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human renal proximal tubular epithelial cells  (ATCC)


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    Structured Review

    ATCC human renal proximal tubular epithelial cells
    Induction and knockdown of IFIT2 in renal tubular <t>epithelial</t> cells. (A–B) IFN‐ γ –induced IFIT2 expression in HK‐2 and RPTEC cells. (C–D) TGF‐ β 1–induced IFIT2 expression in HK‐2 and RPTEC cells. (E–F) Validation of IFIT2 knockdown efficiency by qPCR. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
    Human Renal Proximal Tubular Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 745 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+proximal+tubule+cells/pmc13179815-45-0-11?v=ATCC
    Average 99 stars, based on 745 article reviews
    human renal proximal tubular epithelial cells - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Cross‐Cohort Transcriptomic Integration Identifies IFIT2 as a Translational Diagnostic Biomarker and Functional Driver of Inflammation‐Linked Tubular Injury in Chronic Kidney Disease"

    Article Title: Cross‐Cohort Transcriptomic Integration Identifies IFIT2 as a Translational Diagnostic Biomarker and Functional Driver of Inflammation‐Linked Tubular Injury in Chronic Kidney Disease

    Journal: Human Mutation

    doi: 10.1155/humu/8282277

    Induction and knockdown of IFIT2 in renal tubular epithelial cells. (A–B) IFN‐ γ –induced IFIT2 expression in HK‐2 and RPTEC cells. (C–D) TGF‐ β 1–induced IFIT2 expression in HK‐2 and RPTEC cells. (E–F) Validation of IFIT2 knockdown efficiency by qPCR. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
    Figure Legend Snippet: Induction and knockdown of IFIT2 in renal tubular epithelial cells. (A–B) IFN‐ γ –induced IFIT2 expression in HK‐2 and RPTEC cells. (C–D) TGF‐ β 1–induced IFIT2 expression in HK‐2 and RPTEC cells. (E–F) Validation of IFIT2 knockdown efficiency by qPCR. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Techniques Used: Knockdown, Expressing, Biomarker Discovery

    IFIT2 knockdown attenuates IFN‐ γ –induced injury and apoptosis in renal tubular epithelial cells. (A–B) CCK‐8 assay showing that IFIT2 knockdown alleviates IFN‐ γ –induced reduction of cell viability in HK‐2 and RPTEC cells. (C–F) Annexin V/PI flow cytometry analysis showing that IFIT2 knockdown reduces IFN‐ γ –induced apoptosis in (C, E) HK‐2 and (D, F) RPTEC cells. Data are presented as mean ± SD from three independent experiments. ∗∗∗ p < 0.001.
    Figure Legend Snippet: IFIT2 knockdown attenuates IFN‐ γ –induced injury and apoptosis in renal tubular epithelial cells. (A–B) CCK‐8 assay showing that IFIT2 knockdown alleviates IFN‐ γ –induced reduction of cell viability in HK‐2 and RPTEC cells. (C–F) Annexin V/PI flow cytometry analysis showing that IFIT2 knockdown reduces IFN‐ γ –induced apoptosis in (C, E) HK‐2 and (D, F) RPTEC cells. Data are presented as mean ± SD from three independent experiments. ∗∗∗ p < 0.001.

    Techniques Used: Knockdown, CCK-8 Assay, Flow Cytometry



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    ATCC renal proximal tubule epithelial cell rptec immortalized cell line
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    Image Search Results


    Induction and knockdown of IFIT2 in renal tubular epithelial cells. (A–B) IFN‐ γ –induced IFIT2 expression in HK‐2 and RPTEC cells. (C–D) TGF‐ β 1–induced IFIT2 expression in HK‐2 and RPTEC cells. (E–F) Validation of IFIT2 knockdown efficiency by qPCR. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Journal: Human Mutation

    Article Title: Cross‐Cohort Transcriptomic Integration Identifies IFIT2 as a Translational Diagnostic Biomarker and Functional Driver of Inflammation‐Linked Tubular Injury in Chronic Kidney Disease

    doi: 10.1155/humu/8282277

    Figure Lengend Snippet: Induction and knockdown of IFIT2 in renal tubular epithelial cells. (A–B) IFN‐ γ –induced IFIT2 expression in HK‐2 and RPTEC cells. (C–D) TGF‐ β 1–induced IFIT2 expression in HK‐2 and RPTEC cells. (E–F) Validation of IFIT2 knockdown efficiency by qPCR. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Article Snippet: Human renal proximal tubular epithelial cells, including the HK‐2 cell line (ATCC, RRID: CVCL_0302) and primary RPTEC cells (ATCC, RRID: CVCL_K278), were used in this study.

    Techniques: Knockdown, Expressing, Biomarker Discovery

    IFIT2 knockdown attenuates IFN‐ γ –induced injury and apoptosis in renal tubular epithelial cells. (A–B) CCK‐8 assay showing that IFIT2 knockdown alleviates IFN‐ γ –induced reduction of cell viability in HK‐2 and RPTEC cells. (C–F) Annexin V/PI flow cytometry analysis showing that IFIT2 knockdown reduces IFN‐ γ –induced apoptosis in (C, E) HK‐2 and (D, F) RPTEC cells. Data are presented as mean ± SD from three independent experiments. ∗∗∗ p < 0.001.

    Journal: Human Mutation

    Article Title: Cross‐Cohort Transcriptomic Integration Identifies IFIT2 as a Translational Diagnostic Biomarker and Functional Driver of Inflammation‐Linked Tubular Injury in Chronic Kidney Disease

    doi: 10.1155/humu/8282277

    Figure Lengend Snippet: IFIT2 knockdown attenuates IFN‐ γ –induced injury and apoptosis in renal tubular epithelial cells. (A–B) CCK‐8 assay showing that IFIT2 knockdown alleviates IFN‐ γ –induced reduction of cell viability in HK‐2 and RPTEC cells. (C–F) Annexin V/PI flow cytometry analysis showing that IFIT2 knockdown reduces IFN‐ γ –induced apoptosis in (C, E) HK‐2 and (D, F) RPTEC cells. Data are presented as mean ± SD from three independent experiments. ∗∗∗ p < 0.001.

    Article Snippet: Human renal proximal tubular epithelial cells, including the HK‐2 cell line (ATCC, RRID: CVCL_0302) and primary RPTEC cells (ATCC, RRID: CVCL_K278), were used in this study.

    Techniques: Knockdown, CCK-8 Assay, Flow Cytometry

    Cytotoxicity of HIF inhibitors and sunitinib in renal cell lines: ( A ) 786-O, ( B ) Caki-1, and ( C ) HK-2. Dose–response curves (SRB, 72 h of incubation). Data are presented as mean ± SD from independent biological experiments, each measured in technical replicates ( n = 6). Curves were fitted using four-parameter logistic regression.

    Journal: International Journal of Molecular Sciences

    Article Title: Exploratory Multi-Level Analysis of the HIF Axis in Clear-Cell Renal Cell Carcinoma and Evaluation of GN44028 as an Experimental HIF Pathway-Modulating Compound

    doi: 10.3390/ijms27083505

    Figure Lengend Snippet: Cytotoxicity of HIF inhibitors and sunitinib in renal cell lines: ( A ) 786-O, ( B ) Caki-1, and ( C ) HK-2. Dose–response curves (SRB, 72 h of incubation). Data are presented as mean ± SD from independent biological experiments, each measured in technical replicates ( n = 6). Curves were fitted using four-parameter logistic regression.

    Article Snippet: 786-O (cRL1932TM), Caki-1 (McCoy) human renal cell carcinoma lines, and HK-2 (cRL2190TM) human proximal kidney tubule-derived cell lines were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Incubation

    Cell cycle analysis by propidium iodide staining and flow cytometry in 786-O ( A ), Caki-1 ( B ), and HK-2 ( C ) cells treated with KC7F2, FM19G11, GN44028, and sunitinib at IC 50 concentrations for 24 h. Bar graphs show mean ± SD from independent biological experiments, each measured in technical replicates ( n = 3–19). GN44028 was associated with an increased sub-G1 fraction in ccRCC cell lines and G2/M arrest in HK-2 cells. Sunitinib induces G0/G1 arrest in 786-O cells. **** p < 0.0001, * p < 0.05 vs. DMSO (ANOVA with Dunnett’s test).

    Journal: International Journal of Molecular Sciences

    Article Title: Exploratory Multi-Level Analysis of the HIF Axis in Clear-Cell Renal Cell Carcinoma and Evaluation of GN44028 as an Experimental HIF Pathway-Modulating Compound

    doi: 10.3390/ijms27083505

    Figure Lengend Snippet: Cell cycle analysis by propidium iodide staining and flow cytometry in 786-O ( A ), Caki-1 ( B ), and HK-2 ( C ) cells treated with KC7F2, FM19G11, GN44028, and sunitinib at IC 50 concentrations for 24 h. Bar graphs show mean ± SD from independent biological experiments, each measured in technical replicates ( n = 3–19). GN44028 was associated with an increased sub-G1 fraction in ccRCC cell lines and G2/M arrest in HK-2 cells. Sunitinib induces G0/G1 arrest in 786-O cells. **** p < 0.0001, * p < 0.05 vs. DMSO (ANOVA with Dunnett’s test).

    Article Snippet: 786-O (cRL1932TM), Caki-1 (McCoy) human renal cell carcinoma lines, and HK-2 (cRL2190TM) human proximal kidney tubule-derived cell lines were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Cell Cycle Assay, Staining, Flow Cytometry

    Heatmap of transcriptional responses of hypoxia- and HIF-regulated genes in renal cell carcinoma cell lines following pharmacological inhibition of the HIF pathway. The heatmap shows log 2 (fold change) values of mRNA expression relative to vehicle-treated controls (DMSO) for 786-O and Caki-1 cells after 72 h of treatment with KC7F2, GN44028, FM19G11, or sunitinib (SUN) at IC 50 concentrations. Normal proximal tubule cells (HK-2) were excluded from visualisation. All qPCR data are presented as log 2 fold change relative to the vehicle-treated controls (DMSO). Red, green, and white colours indicate downregulation, upregulation, and no change in expression, respectively. The colour scale represents log 2 FC values ranging from −5 to +5. Genes were hierarchically clustered (average linkage, Euclidean distance), and treatment conditions were ordered manually. Each value represents the mean of two independent biological experiments, each with three technical replicates.

    Journal: International Journal of Molecular Sciences

    Article Title: Exploratory Multi-Level Analysis of the HIF Axis in Clear-Cell Renal Cell Carcinoma and Evaluation of GN44028 as an Experimental HIF Pathway-Modulating Compound

    doi: 10.3390/ijms27083505

    Figure Lengend Snippet: Heatmap of transcriptional responses of hypoxia- and HIF-regulated genes in renal cell carcinoma cell lines following pharmacological inhibition of the HIF pathway. The heatmap shows log 2 (fold change) values of mRNA expression relative to vehicle-treated controls (DMSO) for 786-O and Caki-1 cells after 72 h of treatment with KC7F2, GN44028, FM19G11, or sunitinib (SUN) at IC 50 concentrations. Normal proximal tubule cells (HK-2) were excluded from visualisation. All qPCR data are presented as log 2 fold change relative to the vehicle-treated controls (DMSO). Red, green, and white colours indicate downregulation, upregulation, and no change in expression, respectively. The colour scale represents log 2 FC values ranging from −5 to +5. Genes were hierarchically clustered (average linkage, Euclidean distance), and treatment conditions were ordered manually. Each value represents the mean of two independent biological experiments, each with three technical replicates.

    Article Snippet: 786-O (cRL1932TM), Caki-1 (McCoy) human renal cell carcinoma lines, and HK-2 (cRL2190TM) human proximal kidney tubule-derived cell lines were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Inhibition, Expressing

    Treatment of synchronized kidney and muscle cells with recombinant Fbln5 (10ng/mL) disrupts rhythmic gene expression. A,B) Disrupted expression of Clock and Bmal1 but not C) Per2 in mouse myotube C2C12 cells with Fbln5 treatment. D,E) Disrupted expression of Bmal1 and Per1 but not F) Clock in human renal proximal tubule endothelial cells (RPTEC) with Fbln5. n=3 repetitions with biological triplicate. *p<0.05 Vehicle vs Fbln5. Cells were synchronized with dexamethasone prior to treatment with Fbln5 or vehicle.

    Journal: Comprehensive Physiology

    Article Title: The cardiac circadian clock regulates rhythms in peripheral tissues via Fibulin 5

    doi: 10.1002/cph4.70147

    Figure Lengend Snippet: Treatment of synchronized kidney and muscle cells with recombinant Fbln5 (10ng/mL) disrupts rhythmic gene expression. A,B) Disrupted expression of Clock and Bmal1 but not C) Per2 in mouse myotube C2C12 cells with Fbln5 treatment. D,E) Disrupted expression of Bmal1 and Per1 but not F) Clock in human renal proximal tubule endothelial cells (RPTEC) with Fbln5. n=3 repetitions with biological triplicate. *p<0.05 Vehicle vs Fbln5. Cells were synchronized with dexamethasone prior to treatment with Fbln5 or vehicle.

    Article Snippet: The human Renal Proximal Tubule Epithelial Cell (RPTEC) immortalized cell line (ATCC, PCS-400–010) was cultured in complete growth medium consisting of the base medium containing DMEM: F12 Medium (ATCC 30–2006) and the RPTEC Growth Kit components (ATCC ACS-4007) consisting of 5 pM triiodo-L-thyronine, 10 ng/mL recombinant human EGF, 3.5 μg/mL ascorbic acid, 5.0 μg/mL human transferrin, 5.0 μg/mL insulin, 25 ng/mL prostaglandin E 1 , 25 ng/mL hydrocortisone, 8.65 ng/mL sodium selenite and 1.2 mg/mL sodium bicarbonate.

    Techniques: Recombinant, Gene Expression, Expressing