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A. Representative Hematoxylin and Eosin stained image of healthy skin and skin of patients with myeloid sarcoma (left), representative spatial transcriptomics plot annotated by cluster/tissue region (middle), and SPN/CD43 expression marking the myeloid sarcoma (right). B. Split UMAP visualization of spatial spots annotated by cluster/spatial region. C. Quantification of cluster abundance in each patient. D. UMAPs show expression of epithelial-mesenchymal transition (EMT) transcription factors <t>ZEB2</t> and SNAI2, and the KRAS activity Hallmark UCell score. E. Spatial transcriptomics plots showing ZEB2, SNAI2, and KRAS activity up Hallmark UCell score in healthy skin and skin with myeloid sarcoma. F. Myeloid sarcoma blasts showing expression of the EMT marker ZEB2 (Immunohistochemistry <t>(IHC)</t> with hematoxylin counterstain, 100x).
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A. Representative Hematoxylin and Eosin stained image of healthy skin and skin of patients with myeloid sarcoma (left), representative spatial transcriptomics plot annotated by cluster/tissue region (middle), and SPN/CD43 expression marking the myeloid sarcoma (right). B. Split UMAP visualization of spatial spots annotated by cluster/spatial region. C. Quantification of cluster abundance in each patient. D. UMAPs show expression of epithelial-mesenchymal transition (EMT) transcription factors <t>ZEB2</t> and SNAI2, and the KRAS activity Hallmark UCell score. E. Spatial transcriptomics plots showing ZEB2, SNAI2, and KRAS activity up Hallmark UCell score in healthy skin and skin with myeloid sarcoma. F. Myeloid sarcoma blasts showing expression of the EMT marker ZEB2 (Immunohistochemistry <t>(IHC)</t> with hematoxylin counterstain, 100x).
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SCAND1 promotes colorectal cancer cell proliferation, anti-apoptotic, migration, invasion, and EMT. ( A ) SCAND1 protein expression in normal and various colorectal cancer cell lines. ( B - C ) Protein ( B ) and mRNA ( C ) expression levels of SCAND1 were detected by western blotting and RT-qPCR. ( D ) EDU assay analysis. ( E ) Apoptosis rate was detected by flow cytometry. ( F - G ) Wound healing, migration and invasion assay analysis. ( H ) Western blotting was used to detect the expression levels of <t>ZEB2,</t> E-cadherin, N-cadherin, vimentin, α-SMA, and Twist1 in HCT116 and SW620 cells. ( I - J ) Apoptosis and growth assessment of HCT116 after co-culture with Jurkat cells. EMT: Epithelial–mesenchymal transition. * p < 0.05; ** p < 0.01; *** p < 0.001, compared to the corresponding groups
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SCAND1 promotes colorectal cancer cell proliferation, anti-apoptotic, migration, invasion, and EMT. ( A ) SCAND1 protein expression in normal and various colorectal cancer cell lines. ( B - C ) Protein ( B ) and mRNA ( C ) expression levels of SCAND1 were detected by western blotting and RT-qPCR. ( D ) EDU assay analysis. ( E ) Apoptosis rate was detected by flow cytometry. ( F - G ) Wound healing, migration and invasion assay analysis. ( H ) Western blotting was used to detect the expression levels of <t>ZEB2,</t> E-cadherin, N-cadherin, vimentin, α-SMA, and Twist1 in HCT116 and SW620 cells. ( I - J ) Apoptosis and growth assessment of HCT116 after co-culture with Jurkat cells. EMT: Epithelial–mesenchymal transition. * p < 0.05; ** p < 0.01; *** p < 0.001, compared to the corresponding groups
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Fig. 4. LINC02154 promotes EMT through suppression of miR-200b. (A) Correlation between levels of miR-200b expression and those of LINC02154 expression in TCGA-ESCA dataset. (B) Putative miR-200b-3p binding sites in the LINC02154 sequence. (C) qRT-PCR analysis of miR-200b in TE-5 cells transfected with a control siRNA or siRNAs targeting LINC02154. (n = 3). (D) Western blot analysis of <t>ZEB2</t> in TE-5 cells transfected with the indicated siRNAs. (E) Correlation between levels of miR-200b expression and those of VIM in TCGA-ESCA dataset. (F) Correlation between VIM expression and T-factors (left) and clinical stages (right) in TCGA-ESCA dataset. (G) qRT-PCR analysis of VIM in ESCA cells transfected with a miR-mimic control or a miR-200b mimic. (n = 3). (H) qRT-PCR analysis of VIM in ESCA cells transfected with a miR-inhibitor control or a miR-200b inhibitor. (n = 3). (I, J) Results of cell viability assays in ESCA cells infected with the indicated vectors. Cells were treated with the indicated concentrations of cisplatin (H) or 5-FU (I). (n = 6). Error bars represent SDs. **P < 0.01, ***P < 0.001, NS, not significant.
Rabbit Recombinant Anti Zeb2 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


A. Representative Hematoxylin and Eosin stained image of healthy skin and skin of patients with myeloid sarcoma (left), representative spatial transcriptomics plot annotated by cluster/tissue region (middle), and SPN/CD43 expression marking the myeloid sarcoma (right). B. Split UMAP visualization of spatial spots annotated by cluster/spatial region. C. Quantification of cluster abundance in each patient. D. UMAPs show expression of epithelial-mesenchymal transition (EMT) transcription factors ZEB2 and SNAI2, and the KRAS activity Hallmark UCell score. E. Spatial transcriptomics plots showing ZEB2, SNAI2, and KRAS activity up Hallmark UCell score in healthy skin and skin with myeloid sarcoma. F. Myeloid sarcoma blasts showing expression of the EMT marker ZEB2 (Immunohistochemistry (IHC) with hematoxylin counterstain, 100x).

Journal: bioRxiv

Article Title: Multiomic characterization, early detection, and therapeutic targeting of myeloid sarcoma

doi: 10.64898/2025.12.04.689069

Figure Lengend Snippet: A. Representative Hematoxylin and Eosin stained image of healthy skin and skin of patients with myeloid sarcoma (left), representative spatial transcriptomics plot annotated by cluster/tissue region (middle), and SPN/CD43 expression marking the myeloid sarcoma (right). B. Split UMAP visualization of spatial spots annotated by cluster/spatial region. C. Quantification of cluster abundance in each patient. D. UMAPs show expression of epithelial-mesenchymal transition (EMT) transcription factors ZEB2 and SNAI2, and the KRAS activity Hallmark UCell score. E. Spatial transcriptomics plots showing ZEB2, SNAI2, and KRAS activity up Hallmark UCell score in healthy skin and skin with myeloid sarcoma. F. Myeloid sarcoma blasts showing expression of the EMT marker ZEB2 (Immunohistochemistry (IHC) with hematoxylin counterstain, 100x).

Article Snippet: For Zeb2 IHC, we used Rabbit anti-human unconjugated Zinc Finger E-Box Binding Homeobox 2 (Zeb2), clone 1K22 (Protein Tech Group, catalog #82020, Lot#23004049: RRID: AB_2935598).

Techniques: Staining, Expressing, Activity Assay, Marker, Immunohistochemistry

SCAND1 promotes colorectal cancer cell proliferation, anti-apoptotic, migration, invasion, and EMT. ( A ) SCAND1 protein expression in normal and various colorectal cancer cell lines. ( B - C ) Protein ( B ) and mRNA ( C ) expression levels of SCAND1 were detected by western blotting and RT-qPCR. ( D ) EDU assay analysis. ( E ) Apoptosis rate was detected by flow cytometry. ( F - G ) Wound healing, migration and invasion assay analysis. ( H ) Western blotting was used to detect the expression levels of ZEB2, E-cadherin, N-cadherin, vimentin, α-SMA, and Twist1 in HCT116 and SW620 cells. ( I - J ) Apoptosis and growth assessment of HCT116 after co-culture with Jurkat cells. EMT: Epithelial–mesenchymal transition. * p < 0.05; ** p < 0.01; *** p < 0.001, compared to the corresponding groups

Journal: Journal of Translational Medicine

Article Title: Dynamic remodelling of epithelial plasticity in colorectal cancer from single-cell and spatially resolved perspectives

doi: 10.1186/s12967-025-07380-8

Figure Lengend Snippet: SCAND1 promotes colorectal cancer cell proliferation, anti-apoptotic, migration, invasion, and EMT. ( A ) SCAND1 protein expression in normal and various colorectal cancer cell lines. ( B - C ) Protein ( B ) and mRNA ( C ) expression levels of SCAND1 were detected by western blotting and RT-qPCR. ( D ) EDU assay analysis. ( E ) Apoptosis rate was detected by flow cytometry. ( F - G ) Wound healing, migration and invasion assay analysis. ( H ) Western blotting was used to detect the expression levels of ZEB2, E-cadherin, N-cadherin, vimentin, α-SMA, and Twist1 in HCT116 and SW620 cells. ( I - J ) Apoptosis and growth assessment of HCT116 after co-culture with Jurkat cells. EMT: Epithelial–mesenchymal transition. * p < 0.05; ** p < 0.01; *** p < 0.001, compared to the corresponding groups

Article Snippet: The primary antibodies are used as follows: SCAND1 (1:1,000; Thermofisher, PA5-49816), β-actin (1:4,000; ProteinTech, 66009–1-Ig), ZEB2(1:1,000; ProteinTech, 14026–1-AP), Twist1(1:1,000; ProteinTech, 25465–1-AP), N-Cadherin(1:1,000; ProteinTech, 22018–1-AP), E-Cadherin(1:1,000; ProteinTech, 20874–1-AP), α-SMA(1:1,000; ProteinTech, 14395–1-AP), Vimentin(1:1,000; ProteinTech, 10366–1-AP), β-tubulin (1:4,000; ProteinTech, 10094–1-AP).

Techniques: Migration, Expressing, Western Blot, Quantitative RT-PCR, EdU Assay, Flow Cytometry, Invasion Assay, Co-Culture Assay

Fig. 4. LINC02154 promotes EMT through suppression of miR-200b. (A) Correlation between levels of miR-200b expression and those of LINC02154 expression in TCGA-ESCA dataset. (B) Putative miR-200b-3p binding sites in the LINC02154 sequence. (C) qRT-PCR analysis of miR-200b in TE-5 cells transfected with a control siRNA or siRNAs targeting LINC02154. (n = 3). (D) Western blot analysis of ZEB2 in TE-5 cells transfected with the indicated siRNAs. (E) Correlation between levels of miR-200b expression and those of VIM in TCGA-ESCA dataset. (F) Correlation between VIM expression and T-factors (left) and clinical stages (right) in TCGA-ESCA dataset. (G) qRT-PCR analysis of VIM in ESCA cells transfected with a miR-mimic control or a miR-200b mimic. (n = 3). (H) qRT-PCR analysis of VIM in ESCA cells transfected with a miR-inhibitor control or a miR-200b inhibitor. (n = 3). (I, J) Results of cell viability assays in ESCA cells infected with the indicated vectors. Cells were treated with the indicated concentrations of cisplatin (H) or 5-FU (I). (n = 6). Error bars represent SDs. **P < 0.01, ***P < 0.001, NS, not significant.

Journal: Non-coding RNA research

Article Title: Upregulation of LINC02154 promotes esophageal cancer progression by enhancing cell cycling and epithelial-mesenchymal transition.

doi: 10.1016/j.ncrna.2025.06.001

Figure Lengend Snippet: Fig. 4. LINC02154 promotes EMT through suppression of miR-200b. (A) Correlation between levels of miR-200b expression and those of LINC02154 expression in TCGA-ESCA dataset. (B) Putative miR-200b-3p binding sites in the LINC02154 sequence. (C) qRT-PCR analysis of miR-200b in TE-5 cells transfected with a control siRNA or siRNAs targeting LINC02154. (n = 3). (D) Western blot analysis of ZEB2 in TE-5 cells transfected with the indicated siRNAs. (E) Correlation between levels of miR-200b expression and those of VIM in TCGA-ESCA dataset. (F) Correlation between VIM expression and T-factors (left) and clinical stages (right) in TCGA-ESCA dataset. (G) qRT-PCR analysis of VIM in ESCA cells transfected with a miR-mimic control or a miR-200b mimic. (n = 3). (H) qRT-PCR analysis of VIM in ESCA cells transfected with a miR-inhibitor control or a miR-200b inhibitor. (n = 3). (I, J) Results of cell viability assays in ESCA cells infected with the indicated vectors. Cells were treated with the indicated concentrations of cisplatin (H) or 5-FU (I). (n = 6). Error bars represent SDs. **P < 0.01, ***P < 0.001, NS, not significant.

Article Snippet: A mouse monoclonal anti-GAPDH mAb (1:5000 dilution, HRP-60004, Proteintech, Rosemont, IL, USA), rabbit monoclonal anti-cyclin B1 mAb (1:1000 dilution, #12231, Cell Signaling Technology, Danvers, MA, USA), and rabbit recombinant anti-ZEB2 antibody (1:3000 dilution, 82020-1-RR, Proteintech) were used.

Techniques: Expressing, Binding Assay, Sequencing, Quantitative RT-PCR, Transfection, Control, Western Blot, Infection