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rabbit anti-col4a1  (Novus Biologicals)


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    Structured Review

    Novus Biologicals rabbit anti-col4a1
    Rabbit Anti Col4a1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+col4a1/anti+col4a1/pm39191260-192-70-68
    Average 90 stars, based on 1 article reviews
    rabbit anti-col4a1 - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    other:

    Article Title: β-Catenin and FGFR2 regulate postnatal rosette-based adrenocortical morphogenesis.
    Article Snippet: Primary antibodies used for this application include: Rat antiLaminin β1 (Santa Cruz, sc-33709), Rabbit anti-Gαq (Abcam, ab75825), Rabbit anti-β-catenin (Abcam, ab16051), Rabbit anti-Col4a1 (Novus Biologicals, NB1206586), Rat anti-CD31 (BD Bioscience, 557355), Rabbit anti-Vimentin (Abcam, ab92547), Rabbit anti-N-cadherin (Novus Biologicals, NBP2-38856), Rabbit antiK-cadherin (Abcam, ab133632), and Rat anti-E-cadherin (Abcam, ab11512).

    Article Title: β-Catenin and FGFR2 regulate postnatal rosette-based adrenocortical morphogenesis
    Article Snippet: Primary antibodies used for this application include: Rat anti-Laminin β1 (Santa Cruz, sc-33709), Rabbit anti-Gαq (Abcam, ab75825), Rabbit anti-β-catenin (Abcam, ab16051), Rabbit anti-Col4a1 (Novus Biologicals, NB120-6586), Rat anti-CD31 (BD Bioscience, 557355), Rabbit anti-Vimentin (Abcam, ab92547), Rabbit anti-N-cadherin (Novus Biologicals, NBP2-38856), Rabbit anti-K-cadherin (Abcam, ab133632), and Rat anti-E-cadherin (Abcam, ab11512).



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    Fig. 5. Identification of <t>COL4A1-ITGB1</t> as the most significant interaction between tumorous EMT-UC and TME components. (A) Functional enrichment of the upregulated genes in TME compared to the counterparts in normal tissues. (B) General workflow of the ranking score system for screening the most qualified interaction for therapeutic targeting between tumorous EMT-UC and the TME components. (C) Schematic drawing of the cellular interactions between EMT-UC and TME components. Sender: Ligands from EMT-UC; Receiver: Receptors from TME. (D) Top 10 cellular interactions based on the ranking score system. (E) The interaction intensities of the top 10 cellular interactions between tumorous EMT-UC and each TME component.
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    Image Search Results


    Fig. 5. Identification of COL4A1-ITGB1 as the most significant interaction between tumorous EMT-UC and TME components. (A) Functional enrichment of the upregulated genes in TME compared to the counterparts in normal tissues. (B) General workflow of the ranking score system for screening the most qualified interaction for therapeutic targeting between tumorous EMT-UC and the TME components. (C) Schematic drawing of the cellular interactions between EMT-UC and TME components. Sender: Ligands from EMT-UC; Receiver: Receptors from TME. (D) Top 10 cellular interactions based on the ranking score system. (E) The interaction intensities of the top 10 cellular interactions between tumorous EMT-UC and each TME component.

    Journal: Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

    Article Title: A distinct subset of urothelial cells with enhanced EMT features promotes chemotherapy resistance and cancer recurrence by increasing COL4A1-ITGB1 mediated angiogenesis.

    doi: 10.1016/j.drup.2024.101116

    Figure Lengend Snippet: Fig. 5. Identification of COL4A1-ITGB1 as the most significant interaction between tumorous EMT-UC and TME components. (A) Functional enrichment of the upregulated genes in TME compared to the counterparts in normal tissues. (B) General workflow of the ranking score system for screening the most qualified interaction for therapeutic targeting between tumorous EMT-UC and the TME components. (C) Schematic drawing of the cellular interactions between EMT-UC and TME components. Sender: Ligands from EMT-UC; Receiver: Receptors from TME. (D) Top 10 cellular interactions based on the ranking score system. (E) The interaction intensities of the top 10 cellular interactions between tumorous EMT-UC and each TME component.

    Article Snippet: The supernatant of EMT-UC like cells J. Guo et al. Drug Resistance Updates 76 (2024) 101116 were collected and used to incubate HUVECs at 37◦C for 2–4 h. Specific antibodies targeting COL4A1-ITGB1 (diluted at 1 μg/mL, Abclonal, Cat. No. A10710, A2217) were also added to the conditional medium of certain wells to determine their effects on tube formation.

    Techniques: Functional Assay

    Fig. 7. Targeted blockade of COL4A1-ITGB1 suppressed angiogenesis and chemotherapy resistance of UC. (A) Schematic drawing of PDX model construction and animal experiment design. (B) Tumor growth curves of mice with different treatments. Values were presented as mean ± SD, n = 5, ** p < 0.01, *** p < 0.001. (C) Tumor size of mice with different treatments. (D) Tumor weights of mice with different treatments. Values were presented as mean ± SD, n = 5, * p < 0.05, ** p < 0.01, *** p < 0.001, NS indicated no significance. (E) Histology alterations of tumors from mice with different treatment. (F) Pathology response rate of tumors from mice with different treatment. Values were presented as mean ± SD, n = 5, ** p < 0.01, *** p < 0.001, NS indicated no significance. (G) Tumorous angiogenesis of tumor tissues from mice with different treatments evaluated by CD31 immunostaining. Brown staining indicated CD31 positive signal. Blue staining indicated nuclei stained with hematoxylin. (H). CD31 staining scores of tumors from mice with different treatments evaluated by the staining intensity and positive ratio of CD31. Values were presented as mean ± SD, n = 5, *** p < 0.001, NS indicated no significance.

    Journal: Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

    Article Title: A distinct subset of urothelial cells with enhanced EMT features promotes chemotherapy resistance and cancer recurrence by increasing COL4A1-ITGB1 mediated angiogenesis.

    doi: 10.1016/j.drup.2024.101116

    Figure Lengend Snippet: Fig. 7. Targeted blockade of COL4A1-ITGB1 suppressed angiogenesis and chemotherapy resistance of UC. (A) Schematic drawing of PDX model construction and animal experiment design. (B) Tumor growth curves of mice with different treatments. Values were presented as mean ± SD, n = 5, ** p < 0.01, *** p < 0.001. (C) Tumor size of mice with different treatments. (D) Tumor weights of mice with different treatments. Values were presented as mean ± SD, n = 5, * p < 0.05, ** p < 0.01, *** p < 0.001, NS indicated no significance. (E) Histology alterations of tumors from mice with different treatment. (F) Pathology response rate of tumors from mice with different treatment. Values were presented as mean ± SD, n = 5, ** p < 0.01, *** p < 0.001, NS indicated no significance. (G) Tumorous angiogenesis of tumor tissues from mice with different treatments evaluated by CD31 immunostaining. Brown staining indicated CD31 positive signal. Blue staining indicated nuclei stained with hematoxylin. (H). CD31 staining scores of tumors from mice with different treatments evaluated by the staining intensity and positive ratio of CD31. Values were presented as mean ± SD, n = 5, *** p < 0.001, NS indicated no significance.

    Article Snippet: The supernatant of EMT-UC like cells J. Guo et al. Drug Resistance Updates 76 (2024) 101116 were collected and used to incubate HUVECs at 37◦C for 2–4 h. Specific antibodies targeting COL4A1-ITGB1 (diluted at 1 μg/mL, Abclonal, Cat. No. A10710, A2217) were also added to the conditional medium of certain wells to determine their effects on tube formation.

    Techniques: Immunostaining, Staining