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human renal proximal tubular epithelial cells  (ATCC)


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    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 750 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/renal+proximal+tubules/Primary+Renal+Proximal+Tubule+Epithelial+Cells%3B+Normal%2C+Human/pmc13179815-45-0-11
    Average 99 stars, based on 750 article reviews
    human renal proximal tubular epithelial cells - by Bioz Stars, 2026-09
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    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

    Related Articles

    other:

    Article Title: The role of Toll-like receptor proteins (TLR) 2 and 4 in mediating inflammation in proximal tubules.
    Article Snippet: Harshini Mudaliar, Carol Pollock, Muralikrishna Gangadharan Komala, Steven Chadban, Huiling Wu, and Usha Panchapakesan Renal Research Group, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia; and Renal Medicine, Royal Prince Alfred Hospital and Collaborative Transplant Research Group, University of Sydney, New South Wales, Australia

    Derivative Assay:

    Article Title: Hinokitiol Modulates Nrf2/HO-1 Signaling, Autophagy, and URAT1 in Hyperuricemia and Oxidative Stress Models of Renal Injury.
    Article Snippet: 3 Hyperuricemia (HUA), a metabolic disorder characterized by elevated serum uric acid 4 levels, is a major risk factor for kidney injury and is closely associated with oxidative stress 5 and autophagy dysregulation.. This study investigates the renoprotective effects of 6 hinokitiol, a natural tropolone derivative, in renal tubular epithelial cells and a potassium 7 oxonate (PO)/hypoxanthine (HX)-induced hyperuricemia rat model.. In vitro, hinokitiol 8 significantly attenuated H2O2-induced cytotoxicity and reactive oxygen species (ROS) 9 accumulation, which was associated with the activation of the Nrf2/HO-1 antioxidant 10 pathway.



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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

    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