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aml 12 cell line  (ATCC)


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    Structured Review

    ATCC aml 12 cell line
    Aml 12 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1551 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aml 12 cell line/product/ATCC
    Average 98 stars, based on 1551 article reviews
    aml 12 cell line - by Bioz Stars, 2026-05
    98/100 stars

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    ATCC mouse normal hepatocyte cell line aml12
    ( A ) Liver tumor tissues were collected from the HTVi model and clinical patients and subjected to untargeted metabolomic profiling for pathway enrichment. ( B ) Summarized SLC transporters for TCA cycle intermediates. ( C ) Forest plot showing the hazard ratios (HR) for multiple genes encoding SLC transporters of TCA cycle intermediates in HCC. The horizontal line represents the 95% confidence interval. ( D ) Heatmap of detectable SLC transporters for TCA cycle intermediates in heterogeneous primary liver cancer models generated by genome editing of cancer driver genes selected by mutational frequency from human HCC cohorts (PRJNA674008). ( E ) qPCR analysis to screen candidate SLC transporters for HCC progression based on the relative expression of SLC transporters in the HTVi model ( n = 4 for the control group and n = 5 for the model group), mouse HCC Hepa1-6 cells, <t>AML12</t> cells, and MPHs ( n = 3 independent experiments). ( F ) Venn diagram showing the overlap of significantly differentially expressed SLC transporters in the HTVi model, mouse HCC Hepa1-6 cells, and normal hepatocytes (AML12 and MPHs). ( G and H ) SLC13A2 expression in liver tissues from HTVi, AAV-cMYC/nRAS, and STZ-HFD HCC model. The data are presented as means ± SEM. * P < 0.05; ** P < 0.01, two-tailed unpaired Student’s t test. Ctrl, control; n.d., not determined; NS, not significant.
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    ATCC cell line culture aml12 cell
    ( A ) Liver tumor tissues were collected from the HTVi model and clinical patients and subjected to untargeted metabolomic profiling for pathway enrichment. ( B ) Summarized SLC transporters for TCA cycle intermediates. ( C ) Forest plot showing the hazard ratios (HR) for multiple genes encoding SLC transporters of TCA cycle intermediates in HCC. The horizontal line represents the 95% confidence interval. ( D ) Heatmap of detectable SLC transporters for TCA cycle intermediates in heterogeneous primary liver cancer models generated by genome editing of cancer driver genes selected by mutational frequency from human HCC cohorts (PRJNA674008). ( E ) qPCR analysis to screen candidate SLC transporters for HCC progression based on the relative expression of SLC transporters in the HTVi model ( n = 4 for the control group and n = 5 for the model group), mouse HCC Hepa1-6 cells, <t>AML12</t> cells, and MPHs ( n = 3 independent experiments). ( F ) Venn diagram showing the overlap of significantly differentially expressed SLC transporters in the HTVi model, mouse HCC Hepa1-6 cells, and normal hepatocytes (AML12 and MPHs). ( G and H ) SLC13A2 expression in liver tissues from HTVi, AAV-cMYC/nRAS, and STZ-HFD HCC model. The data are presented as means ± SEM. * P < 0.05; ** P < 0.01, two-tailed unpaired Student’s t test. Ctrl, control; n.d., not determined; NS, not significant.
    Cell Line Culture Aml12 Cell, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC mouse aml12 cell line
    ( A ) Liver tumor tissues were collected from the HTVi model and clinical patients and subjected to untargeted metabolomic profiling for pathway enrichment. ( B ) Summarized SLC transporters for TCA cycle intermediates. ( C ) Forest plot showing the hazard ratios (HR) for multiple genes encoding SLC transporters of TCA cycle intermediates in HCC. The horizontal line represents the 95% confidence interval. ( D ) Heatmap of detectable SLC transporters for TCA cycle intermediates in heterogeneous primary liver cancer models generated by genome editing of cancer driver genes selected by mutational frequency from human HCC cohorts (PRJNA674008). ( E ) qPCR analysis to screen candidate SLC transporters for HCC progression based on the relative expression of SLC transporters in the HTVi model ( n = 4 for the control group and n = 5 for the model group), mouse HCC Hepa1-6 cells, <t>AML12</t> cells, and MPHs ( n = 3 independent experiments). ( F ) Venn diagram showing the overlap of significantly differentially expressed SLC transporters in the HTVi model, mouse HCC Hepa1-6 cells, and normal hepatocytes (AML12 and MPHs). ( G and H ) SLC13A2 expression in liver tissues from HTVi, AAV-cMYC/nRAS, and STZ-HFD HCC model. The data are presented as means ± SEM. * P < 0.05; ** P < 0.01, two-tailed unpaired Student’s t test. Ctrl, control; n.d., not determined; NS, not significant.
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    ATCC hepatocyte cell line aml12
    Co-incubation of platelets and hepatocytes increases hepatocyte lipid. (A) Schematic overview (B–K) Differential protein expression analysis of <t>AML12</t> lysates (Ctrl): tunicamycin-treated (Tuni), platelet co-culture (Plts), combination (TuniPlts). Log 2 -transformed DEseq normalized differential average protein expression (∼7,600 proteins, n = 4) (B) comparing tunicamycin treatment of Ctrl and Plts samples or (C) platelet co-culture of Ctrl and Tuni-treated cells. Fifty-two (tunicamycin) and 27 (platelets) significantly changed proteins (padj <0.05). (D–K) Relative protein expression (normalized log2-intensities): (D) C/EBP homologous protein (CHOP, n = 4), (E) 78-kDa glucose-regulated protein (BIP/GRP78, n = 4), (F) X-box splicing protein (XBP1, n = 2–4), (G) 94 kDa glucose-regulated protein (GRP94, n = 4) and (H) perilipin 2 (Plin2, n = 4), (L) apolipoprotein b (Apob, n = 4), (J) intracellular adhesion molecule 1 (Icam1, n = 4), and (K) vascular cell adhesion molecule 1 (vcam1, n = 4). Gene expression of (L) BIP/GRP78 (n = 4–5), (M) IRE1α (n = 4–5), (N) spliced XBP1 (XBP1spl, n = 4–5), (O) CHOP (n = 4–5). (P,Q) Hepatocyte lipid content (n = 3). (R) Gene expression of very low-density lipoprotein receptor (VLDLR, n = 5), (S) interleukin-6 (IL-6, n = 3–4), (T) inducible nitric oxide synthase (iNOS, n = 3–4). Data represent mean ± SD. Two-way ANOVA; ∗ p <0.05, ∗∗ p <0.01 (platelets); # p <0.05, ## p <0.01, #### p <0.0001 (tunicamycin).
    Hepatocyte Cell Line Aml12, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hepatocyte cell line aml12/product/ATCC
    Average 98 stars, based on 1 article reviews
    hepatocyte cell line aml12 - by Bioz Stars, 2026-05
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    ( A ) Liver tumor tissues were collected from the HTVi model and clinical patients and subjected to untargeted metabolomic profiling for pathway enrichment. ( B ) Summarized SLC transporters for TCA cycle intermediates. ( C ) Forest plot showing the hazard ratios (HR) for multiple genes encoding SLC transporters of TCA cycle intermediates in HCC. The horizontal line represents the 95% confidence interval. ( D ) Heatmap of detectable SLC transporters for TCA cycle intermediates in heterogeneous primary liver cancer models generated by genome editing of cancer driver genes selected by mutational frequency from human HCC cohorts (PRJNA674008). ( E ) qPCR analysis to screen candidate SLC transporters for HCC progression based on the relative expression of SLC transporters in the HTVi model ( n = 4 for the control group and n = 5 for the model group), mouse HCC Hepa1-6 cells, AML12 cells, and MPHs ( n = 3 independent experiments). ( F ) Venn diagram showing the overlap of significantly differentially expressed SLC transporters in the HTVi model, mouse HCC Hepa1-6 cells, and normal hepatocytes (AML12 and MPHs). ( G and H ) SLC13A2 expression in liver tissues from HTVi, AAV-cMYC/nRAS, and STZ-HFD HCC model. The data are presented as means ± SEM. * P < 0.05; ** P < 0.01, two-tailed unpaired Student’s t test. Ctrl, control; n.d., not determined; NS, not significant.

    Journal: Science Advances

    Article Title: SLC13A2-transported citrate remodels transcriptional regulation through protein acetylation to suppress tumor growth

    doi: 10.1126/sciadv.aec4368

    Figure Lengend Snippet: ( A ) Liver tumor tissues were collected from the HTVi model and clinical patients and subjected to untargeted metabolomic profiling for pathway enrichment. ( B ) Summarized SLC transporters for TCA cycle intermediates. ( C ) Forest plot showing the hazard ratios (HR) for multiple genes encoding SLC transporters of TCA cycle intermediates in HCC. The horizontal line represents the 95% confidence interval. ( D ) Heatmap of detectable SLC transporters for TCA cycle intermediates in heterogeneous primary liver cancer models generated by genome editing of cancer driver genes selected by mutational frequency from human HCC cohorts (PRJNA674008). ( E ) qPCR analysis to screen candidate SLC transporters for HCC progression based on the relative expression of SLC transporters in the HTVi model ( n = 4 for the control group and n = 5 for the model group), mouse HCC Hepa1-6 cells, AML12 cells, and MPHs ( n = 3 independent experiments). ( F ) Venn diagram showing the overlap of significantly differentially expressed SLC transporters in the HTVi model, mouse HCC Hepa1-6 cells, and normal hepatocytes (AML12 and MPHs). ( G and H ) SLC13A2 expression in liver tissues from HTVi, AAV-cMYC/nRAS, and STZ-HFD HCC model. The data are presented as means ± SEM. * P < 0.05; ** P < 0.01, two-tailed unpaired Student’s t test. Ctrl, control; n.d., not determined; NS, not significant.

    Article Snippet: The mouse HCC cell line Hepa1-6 and mouse normal hepatocyte cell line AML12 were obtained from the American Type Culture Collection as described previously ( ).

    Techniques: Metabolomic, Generated, Expressing, Control, Two Tailed Test

    Co-incubation of platelets and hepatocytes increases hepatocyte lipid. (A) Schematic overview (B–K) Differential protein expression analysis of AML12 lysates (Ctrl): tunicamycin-treated (Tuni), platelet co-culture (Plts), combination (TuniPlts). Log 2 -transformed DEseq normalized differential average protein expression (∼7,600 proteins, n = 4) (B) comparing tunicamycin treatment of Ctrl and Plts samples or (C) platelet co-culture of Ctrl and Tuni-treated cells. Fifty-two (tunicamycin) and 27 (platelets) significantly changed proteins (padj <0.05). (D–K) Relative protein expression (normalized log2-intensities): (D) C/EBP homologous protein (CHOP, n = 4), (E) 78-kDa glucose-regulated protein (BIP/GRP78, n = 4), (F) X-box splicing protein (XBP1, n = 2–4), (G) 94 kDa glucose-regulated protein (GRP94, n = 4) and (H) perilipin 2 (Plin2, n = 4), (L) apolipoprotein b (Apob, n = 4), (J) intracellular adhesion molecule 1 (Icam1, n = 4), and (K) vascular cell adhesion molecule 1 (vcam1, n = 4). Gene expression of (L) BIP/GRP78 (n = 4–5), (M) IRE1α (n = 4–5), (N) spliced XBP1 (XBP1spl, n = 4–5), (O) CHOP (n = 4–5). (P,Q) Hepatocyte lipid content (n = 3). (R) Gene expression of very low-density lipoprotein receptor (VLDLR, n = 5), (S) interleukin-6 (IL-6, n = 3–4), (T) inducible nitric oxide synthase (iNOS, n = 3–4). Data represent mean ± SD. Two-way ANOVA; ∗ p <0.05, ∗∗ p <0.01 (platelets); # p <0.05, ## p <0.01, #### p <0.0001 (tunicamycin).

    Journal: JHEP Reports

    Article Title: Platelets accelerate endoplasmic reticulum stress and promote hepatic steatosis

    doi: 10.1016/j.jhepr.2026.101767

    Figure Lengend Snippet: Co-incubation of platelets and hepatocytes increases hepatocyte lipid. (A) Schematic overview (B–K) Differential protein expression analysis of AML12 lysates (Ctrl): tunicamycin-treated (Tuni), platelet co-culture (Plts), combination (TuniPlts). Log 2 -transformed DEseq normalized differential average protein expression (∼7,600 proteins, n = 4) (B) comparing tunicamycin treatment of Ctrl and Plts samples or (C) platelet co-culture of Ctrl and Tuni-treated cells. Fifty-two (tunicamycin) and 27 (platelets) significantly changed proteins (padj <0.05). (D–K) Relative protein expression (normalized log2-intensities): (D) C/EBP homologous protein (CHOP, n = 4), (E) 78-kDa glucose-regulated protein (BIP/GRP78, n = 4), (F) X-box splicing protein (XBP1, n = 2–4), (G) 94 kDa glucose-regulated protein (GRP94, n = 4) and (H) perilipin 2 (Plin2, n = 4), (L) apolipoprotein b (Apob, n = 4), (J) intracellular adhesion molecule 1 (Icam1, n = 4), and (K) vascular cell adhesion molecule 1 (vcam1, n = 4). Gene expression of (L) BIP/GRP78 (n = 4–5), (M) IRE1α (n = 4–5), (N) spliced XBP1 (XBP1spl, n = 4–5), (O) CHOP (n = 4–5). (P,Q) Hepatocyte lipid content (n = 3). (R) Gene expression of very low-density lipoprotein receptor (VLDLR, n = 5), (S) interleukin-6 (IL-6, n = 3–4), (T) inducible nitric oxide synthase (iNOS, n = 3–4). Data represent mean ± SD. Two-way ANOVA; ∗ p <0.05, ∗∗ p <0.01 (platelets); # p <0.05, ## p <0.01, #### p <0.0001 (tunicamycin).

    Article Snippet: The hepatocyte cell line AML12 (ATCC, Manassas, Virginia, USA, CRL-2254TM) was cultured in DMEM-F12 medium (Gibco, Waltham, Massachusetts, USA) containing 10% FBS (Sigma, Darmstadt, Germany) and treated with tunicamycin (0.5–1 μg/ml, Sigma, Darmstadt, Germany) ± isolated platelets (500,000 platelets/μl) for 6 h.

    Techniques: Incubation, Expressing, Co-Culture Assay, Transformation Assay, Gene Expression