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goat polyclonal antibody against collagen type iii  (SouthernBiotech)


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    Structured Review

    SouthernBiotech goat polyclonal antibody against collagen type iii
    Immunohistochemistry and unstained SHG images of conjunctival tissues from healthy controls participants and patients with chronic ocular SJS. Left and middle panels showing representative raw immunohistology and corresponding processed grayscale images highlighting collagen Type 1 and Type 3 in the conjunctiva of control and diseased subjects; the green represents antibody positive signals and blue represents cell nuclei; Right panels show representative SHG images of the same control patient and diseased patients; red demarcation line represents the region of interest; bar graph showing higher <t>collagen</t> <t>III</t> / I ratio in diseased tissues compared to normal controls.
    Goat Polyclonal Antibody Against Collagen Type Iii, supplied by SouthernBiotech, used in various techniques. Bioz Stars score: 94/100, based on 151 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/goat polyclonal antibody against collagen type iii/product/SouthernBiotech
    Average 94 stars, based on 151 article reviews
    goat polyclonal antibody against collagen type iii - by Bioz Stars, 2026-04
    94/100 stars

    Images

    1) Product Images from "Quantitative Stain-Free Conjunctival Collagen Imaging in Cicatrizing Conjunctivitis Using Second Harmonic Generation-Two Photon Excitation Technology"

    Article Title: Quantitative Stain-Free Conjunctival Collagen Imaging in Cicatrizing Conjunctivitis Using Second Harmonic Generation-Two Photon Excitation Technology

    Journal: Investigative Ophthalmology & Visual Science

    doi: 10.1167/iovs.66.4.49

    Immunohistochemistry and unstained SHG images of conjunctival tissues from healthy controls participants and patients with chronic ocular SJS. Left and middle panels showing representative raw immunohistology and corresponding processed grayscale images highlighting collagen Type 1 and Type 3 in the conjunctiva of control and diseased subjects; the green represents antibody positive signals and blue represents cell nuclei; Right panels show representative SHG images of the same control patient and diseased patients; red demarcation line represents the region of interest; bar graph showing higher collagen III / I ratio in diseased tissues compared to normal controls.
    Figure Legend Snippet: Immunohistochemistry and unstained SHG images of conjunctival tissues from healthy controls participants and patients with chronic ocular SJS. Left and middle panels showing representative raw immunohistology and corresponding processed grayscale images highlighting collagen Type 1 and Type 3 in the conjunctiva of control and diseased subjects; the green represents antibody positive signals and blue represents cell nuclei; Right panels show representative SHG images of the same control patient and diseased patients; red demarcation line represents the region of interest; bar graph showing higher collagen III / I ratio in diseased tissues compared to normal controls.

    Techniques Used: Immunohistochemistry, Control



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    Fig. 2. CAR suppressed TAC-induced myocardial inflammation and fibrosis in mice. (A) Staining ventricular sections with Masson’s trichrome and quantifying fibrotic areas; (B) Immunofluorescence <t>labeling</t> <t>Collagen</t> <t>III</t> in ventricular sections and quantifying Collagen III positive cell areas; (C) Analyzing Collagen III mRNA levels in each group using qPCR; (D) Displaying H&E staining in upper ventricular sections. Showing IHC staining of CD68 in lower ventricular sections and quantifying CD68 positive cell areas on the right; (E) Analyzing Il1β mRNA levels in each group using qPCR; (F) Detected the protein level of NLRP3, Collagen III and β-actin in each group by Western Blot. Data are presented as mean±SD, two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6; For WB experiments, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.
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    Image Search Results


    Fig. 3 Matrix stiffness mediated by CAFs is closely associated with HCC. (A) Clustering results for aneuploid and euploid samples. The ordinate represents cells, and the abscissa represents chromosome positions. Orange indicates an increase in DNA copy number, while blue indicates a decrease in DNA copy number. (B) The distribution of tumor cells and non-tumor cells after reordering. (C) UMAP visualization of the positional distribution of tumor cells and non-tumor cells. (D) The proportion of tumor cells and non-tumor cells in CAFs across different clusters. (E) The proportion of CAFs from different clusters within tumor cells and non-tumor cells. (F-I) The expression level of COL1A1, COL1A2, COL3A1 and LOX in CAFs from different clusters. (J-M) Violin plot of COL1A1, COL1A2, COL3A1 and LOX expression in tumor tissues, normal tissues, PVTT, and lymph node tissues corresponding to cluster2-CAFs

    Journal: Journal of translational medicine

    Article Title: CAFs activated by YAP1 upregulate cancer matrix stiffness to mediate hepatocellular carcinoma progression.

    doi: 10.1186/s12967-025-06325-5

    Figure Lengend Snippet: Fig. 3 Matrix stiffness mediated by CAFs is closely associated with HCC. (A) Clustering results for aneuploid and euploid samples. The ordinate represents cells, and the abscissa represents chromosome positions. Orange indicates an increase in DNA copy number, while blue indicates a decrease in DNA copy number. (B) The distribution of tumor cells and non-tumor cells after reordering. (C) UMAP visualization of the positional distribution of tumor cells and non-tumor cells. (D) The proportion of tumor cells and non-tumor cells in CAFs across different clusters. (E) The proportion of CAFs from different clusters within tumor cells and non-tumor cells. (F-I) The expression level of COL1A1, COL1A2, COL3A1 and LOX in CAFs from different clusters. (J-M) Violin plot of COL1A1, COL1A2, COL3A1 and LOX expression in tumor tissues, normal tissues, PVTT, and lymph node tissues corresponding to cluster2-CAFs

    Article Snippet: Primary antibodies against COL3A1 (Proteintech, cat.22734-1-AP, 1:1000), YAP1 (Proteintech, cat.135841-AP, 1:3000), COL1A1 (Immunoway, cat. YM 4807, 1:1000), COL1A2 (Immunoway, cat.YT1019, 1:1000), LOX (Immunoway, cat. YN 4611, 1:1000) and GAPDH (Proteintech, cat. No. 60004-1-Ig, 1:50,000) were used for Western blotting.

    Techniques: Expressing

    Fig. 4 High matrix stiffness is negatively correlated with the prognosis of HCC patients. (A-D) Expression levels of COL1A1, COL1A2, COL3A1 and LOX in cancer and normal liver tissues. (E-H) Survival curve for HCC patients with different expression levels of COL1A1, COL1A2, COL3A1 and LOX. * P<0.05

    Journal: Journal of translational medicine

    Article Title: CAFs activated by YAP1 upregulate cancer matrix stiffness to mediate hepatocellular carcinoma progression.

    doi: 10.1186/s12967-025-06325-5

    Figure Lengend Snippet: Fig. 4 High matrix stiffness is negatively correlated with the prognosis of HCC patients. (A-D) Expression levels of COL1A1, COL1A2, COL3A1 and LOX in cancer and normal liver tissues. (E-H) Survival curve for HCC patients with different expression levels of COL1A1, COL1A2, COL3A1 and LOX. * P<0.05

    Article Snippet: Primary antibodies against COL3A1 (Proteintech, cat.22734-1-AP, 1:1000), YAP1 (Proteintech, cat.135841-AP, 1:3000), COL1A1 (Immunoway, cat. YM 4807, 1:1000), COL1A2 (Immunoway, cat.YT1019, 1:1000), LOX (Immunoway, cat. YN 4611, 1:1000) and GAPDH (Proteintech, cat. No. 60004-1-Ig, 1:50,000) were used for Western blotting.

    Techniques: Expressing

    Fig. 9 Verification of cell experiments and animal experiments. (A, B) Tumor volume and Tumor weight distribution maps of the control group, Vertepor fin treatment group and K-975 treatment group. (C-H) The mRNA and protein expression levels of YAP1, COL1A1, COL1A2, COL3A1, and LOX were analyzed in CAFs from the control group, the group treated with Verteporfin, and the group treated with K-975. (I, J) The concentrations of COL1A1 and COL1A2 in the supernatants of CAFs from the control group and the K-975 treatment group were measured. * P<0.05, **P<0.01, ***P<0.001

    Journal: Journal of translational medicine

    Article Title: CAFs activated by YAP1 upregulate cancer matrix stiffness to mediate hepatocellular carcinoma progression.

    doi: 10.1186/s12967-025-06325-5

    Figure Lengend Snippet: Fig. 9 Verification of cell experiments and animal experiments. (A, B) Tumor volume and Tumor weight distribution maps of the control group, Vertepor fin treatment group and K-975 treatment group. (C-H) The mRNA and protein expression levels of YAP1, COL1A1, COL1A2, COL3A1, and LOX were analyzed in CAFs from the control group, the group treated with Verteporfin, and the group treated with K-975. (I, J) The concentrations of COL1A1 and COL1A2 in the supernatants of CAFs from the control group and the K-975 treatment group were measured. * P<0.05, **P<0.01, ***P<0.001

    Article Snippet: Primary antibodies against COL3A1 (Proteintech, cat.22734-1-AP, 1:1000), YAP1 (Proteintech, cat.135841-AP, 1:3000), COL1A1 (Immunoway, cat. YM 4807, 1:1000), COL1A2 (Immunoway, cat.YT1019, 1:1000), LOX (Immunoway, cat. YN 4611, 1:1000) and GAPDH (Proteintech, cat. No. 60004-1-Ig, 1:50,000) were used for Western blotting.

    Techniques: Control, Expressing

    Immunohistochemistry and unstained SHG images of conjunctival tissues from healthy controls participants and patients with chronic ocular SJS. Left and middle panels showing representative raw immunohistology and corresponding processed grayscale images highlighting collagen Type 1 and Type 3 in the conjunctiva of control and diseased subjects; the green represents antibody positive signals and blue represents cell nuclei; Right panels show representative SHG images of the same control patient and diseased patients; red demarcation line represents the region of interest; bar graph showing higher collagen III / I ratio in diseased tissues compared to normal controls.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Quantitative Stain-Free Conjunctival Collagen Imaging in Cicatrizing Conjunctivitis Using Second Harmonic Generation-Two Photon Excitation Technology

    doi: 10.1167/iovs.66.4.49

    Figure Lengend Snippet: Immunohistochemistry and unstained SHG images of conjunctival tissues from healthy controls participants and patients with chronic ocular SJS. Left and middle panels showing representative raw immunohistology and corresponding processed grayscale images highlighting collagen Type 1 and Type 3 in the conjunctiva of control and diseased subjects; the green represents antibody positive signals and blue represents cell nuclei; Right panels show representative SHG images of the same control patient and diseased patients; red demarcation line represents the region of interest; bar graph showing higher collagen III / I ratio in diseased tissues compared to normal controls.

    Article Snippet: Sections on the slides were initially washed in 1× PBS (1st BASE), permeabilized with 0.15% Triton X-100 (Sigma-Aldrich) for 30 minutes, blocked with 2% bovine serum albumin (Sigma-Aldrich) and 5% normal goat serum (Thermo Fisher Scientific) for one hour, and double-stained with a mouse monoclonal antibody against collagen type I (Sigma-Aldrich) and a goat polyclonal antibody against collagen type III (Southern Biotech, Birmingham, AL, USA) at 4°C overnight.

    Techniques: Immunohistochemistry, Control

    Fig. 2. CAR suppressed TAC-induced myocardial inflammation and fibrosis in mice. (A) Staining ventricular sections with Masson’s trichrome and quantifying fibrotic areas; (B) Immunofluorescence labeling Collagen III in ventricular sections and quantifying Collagen III positive cell areas; (C) Analyzing Collagen III mRNA levels in each group using qPCR; (D) Displaying H&E staining in upper ventricular sections. Showing IHC staining of CD68 in lower ventricular sections and quantifying CD68 positive cell areas on the right; (E) Analyzing Il1β mRNA levels in each group using qPCR; (F) Detected the protein level of NLRP3, Collagen III and β-actin in each group by Western Blot. Data are presented as mean±SD, two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6; For WB experiments, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.

    Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

    Article Title: Cardamonin intervenes in myocardial hypertrophy progression by regulating Usp18.

    doi: 10.1016/j.phymed.2024.155970

    Figure Lengend Snippet: Fig. 2. CAR suppressed TAC-induced myocardial inflammation and fibrosis in mice. (A) Staining ventricular sections with Masson’s trichrome and quantifying fibrotic areas; (B) Immunofluorescence labeling Collagen III in ventricular sections and quantifying Collagen III positive cell areas; (C) Analyzing Collagen III mRNA levels in each group using qPCR; (D) Displaying H&E staining in upper ventricular sections. Showing IHC staining of CD68 in lower ventricular sections and quantifying CD68 positive cell areas on the right; (E) Analyzing Il1β mRNA levels in each group using qPCR; (F) Detected the protein level of NLRP3, Collagen III and β-actin in each group by Western Blot. Data are presented as mean±SD, two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6; For WB experiments, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.

    Article Snippet: They were blocked with 5 %bovine serum albumin (BSA) at room temperature for 1 hour, followed by the addition of primary antibody against Collagen III (1:150, 22,734–1-AP, Proteintech), CD68 (1:200, ARG10514, arigobio) drops to the sections, incubated at 4 ◦C overnight, re-washed sections with PBS, and incubated with a Goat anti-Rabbit IgG (H + l) Highly Cross-Adsorbed Secondary Antibody, Alexa FluorTM Plus 488 (Invitrogen, A32731) or Goat antiMouse IgG (H + l) Highly Cross-Adsorbed Secondary Antibody, Alexa FluorTM Plus 555 (Invitrogen, A32727) at room temperature for 1 hour.

    Techniques: Staining, Immunofluorescence, Labeling, Immunohistochemistry, Western Blot, In Vivo

    Fig. 5. Usp18 knockout can inhibit the anti-inflammatory and anti-fibrotic effects of CAR. (A) Ventricular sections were stained using Masson’s trichrome technique (upper), and Collagen III (lower) immunofluorescence. (B) The mRNA levels of Collagen III were measured in each group using qPCR. (C) Ventricular sections were stained with H&E (upper) and immunohistochemistry using the CD68 antibody (lower), with quantification of CD68 positive cell areas (right); (D) The mRNA levels of Il1β were measured in each group using qPCR. Data are presented as mean±SD. two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.

    Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

    Article Title: Cardamonin intervenes in myocardial hypertrophy progression by regulating Usp18.

    doi: 10.1016/j.phymed.2024.155970

    Figure Lengend Snippet: Fig. 5. Usp18 knockout can inhibit the anti-inflammatory and anti-fibrotic effects of CAR. (A) Ventricular sections were stained using Masson’s trichrome technique (upper), and Collagen III (lower) immunofluorescence. (B) The mRNA levels of Collagen III were measured in each group using qPCR. (C) Ventricular sections were stained with H&E (upper) and immunohistochemistry using the CD68 antibody (lower), with quantification of CD68 positive cell areas (right); (D) The mRNA levels of Il1β were measured in each group using qPCR. Data are presented as mean±SD. two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.

    Article Snippet: They were blocked with 5 %bovine serum albumin (BSA) at room temperature for 1 hour, followed by the addition of primary antibody against Collagen III (1:150, 22,734–1-AP, Proteintech), CD68 (1:200, ARG10514, arigobio) drops to the sections, incubated at 4 ◦C overnight, re-washed sections with PBS, and incubated with a Goat anti-Rabbit IgG (H + l) Highly Cross-Adsorbed Secondary Antibody, Alexa FluorTM Plus 488 (Invitrogen, A32731) or Goat antiMouse IgG (H + l) Highly Cross-Adsorbed Secondary Antibody, Alexa FluorTM Plus 555 (Invitrogen, A32727) at room temperature for 1 hour.

    Techniques: Knock-Out, Staining, Immunofluorescence, Immunohistochemistry, In Vivo

    Fig. 6. Cardiac-specific overexpression of Usp18 can improve the anti-cardiac remodeling effects of CAR. (A) Experimental operation flowchart; (B) each group of HW/BW ratios; (B) Detected the mRNA level of Nox4 in ecah group by qPCR; (C) Representative M-mode echocardiography of left ventricular chamber and each group of echocardiographic assessment of EF%; (D) DHE staining of cardiac sections in ecah group; (E) WGA staining of cardiac sections in ecah group; (F) Illustration of ventricular sections with Representative H&E staining; (G) Visualization of Collagen III in ventricular sections along with Representative IF and quantification of Collagen III-positive cell areas. Data are presented as mean±SD, Student’s t-test for AAV9-control vs AAV9-Usp18. two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.

    Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

    Article Title: Cardamonin intervenes in myocardial hypertrophy progression by regulating Usp18.

    doi: 10.1016/j.phymed.2024.155970

    Figure Lengend Snippet: Fig. 6. Cardiac-specific overexpression of Usp18 can improve the anti-cardiac remodeling effects of CAR. (A) Experimental operation flowchart; (B) each group of HW/BW ratios; (B) Detected the mRNA level of Nox4 in ecah group by qPCR; (C) Representative M-mode echocardiography of left ventricular chamber and each group of echocardiographic assessment of EF%; (D) DHE staining of cardiac sections in ecah group; (E) WGA staining of cardiac sections in ecah group; (F) Illustration of ventricular sections with Representative H&E staining; (G) Visualization of Collagen III in ventricular sections along with Representative IF and quantification of Collagen III-positive cell areas. Data are presented as mean±SD, Student’s t-test for AAV9-control vs AAV9-Usp18. two-way ANOVA analyses were conducted to assess the statistical differences between the groups. For in vivo experiments, n = 6. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns=not significant.

    Article Snippet: They were blocked with 5 %bovine serum albumin (BSA) at room temperature for 1 hour, followed by the addition of primary antibody against Collagen III (1:150, 22,734–1-AP, Proteintech), CD68 (1:200, ARG10514, arigobio) drops to the sections, incubated at 4 ◦C overnight, re-washed sections with PBS, and incubated with a Goat anti-Rabbit IgG (H + l) Highly Cross-Adsorbed Secondary Antibody, Alexa FluorTM Plus 488 (Invitrogen, A32731) or Goat antiMouse IgG (H + l) Highly Cross-Adsorbed Secondary Antibody, Alexa FluorTM Plus 555 (Invitrogen, A32727) at room temperature for 1 hour.

    Techniques: Over Expression, Staining, Control, In Vivo

    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers (COL I, COL III, α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: International Journal of Nanomedicine

    Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

    doi: 10.2147/ijn.s466312

    Figure Lengend Snippet: Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers (COL I, COL III, α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: Evaluation of Anti-Fibrotic Effects of the Biomaterials by Immunofluorescent Staining at Six Weeks The fresh tissue sections were incubated with rabbit anti-rat antibodies against COL III (1:200; Cat#22734-1-AP, Proteintech, USA) and α-SMA (1:200; Cat#19245S, Cell Signaling Technology, USA) at 4°C overnight.

    Techniques: Immunofluorescence, Staining, Membrane

    Figure 6 RCDs/UA@Lipo-HAMA reduced adhesion of injured tendons at macroscopic and histological levels at various time points post-injury. (A) Schematic diagram of surgical procedures of the ATI. (B) Gross view of ATI. (C)Representative images of immunofluorescence staining of tendon antioxidant (Nrf-2, HO-1) and anti-inflammatory markers (CD68, iNOS) at 2 weeks post-injury (n = 3). (D) Representative images of immunofluorescence staining of tendon antifibrosis (COL III, α-SMA) at 6 weeks post- injury (n = 3). (E) Representative images of immunohistochemical staining of tendon markers (Vimentin, MMP2, α-SMA) antifibrosis at 6 weeks post-injury (n = 4). (F–N) Semiquantitative analysis of expression level of tendon marker of (C–E), respectively. Data are presented as mean ± SD; comparisons between the groups were performed by one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: International Journal of Nanomedicine

    Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

    doi: 10.2147/ijn.s466312

    Figure Lengend Snippet: Figure 6 RCDs/UA@Lipo-HAMA reduced adhesion of injured tendons at macroscopic and histological levels at various time points post-injury. (A) Schematic diagram of surgical procedures of the ATI. (B) Gross view of ATI. (C)Representative images of immunofluorescence staining of tendon antioxidant (Nrf-2, HO-1) and anti-inflammatory markers (CD68, iNOS) at 2 weeks post-injury (n = 3). (D) Representative images of immunofluorescence staining of tendon antifibrosis (COL III, α-SMA) at 6 weeks post- injury (n = 3). (E) Representative images of immunohistochemical staining of tendon markers (Vimentin, MMP2, α-SMA) antifibrosis at 6 weeks post-injury (n = 4). (F–N) Semiquantitative analysis of expression level of tendon marker of (C–E), respectively. Data are presented as mean ± SD; comparisons between the groups were performed by one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: Evaluation of Anti-Fibrotic Effects of the Biomaterials by Immunofluorescent Staining at Six Weeks The fresh tissue sections were incubated with rabbit anti-rat antibodies against COL III (1:200; Cat#22734-1-AP, Proteintech, USA) and α-SMA (1:200; Cat#19245S, Cell Signaling Technology, USA) at 4°C overnight.

    Techniques: Immunofluorescence, Staining, Immunohistochemical staining, Expressing, Marker