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am 80  (Bio-Techne corporation)


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    Bio-Techne corporation am 80
    Am 80, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 94/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/am+80/custom%403507%4042138197?v=Bio-Techne+corporation
    Average 94 stars, based on 19 article reviews
    am 80 - by Bioz Stars, 2026-07
    94/100 stars

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    am80  (Tocris)
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    ATF5 is highly localized in the nuclei of human and mouse pancreatic cancer cells in stiff tumors (A) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in adjacent normal, and collagen-poor and collagen-rich tumor regions of human pancreatic ductal adenocarcinoma. The areas of black rectangles are magnified. (B) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined via immunohistochemistry, followed by quantification. (C) Proportions of cells negative for EGR1 (−), nuclear-positive for EGR1 (Nuc(+)), and nuclear-negative and cytoplasm-positive for EGR1 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined by immunohistochemistry, followed by quantification. (D) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in control pancreatic tumors and those treated with <t>AM80.</t> The areas of black rectangles are magnified. Note that AM80 is reported to reduce tumor stiffness by inducing changes in the phenotype of CAFs. (E) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. (F) Proportions of cells negative for EGR1 (−), nuclear positive for EGR1 (Nuc(+)), and nuclear negative and cytoplasm-positive for EGR1 (Other(+)) on tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. Scale bar = 100 μm; mean with S.D. and each data point is shown; †, statistical significance ( p < 0.05) determined via Student’s t test; ‡, statistical significance ( p < 0.05) determined via Welch’s t-test; ¥, statistical significance ( p < 0.05) determined via Wilcoxon rank-sum test; §, statistical significance ( p < 0.05) determined via paired t-test. For multiple comparisons, we analyzed significance using the Bonferroni correction.
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    ATF5 is highly localized in the nuclei of human and mouse pancreatic cancer cells in stiff tumors (A) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in adjacent normal, and collagen-poor and collagen-rich tumor regions of human pancreatic ductal adenocarcinoma. The areas of black rectangles are magnified. (B) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined via immunohistochemistry, followed by quantification. (C) Proportions of cells negative for EGR1 (−), nuclear-positive for EGR1 (Nuc(+)), and nuclear-negative and cytoplasm-positive for EGR1 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined by immunohistochemistry, followed by quantification. (D) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in control pancreatic tumors and those treated with <t>AM80.</t> The areas of black rectangles are magnified. Note that AM80 is reported to reduce tumor stiffness by inducing changes in the phenotype of CAFs. (E) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. (F) Proportions of cells negative for EGR1 (−), nuclear positive for EGR1 (Nuc(+)), and nuclear negative and cytoplasm-positive for EGR1 (Other(+)) on tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. Scale bar = 100 μm; mean with S.D. and each data point is shown; †, statistical significance ( p < 0.05) determined via Student’s t test; ‡, statistical significance ( p < 0.05) determined via Welch’s t-test; ¥, statistical significance ( p < 0.05) determined via Wilcoxon rank-sum test; §, statistical significance ( p < 0.05) determined via paired t-test. For multiple comparisons, we analyzed significance using the Bonferroni correction.
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    Image Search Results


    ATF5 is highly localized in the nuclei of human and mouse pancreatic cancer cells in stiff tumors (A) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in adjacent normal, and collagen-poor and collagen-rich tumor regions of human pancreatic ductal adenocarcinoma. The areas of black rectangles are magnified. (B) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined via immunohistochemistry, followed by quantification. (C) Proportions of cells negative for EGR1 (−), nuclear-positive for EGR1 (Nuc(+)), and nuclear-negative and cytoplasm-positive for EGR1 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined by immunohistochemistry, followed by quantification. (D) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in control pancreatic tumors and those treated with AM80. The areas of black rectangles are magnified. Note that AM80 is reported to reduce tumor stiffness by inducing changes in the phenotype of CAFs. (E) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. (F) Proportions of cells negative for EGR1 (−), nuclear positive for EGR1 (Nuc(+)), and nuclear negative and cytoplasm-positive for EGR1 (Other(+)) on tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. Scale bar = 100 μm; mean with S.D. and each data point is shown; †, statistical significance ( p < 0.05) determined via Student’s t test; ‡, statistical significance ( p < 0.05) determined via Welch’s t-test; ¥, statistical significance ( p < 0.05) determined via Wilcoxon rank-sum test; §, statistical significance ( p < 0.05) determined via paired t-test. For multiple comparisons, we analyzed significance using the Bonferroni correction.

    Journal: iScience

    Article Title: Stiff extracellular matrix activates the transcription factor ATF5 to promote the proliferation of cancer cells

    doi: 10.1016/j.isci.2025.112057

    Figure Lengend Snippet: ATF5 is highly localized in the nuclei of human and mouse pancreatic cancer cells in stiff tumors (A) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in adjacent normal, and collagen-poor and collagen-rich tumor regions of human pancreatic ductal adenocarcinoma. The areas of black rectangles are magnified. (B) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined via immunohistochemistry, followed by quantification. (C) Proportions of cells negative for EGR1 (−), nuclear-positive for EGR1 (Nuc(+)), and nuclear-negative and cytoplasm-positive for EGR1 (Other(+)) in human pancreatic cancer tissues ( n = 9 patients) were examined by immunohistochemistry, followed by quantification. (D) Representative staining images of hematoxylin and eosin (HE) and immunohistochemistry for ATF5 and EGR1 in control pancreatic tumors and those treated with AM80. The areas of black rectangles are magnified. Note that AM80 is reported to reduce tumor stiffness by inducing changes in the phenotype of CAFs. (E) Proportions of cells negative for ATF5 (−), nuclear positive for ATF5 (Nuc(+)), and nuclear negative and cytoplasm-positive for ATF5 (Other(+)) in tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. (F) Proportions of cells negative for EGR1 (−), nuclear positive for EGR1 (Nuc(+)), and nuclear negative and cytoplasm-positive for EGR1 (Other(+)) on tumor tissues obtained from control mice ( n = 9) and those administered AM80 ( n = 10) were examined via immunohistochemistry followed by quantification. Scale bar = 100 μm; mean with S.D. and each data point is shown; †, statistical significance ( p < 0.05) determined via Student’s t test; ‡, statistical significance ( p < 0.05) determined via Welch’s t-test; ¥, statistical significance ( p < 0.05) determined via Wilcoxon rank-sum test; §, statistical significance ( p < 0.05) determined via paired t-test. For multiple comparisons, we analyzed significance using the Bonferroni correction.

    Article Snippet: AM80 , Tocris , Cat# 3507.

    Techniques: Staining, Immunohistochemistry, Control

    Journal: iScience

    Article Title: Stiff extracellular matrix activates the transcription factor ATF5 to promote the proliferation of cancer cells

    doi: 10.1016/j.isci.2025.112057

    Figure Lengend Snippet:

    Article Snippet: AM80 , Tocris , Cat# 3507.

    Techniques: Purification, Recombinant, Plasmid Preparation, Modification, Cloning, Transfection, In Vitro, Isolation, Staining, Control, Western Blot, Microarray, shRNA, Software