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Mouse Monoclonal Anti Tubulin E7, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc anti β actin mouse monoclonal antibody
Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. <t>β-Actin</t> was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
Anti β Actin Mouse Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Merck & Co mouse monoclonal anti tuj1
Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. <t>β-Actin</t> was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
Mouse Monoclonal Anti Tuj1, supplied by Merck & Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology mouse monoclonal anti c fos e 8
Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. <t>β-Actin</t> was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
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Developmental Studies Hybridoma Bank mouse monoclonal anti fasciculin iii
Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. <t>β-Actin</t> was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
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OriGene villin antibodies
<t>Immunohistochemical</t> staining results suggesting that the tumor is an intestinal-type adenocarcinoma. Original magnification, ×100. (A) CK7(−), (B) CK20(+), (C) CDX2(+) and (D) <t>villin(+).</t> CK, cytokeratin; CDX2, caudal-type homeobox 2.
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OriGene eber monoclonal antibody
Pathology and IHC of the pulmonary lymphoepithelioma-like carcinoma. (A and B) Histological analysis. (A) heterologous cells were arranged in clusters (magnification, ×40); (B) the nuclei of heterologous cells were vacuolated and the nucleoli were clear (magnification, ×200; H&E staining); the arrows point at heterologous cells. (C-I) IHC analysis. (C) Cytoplasmic CK5/6 was positive, the arrows point at positive CK5/6 cytoplasm; (D) nuclear P40 was positive; the arrows point at positive P40 nuclear; (E) thyroid transcription factor-1 was negative; (F) Napsin A was negative; (G) nuclear <t>EBER</t> was positive; the arrows point at positive EBER nuclear; (H) proliferation index Ki-67 positive ~50%, the arrows point at positive Ki-67 nuclear; (I) PD-L1 detection microscopic image: Tumor proportion score=55% (magnification, ×100), the arrows point at positive PD-L1 nuclear. CK, cytokeratin; PD-L1, programmed cell death ligand 1; EBER, Epstein-Barr virus-encoded small RNA; IHC, immunohistochemistry.
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Proteintech mouse anti gapdh
Pathology and IHC of the pulmonary lymphoepithelioma-like carcinoma. (A and B) Histological analysis. (A) heterologous cells were arranged in clusters (magnification, ×40); (B) the nuclei of heterologous cells were vacuolated and the nucleoli were clear (magnification, ×200; H&E staining); the arrows point at heterologous cells. (C-I) IHC analysis. (C) Cytoplasmic CK5/6 was positive, the arrows point at positive CK5/6 cytoplasm; (D) nuclear P40 was positive; the arrows point at positive P40 nuclear; (E) thyroid transcription factor-1 was negative; (F) Napsin A was negative; (G) nuclear <t>EBER</t> was positive; the arrows point at positive EBER nuclear; (H) proliferation index Ki-67 positive ~50%, the arrows point at positive Ki-67 nuclear; (I) PD-L1 detection microscopic image: Tumor proportion score=55% (magnification, ×100), the arrows point at positive PD-L1 nuclear. CK, cytokeratin; PD-L1, programmed cell death ligand 1; EBER, Epstein-Barr virus-encoded small RNA; IHC, immunohistochemistry.
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Image Search Results


Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

Journal: Cancer Pathogenesis and Therapy

Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target

doi: 10.1016/j.cpt.2025.08.002

Figure Lengend Snippet: Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

Article Snippet: Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an anti-β-actin mouse monoclonal antibody (Cat# 3700, CST, MA, USA).

Techniques: Knockdown, Staining, Fluorescence, Membrane, Quantitative RT-PCR, Quantitation Assay, Activity Assay, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction

Immunohistochemical staining results suggesting that the tumor is an intestinal-type adenocarcinoma. Original magnification, ×100. (A) CK7(−), (B) CK20(+), (C) CDX2(+) and (D) villin(+). CK, cytokeratin; CDX2, caudal-type homeobox 2.

Journal: Oncology Letters

Article Title: Comprehensive treatment for intracranial invasive sinonasal intestinal-type adenocarcinoma with a focus on radiotherapy dosage and immunological combination therapy: A case report

doi: 10.3892/ol.2026.15571

Figure Lengend Snippet: Immunohistochemical staining results suggesting that the tumor is an intestinal-type adenocarcinoma. Original magnification, ×100. (A) CK7(−), (B) CK20(+), (C) CDX2(+) and (D) villin(+). CK, cytokeratin; CDX2, caudal-type homeobox 2.

Article Snippet: Immunohistochemical staining with CK7, CK20, CDX-2 and villin antibodies (Beijing Zhongshan Jinqiao Biotechnology Co., Ltd.) was performed by the Department of Pathology.

Techniques: Immunohistochemical staining, Staining

Pathology and IHC of the pulmonary lymphoepithelioma-like carcinoma. (A and B) Histological analysis. (A) heterologous cells were arranged in clusters (magnification, ×40); (B) the nuclei of heterologous cells were vacuolated and the nucleoli were clear (magnification, ×200; H&E staining); the arrows point at heterologous cells. (C-I) IHC analysis. (C) Cytoplasmic CK5/6 was positive, the arrows point at positive CK5/6 cytoplasm; (D) nuclear P40 was positive; the arrows point at positive P40 nuclear; (E) thyroid transcription factor-1 was negative; (F) Napsin A was negative; (G) nuclear EBER was positive; the arrows point at positive EBER nuclear; (H) proliferation index Ki-67 positive ~50%, the arrows point at positive Ki-67 nuclear; (I) PD-L1 detection microscopic image: Tumor proportion score=55% (magnification, ×100), the arrows point at positive PD-L1 nuclear. CK, cytokeratin; PD-L1, programmed cell death ligand 1; EBER, Epstein-Barr virus-encoded small RNA; IHC, immunohistochemistry.

Journal: Oncology Letters

Article Title: Adjuvant immunotherapy plus chemotherapy and maintenance immunotherapy for pulmonary lymphoepithelioma-like carcinoma with hepatitis B virus infection, KRAS mutation and high expression of programmed death ligand 1: A case report

doi: 10.3892/ol.2026.15612

Figure Lengend Snippet: Pathology and IHC of the pulmonary lymphoepithelioma-like carcinoma. (A and B) Histological analysis. (A) heterologous cells were arranged in clusters (magnification, ×40); (B) the nuclei of heterologous cells were vacuolated and the nucleoli were clear (magnification, ×200; H&E staining); the arrows point at heterologous cells. (C-I) IHC analysis. (C) Cytoplasmic CK5/6 was positive, the arrows point at positive CK5/6 cytoplasm; (D) nuclear P40 was positive; the arrows point at positive P40 nuclear; (E) thyroid transcription factor-1 was negative; (F) Napsin A was negative; (G) nuclear EBER was positive; the arrows point at positive EBER nuclear; (H) proliferation index Ki-67 positive ~50%, the arrows point at positive Ki-67 nuclear; (I) PD-L1 detection microscopic image: Tumor proportion score=55% (magnification, ×100), the arrows point at positive PD-L1 nuclear. CK, cytokeratin; PD-L1, programmed cell death ligand 1; EBER, Epstein-Barr virus-encoded small RNA; IHC, immunohistochemistry.

Article Snippet: Hybridization in situ : EBER monoclonal antibody (cat. no. 25080502; dilution, ready-to-use; Beijing Zhongshan Jinqiao Biotechnology Co., Ltd.).

Techniques: Staining, Virus, Immunohistochemistry