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human normal kidney cell lines hk 2  (ATCC)


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    ATCC human normal kidney cell lines hk 2
    Human Normal Kidney Cell Lines Hk 2, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4423 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+normal+kidney+cell+lines+hk+2/pmc12852824-329-10-22?v=ATCC
    Average 99 stars, based on 4423 article reviews
    human normal kidney cell lines hk 2 - by Bioz Stars, 2026-07
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    STAP2 regulates the advancement of renal fibrosis through the HSP27-PI3K/AKT signaling pathway. After various factors lead to renal injury, the upregulation of STAP2 promotes the interaction between STAP2 and HSP27, further enhancing the phosphorylation of HSP27 and activation of the PI3K/AKT signaling pathway, which results in the loss of <t>epithelial</t> phenotype in epithelial cells, activation of fibroblasts and ultimately results in renal interstitial fibrosis
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    ATCC normal human tubular kidney epithelial cell line
    STAP2 regulates the advancement of renal fibrosis through the HSP27-PI3K/AKT signaling pathway. After various factors lead to renal injury, the upregulation of STAP2 promotes the interaction between STAP2 and HSP27, further enhancing the phosphorylation of HSP27 and activation of the PI3K/AKT signaling pathway, which results in the loss of <t>epithelial</t> phenotype in epithelial cells, activation of fibroblasts and ultimately results in renal interstitial fibrosis
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    STAP2 regulates the advancement of renal fibrosis through the HSP27-PI3K/AKT signaling pathway. After various factors lead to renal injury, the upregulation of STAP2 promotes the interaction between STAP2 and HSP27, further enhancing the phosphorylation of HSP27 and activation of the PI3K/AKT signaling pathway, which results in the loss of <t>epithelial</t> phenotype in epithelial cells, activation of fibroblasts and ultimately results in renal interstitial fibrosis
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    Procell Inc normal human kidney proximal tubular cell line (cl-0109), hk-2
    Establishment and verification of the prognosis score (Riskscore). (a) Error rate for the random trees and importance values for the 12 metabolism-related genes. (b) Riskscore modeling score, clinical characteristics, and specific expression of 12 genes. (c) Survival analysis of FZD1 , SALL1 , SLC1A1 , and MALAT1 . (d) Relative mRNA expressions of FZD1 , SALL1 , SLC1A1 , and MALAT1 in <t>HK-2</t> (normal cells) and CAKI-1 (cell models of ccRCC). (e) Survival analysis of Riskscore in the TCGA datasets (KIRC). (f) Survival analysis of Riskscore in the independent verification set (GSE29609). ∗ Compared with the HK-2 group, P < 0.05.
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    Keygen Biotech human proximal tubular cell line derived normal kidney (hk-2
    PLD1 expression is inhibited significantly by Cd exposure in renal tubular cell lines. (a) The viability of NRK-52E and <t>HK-2</t> cells after Cd exposure measured by CCK-8 assay. (b) The mRNA expression of PLD1 was decreased after Cd exposure. (c) The protein expression of PLD1 was decreased after Cd exposure. (d) Apoptosis ameliorated in renal tubular cells exposed to Cd performed by flow cytometry. Con: control group. Rats exposed to Cd at 0.6 mg/kg/d for 5 days per week for 12 weeks. NRK-52E cells exposed at 8 μ M CdCl 2 for 48 h, HK-2 cells exposed at 40 μ M CdCl 2 for 48 h. NS: nonspecific band. Data are mean ± SD. ∗ p < 0.05 and ∗∗ p < 0.01.
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    STAP2 regulates the advancement of renal fibrosis through the HSP27-PI3K/AKT signaling pathway. After various factors lead to renal injury, the upregulation of STAP2 promotes the interaction between STAP2 and HSP27, further enhancing the phosphorylation of HSP27 and activation of the PI3K/AKT signaling pathway, which results in the loss of epithelial phenotype in epithelial cells, activation of fibroblasts and ultimately results in renal interstitial fibrosis

    Journal: Journal of Translational Medicine

    Article Title: STAP2 promotes the progression of renal fibrosis via HSP27

    doi: 10.1186/s12967-024-05776-6

    Figure Lengend Snippet: STAP2 regulates the advancement of renal fibrosis through the HSP27-PI3K/AKT signaling pathway. After various factors lead to renal injury, the upregulation of STAP2 promotes the interaction between STAP2 and HSP27, further enhancing the phosphorylation of HSP27 and activation of the PI3K/AKT signaling pathway, which results in the loss of epithelial phenotype in epithelial cells, activation of fibroblasts and ultimately results in renal interstitial fibrosis

    Article Snippet: The China Center for Type Culture Collection (Wuhan, China) provided the normal human kidney proximal tubule epithelial cell line (HK-2), which was grown in a DMEM/F12 medium (#G4610-500ML, Servicebio, Wuhan, China) supplemented with 10% fetal bovine serum (FBS, Gibco, USA).

    Techniques: Phospho-proteomics, Activation Assay

    Establishment and verification of the prognosis score (Riskscore). (a) Error rate for the random trees and importance values for the 12 metabolism-related genes. (b) Riskscore modeling score, clinical characteristics, and specific expression of 12 genes. (c) Survival analysis of FZD1 , SALL1 , SLC1A1 , and MALAT1 . (d) Relative mRNA expressions of FZD1 , SALL1 , SLC1A1 , and MALAT1 in HK-2 (normal cells) and CAKI-1 (cell models of ccRCC). (e) Survival analysis of Riskscore in the TCGA datasets (KIRC). (f) Survival analysis of Riskscore in the independent verification set (GSE29609). ∗ Compared with the HK-2 group, P < 0.05.

    Journal: Journal of Oncology

    Article Title: Identification of Prognostic Metabolism-Related Genes in Clear Cell Renal Cell Carcinoma

    doi: 10.1155/2021/2042114

    Figure Lengend Snippet: Establishment and verification of the prognosis score (Riskscore). (a) Error rate for the random trees and importance values for the 12 metabolism-related genes. (b) Riskscore modeling score, clinical characteristics, and specific expression of 12 genes. (c) Survival analysis of FZD1 , SALL1 , SLC1A1 , and MALAT1 . (d) Relative mRNA expressions of FZD1 , SALL1 , SLC1A1 , and MALAT1 in HK-2 (normal cells) and CAKI-1 (cell models of ccRCC). (e) Survival analysis of Riskscore in the TCGA datasets (KIRC). (f) Survival analysis of Riskscore in the independent verification set (GSE29609). ∗ Compared with the HK-2 group, P < 0.05.

    Article Snippet: The cell line and the medium above were purchased from Shanghai Zhong Qiao Xin Zhou Biotechnology Co., Ltd. A normal human kidney proximal tubular cell line (CL-0109), HK-2, and its special medium (CM-0109) were purchased from Procell Life Science & Technology Co., Ltd.

    Techniques: Expressing

    PLD1 expression is inhibited significantly by Cd exposure in renal tubular cell lines. (a) The viability of NRK-52E and HK-2 cells after Cd exposure measured by CCK-8 assay. (b) The mRNA expression of PLD1 was decreased after Cd exposure. (c) The protein expression of PLD1 was decreased after Cd exposure. (d) Apoptosis ameliorated in renal tubular cells exposed to Cd performed by flow cytometry. Con: control group. Rats exposed to Cd at 0.6 mg/kg/d for 5 days per week for 12 weeks. NRK-52E cells exposed at 8 μ M CdCl 2 for 48 h, HK-2 cells exposed at 40 μ M CdCl 2 for 48 h. NS: nonspecific band. Data are mean ± SD. ∗ p < 0.05 and ∗∗ p < 0.01.

    Journal: BioMed Research International

    Article Title: Phospholipase D1 Ameliorates Apoptosis in Chronic Renal Toxicity Caused by Low-Dose Cadmium Exposure

    doi: 10.1155/2020/7091053

    Figure Lengend Snippet: PLD1 expression is inhibited significantly by Cd exposure in renal tubular cell lines. (a) The viability of NRK-52E and HK-2 cells after Cd exposure measured by CCK-8 assay. (b) The mRNA expression of PLD1 was decreased after Cd exposure. (c) The protein expression of PLD1 was decreased after Cd exposure. (d) Apoptosis ameliorated in renal tubular cells exposed to Cd performed by flow cytometry. Con: control group. Rats exposed to Cd at 0.6 mg/kg/d for 5 days per week for 12 weeks. NRK-52E cells exposed at 8 μ M CdCl 2 for 48 h, HK-2 cells exposed at 40 μ M CdCl 2 for 48 h. NS: nonspecific band. Data are mean ± SD. ∗ p < 0.05 and ∗∗ p < 0.01.

    Article Snippet: A human proximal tubular cell line derived from a normal kidney (HK-2) and rat renal tubular epithelial cell lines (NRK-52E) were purchased from KeyGen BioTech, Nanjing, China.

    Techniques: Expressing, CCK-8 Assay, Flow Cytometry

    PLD1 and its downstream product PA protect cells from Cd-induced renal impairment. (a) Apoptosis was ameliorated after overexpression of PLD1 in HK-2 cells. (b) Cell survival rate was increased after overexpression of PLD1 in HK-2 cells assayed with CCK-8. (c) The concentration of PA in HK-2 cells detected with ELISA. (d) Apoptosis was ameliorated by PA treatment in HK-2 and NRK-52E cells. (e) Apoptosis was ameliorated by PA treatment detected in HK-2 and NRK-52E cells by flow cytometry. OE: overexpression of PLD1 with adenovirus vector. Data are mean ± SD from three experiments. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Journal: BioMed Research International

    Article Title: Phospholipase D1 Ameliorates Apoptosis in Chronic Renal Toxicity Caused by Low-Dose Cadmium Exposure

    doi: 10.1155/2020/7091053

    Figure Lengend Snippet: PLD1 and its downstream product PA protect cells from Cd-induced renal impairment. (a) Apoptosis was ameliorated after overexpression of PLD1 in HK-2 cells. (b) Cell survival rate was increased after overexpression of PLD1 in HK-2 cells assayed with CCK-8. (c) The concentration of PA in HK-2 cells detected with ELISA. (d) Apoptosis was ameliorated by PA treatment in HK-2 and NRK-52E cells. (e) Apoptosis was ameliorated by PA treatment detected in HK-2 and NRK-52E cells by flow cytometry. OE: overexpression of PLD1 with adenovirus vector. Data are mean ± SD from three experiments. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Article Snippet: A human proximal tubular cell line derived from a normal kidney (HK-2) and rat renal tubular epithelial cell lines (NRK-52E) were purchased from KeyGen BioTech, Nanjing, China.

    Techniques: Over Expression, CCK-8 Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Plasmid Preparation

    The miR-122-5p downregulates the expression of PLD1 to promote apoptosis. (a) Screening of candidate regulatory miRNAs for PLD1 in online databases (miRWalk, miRanda, and miTarget). (b) Expression of miR-122-5p was increased after Cd exposure in NRK-52E and HK-2 cells. (c) Regulatory effect of miR-122-5p on PLD1 3′UTR determined with dual-luciferase reporter assay. (d) miR-122-5p repressed mRNA expression of PLD1 while cotransfected with miR-122-5p and overexpression of PLD1 in NRK-52E cells. (e) miR-122-5p repressed protein expression of PLD1 in NRK-52E cells. (f) miR-122-5p promoted apoptosis in NRK-52E cells. Data are represented as mean ± SD, N = 3. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Journal: BioMed Research International

    Article Title: Phospholipase D1 Ameliorates Apoptosis in Chronic Renal Toxicity Caused by Low-Dose Cadmium Exposure

    doi: 10.1155/2020/7091053

    Figure Lengend Snippet: The miR-122-5p downregulates the expression of PLD1 to promote apoptosis. (a) Screening of candidate regulatory miRNAs for PLD1 in online databases (miRWalk, miRanda, and miTarget). (b) Expression of miR-122-5p was increased after Cd exposure in NRK-52E and HK-2 cells. (c) Regulatory effect of miR-122-5p on PLD1 3′UTR determined with dual-luciferase reporter assay. (d) miR-122-5p repressed mRNA expression of PLD1 while cotransfected with miR-122-5p and overexpression of PLD1 in NRK-52E cells. (e) miR-122-5p repressed protein expression of PLD1 in NRK-52E cells. (f) miR-122-5p promoted apoptosis in NRK-52E cells. Data are represented as mean ± SD, N = 3. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Article Snippet: A human proximal tubular cell line derived from a normal kidney (HK-2) and rat renal tubular epithelial cell lines (NRK-52E) were purchased from KeyGen BioTech, Nanjing, China.

    Techniques: Expressing, Luciferase, Reporter Assay, Over Expression