteintech), pSTAT3 (Epitomics), STAT3 (2281-1; Epitomics), AKT1 (10176-2-AP; Proteintech), pERK1/2 (sc-7883; Santa Cruz Biotechnology), ERK1/2 (sc-66192-1-Ig [Proteintech] or sc-514302 [Santa Cruz Biotechnology]), GAPDH (MAB374; EMD Millipore), pSMAD2 (GTX13364; GeneTex), SMAD2 (GTX111075; GeneTex), pSMAD1/5 (41D10; Cell Signaling), and SMAD1 (D49D7; Cell Signaling).

Techniques: Expressing

Journal: Discover Oncology

Article Title: Spatial transcriptomics of urothelial carcinoma with basal/squamous differentiation identifies Galectin-7 as a specific marker of squamous lineage commitment

doi: 10.1007/s12672-026-04927-z

Figure Lengend Snippet: LGALS7 is selectively expressed in Ba/Sq differentiation and promotes squamous carcinoma cell proliferation. A The H&E image from Fig. B is shown again, with a red box indicating the region analyzed in this figure. Spatial transcriptomic maps display TP63 and LGALS7 expression patterns within the boxed region, corresponding to the UC–Ba/Sq interface. B Cluster-level expression of TP63 and LGALS7. C Immunohistochemistry (IHC) of the cystectomy specimen showing diffuse p63 positivity in both urothelial carcinoma (UC) and Ba/Sq-differentiated tumor components, and selective Galectin-7 expression restricted to Ba/Sq-differentiated tumor nests. Scale bars, 1 mm. D Western blot showing Galectin-7 expression across cancer cell lines (left), and immunofluorescence (IF) of SCaBER cells showing cytoplasmic localization (right). E Proliferation assay of SCaBER cells following LGALS7 knockdown

Article Snippet: Sections were then incubated overnight at 4 °C with primary antibodies against p63 (mouse monoclonal, clone 4A4, ready-to-use; Nichirei Biosciences) and Galectin-7 (rabbit monoclonal, clone EPR4287, 1:1500; Abcam).

Techniques: Expressing, Immunohistochemistry, Western Blot, Immunofluorescence, Proliferation Assay, Knockdown

Journal: Discover Oncology

Article Title: Spatial transcriptomics of urothelial carcinoma with basal/squamous differentiation identifies Galectin-7 as a specific marker of squamous lineage commitment

doi: 10.1007/s12672-026-04927-z

Figure Lengend Snippet: Diagnostic and prognostic value of Galectin-7 in urothelial carcinoma. A Immunohistochemistry (IHC) for p63 and Galectin-7 in UC with Ba/Sq features ( n = 28) and UC without Ba/Sq ( n = 64). B Immunohistochemistry (IHC) of three representative UC with Ba/Sq differentiation cases showing diffuse p63 positivity in both urothelial carcinoma (UC) and Ba/Sq-differentiated tumor components, and selective Galectin-7 expression restricted to Ba/Sq-differentiated tumor nests. Scale bars, 100 μm. C Summary of key clinicopathological parameters associated with Galectin-7 (G7) expression. Detailed clinicopathological data are provided in Supplementary Table 1. Kaplan–Meier analysis of progression-free survival stratified by Galectin-7 expression

Article Snippet: Sections were then incubated overnight at 4 °C with primary antibodies against p63 (mouse monoclonal, clone 4A4, ready-to-use; Nichirei Biosciences) and Galectin-7 (rabbit monoclonal, clone EPR4287, 1:1500; Abcam).

Techniques: Diagnostic Assay, Immunohistochemistry, Expressing

Journal: Cancer Research

Article Title: miR-31 Displays Subtype Specificity in Lung Cancer

doi: 10.1158/0008-5472.can-20-2769

Figure Lengend Snippet: Figure 1. miR-31 is overexpressed in specific histologic subtypes of lung cancer. A, IHC of patient tumors from each histologic subtype with markers of each (10) and ISH of miR-31 (100) depicting overexpression of miR-31 in lung adenocarcinoma (LUAD), SQCC, ADSQ, and LCNEC, but not in SCLC. TTF-1 is a marker of LUAD, p63 of SQCC, and synaptophysin (SYN) of neuroendocrine carcinomas. B and C, miR-31 levels determined with Taqman qRT-PCR. Expression normalized to endogenous control RNU6B. B, Archived patient tissue from 2016–2019 of normal, lung adenocarcinoma, SQCC, ADSQ, LCNEC, SCLC, and atypical carcinoid (AC) lung tumors. C, Cell lines. Mean miR-31 expression (error bars SEM: , P < 0.05; Student t test). Number (n) samples indicated.

Article Snippet: IHC was performed by Vanderbilt University Medical Center TPSR: anti-p63 antibody [4A4] SKU: CM163A, TTF-1 Leica PA0364, SYP Leica PA0299, CSK ProteinTech 17720–1 -AP, ATM Invitrogen MA5–32063, EPHB4 Cell Signaling Technology14960

Techniques: Over Expression, Marker, Quantitative RT-PCR, Expressing, Control