Review

trp73 (Cell Signaling Technology Inc)

Cell Signaling Technology Inc is a verified supplier

Cell Signaling Technology Inc manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cell Signaling Technology Inc trp73

(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) <t>TRP73</t> 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).

Trp73, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 52 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+p73/p73+Rabbit+mAb/bio_rxiv__64898__2026__02__09__704731-121-40-43
Average 94 stars, based on 52 article reviews

trp73 - by Bioz Stars, 2026-09

94/100 stars

Images

1) Product Images from "Cajal-Retzius fate specification is disrupted by constitutive activation of β-Catenin in hem progenitors"

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

Journal: bioRxiv

doi: 10.64898/2026.02.09.704731

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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 Used: Control, Derivative Assay, Expressing, Staining, Activity Assay, MANN-WHITNEY, IF-P

other:

Article Title: Actein enhances TRAIL effects on suppressing gastric cancer progression by activating p53/Caspase-3 signaling.
Article Snippet: Accepted Manuscript Actein enhances TRAIL effects on suppressing gastric cancer progression by activating p53/Caspase-3 signaling Zhi-Chao Yang, Ji Ma PII: S0006-291X(16)32036-8 DOI: 10.1016/j.bbrc.2016.11.162 Reference: YBBRC 36866 To appear in: Biochemical and Biophysical Research Communications Received Date: 23 November 2016 Accepted Date: 29 November 2016 Please cite this article as: Z.-C. Yang, J. Ma, Actein enhances TRAIL effects on suppressing gastric cancer progression by activating p53/Caspase-3 signaling, Biochemical and Biophysical Research Communications (2016), doi: 10.1016/j.bbrc.2016.11.162.. This is a PDF file of an unedited manuscript that has been accepted for publication.. As a service to our customers we are providing this early version of the manuscript.

Immunohistochemistry:

Article Title: GVHD-Related, Cytokine-Driven Apoptosis Depends on p73 in Cytokeratin 15-Positive Target Cells
Article Snippet: .. Antibodies The primary Ab used for immunohistochemistry and immunofluorescence were rat anti-mouse CD4 (BD Biosciences, San Diego, CA), mouse anti-K15 (Thermo Fisher Scientific, Fremont, CA), rabbit anti-p73 (Cell Signaling, Danvers, MA), rabbit anti-Phospho-p73(Tyr99) (Abcam, Cambridge, MA), sheep anti-digoxigenin (DIG)-peroxidase and sheep anti-DIG-fluorescein (Roche, Indianapolis, IN). .. The secondary Ab used were horse anti-mouse IgG-peroxidase (Vector laboratories, Burlingame, CA), goat anti-rabbit IgG-peroxidase (Vector Laboratories), donkey anti-mouse IgG-Alexa Fluor 488 (Invitrogen, Carlsbad, CA), donkey anti-rabbit IgG-Alexa Fluor 488 or 594 (Invitrogen), donkey anti-rat IgG-Alexa Fluor 594 (Invitrogen).

Article Title: GVHD-Related, Cytokine-Driven Apoptosis Depends on p73 in Cytokeratin 15-Positive Target Cells
Article Snippet: .. The primary Ab used for immunohistochemistry and immunofluorescence were rat anti-mouse CD4 (BD Biosciences, San Diego, CA), mouse anti-K15 (Thermo Fisher Scientific, Fremont, CA), rabbit anti-p73 (Cell Signaling, Danvers, MA), rabbit anti-Phospho-p73(Tyr99) (Abcam, Cambridge, MA), sheep anti-digoxigenin (DIG)-peroxidase and sheep anti-DIG-fluorescein (Roche, Indianapolis, IN). .. The secondary Ab used were horse anti-mouse IgG-peroxidase (Vector laboratories, Burlingame, CA), goat anti-rabbit IgG-peroxidase (Vector Laboratories), donkey anti-mouse IgG-Alexa Fluor 488 (Invitrogen, Carlsbad, CA), donkey anti-rabbit IgG-Alexa Fluor 488 or 594 (Invitrogen), donkey anti-rat IgG-Alexa Fluor 594 (Invitrogen).

Immunofluorescence:

Image Search Results

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

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

( A ) p73 protein expression following treatment with 10 µM Q12 (1, 6, 12, 24 h) compared to vehicle-treated (DMSO) control ( n = 3). ( B ) CDK8 protein expression in MDA-MB-468 cell line following 24 h treatment with 10 µM Q12 ( n = 3). Images are representative of three independent experiments. Error bars represent mean ± SD. Unpaired Student’s t -test was used to determine significance. ** ρ < 0.01.

Journal: International Journal of Molecular Sciences

Article Title: CDK8 Inhibition Increases E2F1 Transcriptional Activity and Promotes STAT3-Dependent Suppression of Mcl-1 in Triple-Negative Breast Cancer Cell Line MDA-MB-468

doi: 10.3390/ijms27020897

Figure Lengend Snippet: ( A ) p73 protein expression following treatment with 10 µM Q12 (1, 6, 12, 24 h) compared to vehicle-treated (DMSO) control ( n = 3). ( B ) CDK8 protein expression in MDA-MB-468 cell line following 24 h treatment with 10 µM Q12 ( n = 3). Images are representative of three independent experiments. Error bars represent mean ± SD. Unpaired Student’s t -test was used to determine significance. ** ρ < 0.01.

Article Snippet: Rabbit anti-E2F-1 (#3742S (dil. 1:1000)), anti-Cdk8 (G398, #4101S) (dil. 1:1000), anti-STAT3 (#30835S) (dil. 1:1000), anti-pSTAT3(S727) (#9134S) (dil. 1:1000), anti-p73 (#14620) (dil. 1:1000), and anti-GAPDH (4C10, #5174S) (dil. 1:5000) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Expressing, Control

(A) Gene expression in E12 CRs subtypes and other glutamatergic neurons from the dorsal and lateral cortex (extracted from https://apps.institutimagine.org/mouse_pallium/ ). (B) Expression of Nhlh2 per cell type and stage in scRNAseq data from the somatosensory cortex. Grey squares indicate no cells were sampled. Note that Nhlh2 expression is restricted to CRs except at early stages where it is also detected in intermediate progenitors and immature neurons. (C, D) In situ hybridization for Nhlh2 on coronal sections of the cerebral cortex from E14 (C) and E18 (D) control and Gmnc -/- embryos. The presence/absence of Nhlh2 + cells in the MZ is indicated by filled/empty arrowheads, respectively. (E) High magnification of the dorsal or lateral cortex MZ after in situ hybridization for Tbr1 and Calb2 at E18, and Lhx5 at P1. (F) In situ hybridization for Nhlh2 and Trp73 on coronal sections of the E18 hippocampus. (G) In situ hybridization for Trp73 on coronal sections of the E14 dorsomedial cortex. (H) Immunostaining for P73 on coronal sections of the E18 hippocampus and dorsomedial cortex. (I) Quantification of the density of P73 + cells in the hippocampal and neocortical MZ of E18 control and Gmnc -/- embryos. Each dot corresponds to one measurement, 3 animals (color-coded) and 3 rostro-caudal levels (shape) were considered. (J) Immunostaining for P73, and Tomato in the hippocampus at P0 following genetic tracing of hem derivatives in a Gmnc -/- background, showing residual hem-derived CRs in mutants. (K) Immunostaining for Tomato and DAPI in the dorsal cortex at P0 following genetic tracing of hem derivatives in either control or Gmnc -/- background, showing the complete absence of Tomato + cells in the mutant neocortical MZ. (L) Schematic representation of the temporal dynamics of CRs depletion in Gmnc -/- mutants. Scale bars: 200µm in C, F, G, H, 500µm in D, 50µm in high magnification panels in C, D, E and in J, K.

Journal: bioRxiv

Article Title: Differential contribution of P73 + Cajal-Retzius cells and Reelin to cortical morphogenesis

doi: 10.1101/2024.10.15.618167

Figure Lengend Snippet: (A) Gene expression in E12 CRs subtypes and other glutamatergic neurons from the dorsal and lateral cortex (extracted from https://apps.institutimagine.org/mouse_pallium/ ). (B) Expression of Nhlh2 per cell type and stage in scRNAseq data from the somatosensory cortex. Grey squares indicate no cells were sampled. Note that Nhlh2 expression is restricted to CRs except at early stages where it is also detected in intermediate progenitors and immature neurons. (C, D) In situ hybridization for Nhlh2 on coronal sections of the cerebral cortex from E14 (C) and E18 (D) control and Gmnc -/- embryos. The presence/absence of Nhlh2 + cells in the MZ is indicated by filled/empty arrowheads, respectively. (E) High magnification of the dorsal or lateral cortex MZ after in situ hybridization for Tbr1 and Calb2 at E18, and Lhx5 at P1. (F) In situ hybridization for Nhlh2 and Trp73 on coronal sections of the E18 hippocampus. (G) In situ hybridization for Trp73 on coronal sections of the E14 dorsomedial cortex. (H) Immunostaining for P73 on coronal sections of the E18 hippocampus and dorsomedial cortex. (I) Quantification of the density of P73 + cells in the hippocampal and neocortical MZ of E18 control and Gmnc -/- embryos. Each dot corresponds to one measurement, 3 animals (color-coded) and 3 rostro-caudal levels (shape) were considered. (J) Immunostaining for P73, and Tomato in the hippocampus at P0 following genetic tracing of hem derivatives in a Gmnc -/- background, showing residual hem-derived CRs in mutants. (K) Immunostaining for Tomato and DAPI in the dorsal cortex at P0 following genetic tracing of hem derivatives in either control or Gmnc -/- background, showing the complete absence of Tomato + cells in the mutant neocortical MZ. (L) Schematic representation of the temporal dynamics of CRs depletion in Gmnc -/- mutants. Scale bars: 200µm in C, F, G, H, 500µm in D, 50µm in high magnification panels in C, D, E and in J, K.

Article Snippet: The following primary antibodies were used: goat anti-Brn2 (POU3F2, Abcam ab101726 1:1000), rat anti-CTIP2 (BCL11B, Abcam ab18465 1:600), rabbit anti-FOXG1 (Abcam ab18259 1:2000), rabbit anti-Laminin (Sigma-Aldrich L9393 1:600), goat anti-Neuropilin-1 (R&D Systems AF566 1:800), rabbit anti-p73 (Cell signaling 14620 1:250), goat anti-Nurr1 (NR4A2, R&D Systems AF2156 1:200), goat anti-Prox1 (R&D Systems AF2727 1:1000), goat anti-Reelin (R&D Systems AF3820 1:2000), rabbit anti-TBR1 (Abcam ab31940 1:1000).

Techniques: Expressing, In Situ Hybridization, Control, Immunostaining, Derivative Assay, Mutagenesis

Journal: Cell reports

Article Title: Ceramide-induced cleavage of GPR64 intracellular domain drives Ewing sarcoma

doi: 10.1016/j.celrep.2024.114497

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: The following antibodies were used: sheep polyclonal anti-GPR64 (AF7977, R & D Systems); rabbit polyclonal anti-GPR64 C terminus (GTX70517, GeneTex); goat polyclonal anti-SMPD1 (AF5348, R & D Systems); mouse monoclonal anti-tubulin (DM1A, Thermo Fisher Scientific); mouse monoclonal anti-FLAG (F1804, Sigma-Aldrich); rabbit polyclonal anti-FLI1 (ab15289, Abcam), rabbit monoclonal anti-HA (3724, Cell Signaling Technology); rabbit monoclonal anti-Phospho-CREB (Ser133) (9198, Cell Signaling Technology); rabbit monoclonal anti-CREB (9197, Cell Signaling Technology); rabbit monoclonal anti-RIF1 (95558, Cell Signaling Technology); rabbit polyclonal anti-SPOP (16750-1-AP, Proteintech); mouse monoclonal anti-p21 (2946, Cell Signaling Technology); mouse monoclonal anti-p27 (sc-528, Santa Cruz Biotechnology); rabbit polyclonal antibody anti-p16 (sc-468, Santa Cruz Biotechnology); rabbit monoclonal anti-p73 (14620, Cell Signaling Technology); rabbit monoclonal anti-β3-Tubulin (5568, Cell Signaling Technology); rabbit monoclonal anti-Neurofilament-L (2837, Cell Signaling Technology); rabbit monoclonal anti-caspase-3 (9665, Cell Signaling Technology); mouse monoclonal anti-PARP1 (9542,Cell Signaling Technology); anti-rabbit IgG, HRP-linked antibody (7074, Cell Signaling Technology); anti-mouse IgG, HRP-linked antibody (7076, Cell Signaling Technology); rabbit anti-goat IgG HRP-linked antibody (HAF017, R & D Systems); and donkey anti-Sheep IgG HRP-linked antibody (HAF016, R & D Systems).

Techniques: Control, Virus, Recombinant, Transfection, SYBR Green Assay, Reverse Transcription, Enzyme-linked Immunosorbent Assay, Mass Spectrometry, Plasmid Preparation

Review

trp73 (Cell Signaling Technology Inc)

Structured Review

Images

1) Product Images from "Cajal-Retzius fate specification is disrupted by constitutive activation of β-Catenin in hem progenitors"

Related Articles

other:

Immunohistochemistry:

Immunofluorescence:

Similar Products

Image Search Results