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crl (ATCC)

Name: crl
Brand: ATCC
Rating: 99 (2339 reviews)

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ATCC crl
Crl, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2339 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/crl/product/ATCC
Average 99 stars, based on 2339 article reviews

crl - by Bioz Stars, 2026-02

99/100 stars

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Evaluation of the in vitro antitumor efficacy of Allo CAR70-NKT cells (A) Experimental design to study the in vitro antitumor efficacy of Allo CAR70-NKT cells against human RCC cell lines. (B) Schematics showing the indicated human tumor cell lines. (C) Tumor cell killing data at 24 h (n = 4). (D) ELISA analyses of IFN-γ and TNF-α production by Allo CAR70-NKT cells after 24-hour coculture with 786-O-FG cells (n = 4). (E) Experimental design to Study the tumor cell killing mechanisms of Allo CAR70-NKT cells mediated by NKRs. (F) Tumor cell killing data at 24 h (E:T ratio = 0.5:1; n = 4). Representative of 3 experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 by Student’s t test (D) or one-way ANOVA (C and F).

Journal: STAR Protocols

Article Title: Protocol to generate human stem cell-derived CD70-directed allogeneic CAR-NKT cells for treating renal cell carcinoma

doi: 10.1016/j.xpro.2025.104340

Figure Lengend Snippet: Evaluation of the in vitro antitumor efficacy of Allo CAR70-NKT cells (A) Experimental design to study the in vitro antitumor efficacy of Allo CAR70-NKT cells against human RCC cell lines. (B) Schematics showing the indicated human tumor cell lines. (C) Tumor cell killing data at 24 h (n = 4). (D) ELISA analyses of IFN-γ and TNF-α production by Allo CAR70-NKT cells after 24-hour coculture with 786-O-FG cells (n = 4). (E) Experimental design to Study the tumor cell killing mechanisms of Allo CAR70-NKT cells mediated by NKRs. (F) Tumor cell killing data at 24 h (E:T ratio = 0.5:1; n = 4). Representative of 3 experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 by Student’s t test (D) or one-way ANOVA (C and F).

Article Snippet: Human renal cell carcinoma cell line 786-O , ATCC , CRL-1932.

Techniques: In Vitro, Enzyme-linked Immunosorbent Assay

ZNF395 regulates the expression of key metabolic enzymes in hypoxia a) eGFP was introduced downstream of the ZNF395 locus using CRISPR genome editing. ChIP-seq of eGFP-tagged ZNF395 was performed in 786-O and A-498 cells. b) Genomic distribution of ZNF395 ChIP-seq peaks profiled by ChIPseeker c) De novo motif discovery using HOMER identified a motif that resembles CTCFL (aka BORIS), another C2H2 zinc finger protein. d) Nearest genes were mapped to the ZNF395 binding sites and enrichment of GO biological processes was performed using GREAT e) qPCR validation of a set of metabolic genes downregulated by ZNF395 shRNA-mediated knockdown f) Immunoblotting of metabolic enzymes following shRNA-mediated knockdown of ZNF395 in A-498 and 786-O cells g) Browser view of ChIP-seq profiles at the loci of metabolic enzymes GLS , IDH2 and PDK2 h) Genomic occupancy of ZNF395, HIF2α, HIF1β and MYC at ZNF395 or HIF2α binding sites in 786-O cells i) Overlap of ZNF395, HIF2α and MYC ChIP-seq peaks in 786-O cells using ChIPpeakAnno

Journal: Cancer research

Article Title: ZNF395 is a Hypoxia-Responsive Regulator of Mitochondrial Glutaminolysis in Clear Cell Renal Cell Carcinoma

doi: 10.1158/0008-5472.CAN-24-4745

Figure Lengend Snippet: ZNF395 regulates the expression of key metabolic enzymes in hypoxia a) eGFP was introduced downstream of the ZNF395 locus using CRISPR genome editing. ChIP-seq of eGFP-tagged ZNF395 was performed in 786-O and A-498 cells. b) Genomic distribution of ZNF395 ChIP-seq peaks profiled by ChIPseeker c) De novo motif discovery using HOMER identified a motif that resembles CTCFL (aka BORIS), another C2H2 zinc finger protein. d) Nearest genes were mapped to the ZNF395 binding sites and enrichment of GO biological processes was performed using GREAT e) qPCR validation of a set of metabolic genes downregulated by ZNF395 shRNA-mediated knockdown f) Immunoblotting of metabolic enzymes following shRNA-mediated knockdown of ZNF395 in A-498 and 786-O cells g) Browser view of ChIP-seq profiles at the loci of metabolic enzymes GLS , IDH2 and PDK2 h) Genomic occupancy of ZNF395, HIF2α, HIF1β and MYC at ZNF395 or HIF2α binding sites in 786-O cells i) Overlap of ZNF395, HIF2α and MYC ChIP-seq peaks in 786-O cells using ChIPpeakAnno

Article Snippet: Commercial cell lines, 786-O (RRID:CVCL_1051), A-498 (RRID:CVCL_1056), HK-2 (RRID:CVCL_0302), ACHN (RRID:CVCL_1067), Caki-1 (RRID:CVCL_0234) and HEK293 (RRID:CVCL_0045) were purchased from ATCC.

Techniques: Expressing, CRISPR, ChIP-sequencing, Binding Assay, Biomarker Discovery, shRNA, Knockdown, Western Blot

ZNF395 maintains TCA anaplerosis a) Levels of TCA cycle intermediates measured by GC-MS in A-498 cells following shRNA-mediated knockdown of ZNF395 b) Levels of amino acids measured by LC-MS in A-498 cells following shRNA-mediated knockdown of ZNF395 c) NADPH/NADP levels measured using NADP/NADPH-Glo ™ assay in A-498 cells following shRNA-mediated knockdown of ZNF395 d) GSH/GSSG measured using GSH/GSSG-Glo ™ assay in A-498 cells following shRNA-mediated knockdown of ZNF395 e) Levels of reactive oxygen species (ROS) in A-498 cells following shRNA-mediated knockdown of ZNF395 determined by staining cells with MitoSOX ™ Red mitochondrial superoxide indicator and quantifying by flow cytometry f) Cell viability measured by CCK8 after 24 hr treatment of H 2 O 2 in A-498 cells g) Isotope tracing using 13 C 5 -glutamine was performed to determine the abundance of TCA cycle intermediates, glutathione, pyrimidine nucleotides and amino acids derived from glutaminolysis h) Levels of TCA cycle intermediates, glutathione and pyrimidine nucleotides detected in A-498 cells following shRNA-mediated knockdown of ZNF395 from experiment in g) split by oxidative and reductive pathways i) Levels of GSH and GSSG from experiment g) j) Levels of amino acids from experiment g) k) Levels of TCA cycle intermediates measured by GC-MS in 786-O cells following shRNA-mediated knockdown of ZNF395 propagated in vivo l) Levels of amino acids measured by LC-MS in 786-O cells following shRNA-mediated knockdown of ZNF395 propagated in vivo

Journal: Cancer research

Article Title: ZNF395 is a Hypoxia-Responsive Regulator of Mitochondrial Glutaminolysis in Clear Cell Renal Cell Carcinoma

doi: 10.1158/0008-5472.CAN-24-4745

Figure Lengend Snippet: ZNF395 maintains TCA anaplerosis a) Levels of TCA cycle intermediates measured by GC-MS in A-498 cells following shRNA-mediated knockdown of ZNF395 b) Levels of amino acids measured by LC-MS in A-498 cells following shRNA-mediated knockdown of ZNF395 c) NADPH/NADP levels measured using NADP/NADPH-Glo ™ assay in A-498 cells following shRNA-mediated knockdown of ZNF395 d) GSH/GSSG measured using GSH/GSSG-Glo ™ assay in A-498 cells following shRNA-mediated knockdown of ZNF395 e) Levels of reactive oxygen species (ROS) in A-498 cells following shRNA-mediated knockdown of ZNF395 determined by staining cells with MitoSOX ™ Red mitochondrial superoxide indicator and quantifying by flow cytometry f) Cell viability measured by CCK8 after 24 hr treatment of H 2 O 2 in A-498 cells g) Isotope tracing using 13 C 5 -glutamine was performed to determine the abundance of TCA cycle intermediates, glutathione, pyrimidine nucleotides and amino acids derived from glutaminolysis h) Levels of TCA cycle intermediates, glutathione and pyrimidine nucleotides detected in A-498 cells following shRNA-mediated knockdown of ZNF395 from experiment in g) split by oxidative and reductive pathways i) Levels of GSH and GSSG from experiment g) j) Levels of amino acids from experiment g) k) Levels of TCA cycle intermediates measured by GC-MS in 786-O cells following shRNA-mediated knockdown of ZNF395 propagated in vivo l) Levels of amino acids measured by LC-MS in 786-O cells following shRNA-mediated knockdown of ZNF395 propagated in vivo

Techniques: Gas Chromatography-Mass Spectrometry, shRNA, Knockdown, Liquid Chromatography with Mass Spectroscopy, Glo Assay, Staining, Flow Cytometry, Derivative Assay, In Vivo

ZNF395 maintains mitochondrial respiration a) Levels of NADH, NAD+ and NADH/NAD+ ratio following dox-inducible shRNA-mediated knockdown of non-targeting control (NTC) or ZNF395. ***p-value < 0.001, **p-value < 0.01, two-tailed t-test b) Seahorse mito stress test was performed in 786-O expressing two dox-inducible shRNA against ZNF395 or non-targeting control (shNTC) c) Mitochondrial respiration rate from b). ****p-value < 0.0001, **p-value < 0.01, *p-value <0.05, two-tailed t-test d) Seahorse mito stress test was performed in 786-O cells expressing either empty vector or NDI-1, a yeast mitochondrial NADH dehydrogenase that oxidizes NADH to NAD+ and thus supplements the mammalian complex I. These two cell lines were further subjected to ZNF395 shRNA-mediated knockdown. e) Mitochondrial respiration rate from d) f) Same as d) but performed in A-498 cells g) Same as e) but performed in A-498 cells h) Colony formation assay of 786-O and A-498 with either empty vector or NDI-1 paired with shRNA against non-targeting control (NTC) or ZNF395

Journal: Cancer research

Article Title: ZNF395 is a Hypoxia-Responsive Regulator of Mitochondrial Glutaminolysis in Clear Cell Renal Cell Carcinoma

doi: 10.1158/0008-5472.CAN-24-4745

Figure Lengend Snippet: ZNF395 maintains mitochondrial respiration a) Levels of NADH, NAD+ and NADH/NAD+ ratio following dox-inducible shRNA-mediated knockdown of non-targeting control (NTC) or ZNF395. ***p-value < 0.001, **p-value < 0.01, two-tailed t-test b) Seahorse mito stress test was performed in 786-O expressing two dox-inducible shRNA against ZNF395 or non-targeting control (shNTC) c) Mitochondrial respiration rate from b). ****p-value < 0.0001, **p-value < 0.01, *p-value <0.05, two-tailed t-test d) Seahorse mito stress test was performed in 786-O cells expressing either empty vector or NDI-1, a yeast mitochondrial NADH dehydrogenase that oxidizes NADH to NAD+ and thus supplements the mammalian complex I. These two cell lines were further subjected to ZNF395 shRNA-mediated knockdown. e) Mitochondrial respiration rate from d) f) Same as d) but performed in A-498 cells g) Same as e) but performed in A-498 cells h) Colony formation assay of 786-O and A-498 with either empty vector or NDI-1 paired with shRNA against non-targeting control (NTC) or ZNF395

Techniques: shRNA, Knockdown, Control, Two Tailed Test, Expressing, Plasmid Preparation, Colony Assay

( A ) Epigenomic datasets generated from 4 tRCC (s-TFE, FU-UR-1, UOK109, and UOK146) and 6 ccRCC (Caki-1, A-498, RFX393, 786-O, 769-P, and KMRC-1) cell lines, either in-house or in a previously published study ( , ). ( B ) Unsupervised hierarchical clustering of the H3K4me3 ChIP-seq, H3K27ac ChIP-seq, and MeDIP-seq consensus peaks across tRCC and ccRCC cell lines analyzed in this study. ( C ) Volcano plots showing differentially marked peaks between tRCC and ccRCC cell lines for H3K4me3 ChIP-Seq, H3K27ac ChIP-seq, and MeDIP-seq. Thresholds for significance were set at FDR-q < 0.01 and log 2 FC > 1 for H3K27ac and MeDIP and > 2 for H3K4me3.

Journal: The Journal of Clinical Investigation

Article Title: Cell-free DNA epigenomic profiling enables noninvasive detection and monitoring of translocation renal cell carcinoma

doi: 10.1172/JCI195725

Figure Lengend Snippet: ( A ) Epigenomic datasets generated from 4 tRCC (s-TFE, FU-UR-1, UOK109, and UOK146) and 6 ccRCC (Caki-1, A-498, RFX393, 786-O, 769-P, and KMRC-1) cell lines, either in-house or in a previously published study ( , ). ( B ) Unsupervised hierarchical clustering of the H3K4me3 ChIP-seq, H3K27ac ChIP-seq, and MeDIP-seq consensus peaks across tRCC and ccRCC cell lines analyzed in this study. ( C ) Volcano plots showing differentially marked peaks between tRCC and ccRCC cell lines for H3K4me3 ChIP-Seq, H3K27ac ChIP-seq, and MeDIP-seq. Thresholds for significance were set at FDR-q < 0.01 and log 2 FC > 1 for H3K27ac and MeDIP and > 2 for H3K4me3.

Article Snippet: The cell lines 786-O (ATCC, CRL-1932; RRID: CVCL_1051), 293T (ATCC, CRL-11268; RRID: CVCL_0063), A-498 (ATCC, HTB-44; RRID: CVCL_1056), 769-P (ATCC, CRL-1933; RRID: CVCL_1050), KMRC-1 (JCRB1010; RRID: CVCL_2983), Caki-1 (ATCC, HTB-46; RRID: CVCL_0234), UOK109 (RRID: CVCL_B123), and UOK146 (RRID: CVCL_B123) were obtained from W. Marston Linehan’s laboratory (National Cancer Institute).

Techniques: Generated, ChIP-sequencing, Methylated DNA Immunoprecipitation

$( A ) Epigenomic datasets generated from 51 plasma samples collected from patients with metastatic tRCC ( N = 30; 10 patients), metastatic ccRCC ( N = 12; 12 patients), or those acting as healthy controls ( N = 9; 9 individuals). ( B ) Integrative Genomics Viewer tracks from ChIP-seq profiles for H3K4me3, H3K27ac, and TFE3 in cell lines (tRCC: UOK109, s-TFE; ccRCC: 786-O, A-498) and plasma samples at representative tRCC-selective ( GPR143 ) or ccRCC-selective ( C1Q1L ) loci. ( C ) Aggregated cf-ChIP signal compared among tRCC, ccRCC, and healthy plasma samples for the following marks; the box plots quantify the AUCs for each histone mark (left to right): H3K4me3 signal at cell line–informed H3K4me3 tRCC-up sites was significantly higher in 28 tRCC samples from 10 patients compared with 11 ccRCC samples from 11 patients ( P = 0.0027) and showed a trend when compared with 9 healthy control samples ( P = 0.079); H3K27ac signal at cell line–informed H3K27ac tRCC-up sites was significantly higher in 27 tRCC samples from 10 patients compared with 12 ccRCC samples from 12 patients ( P = 0.0029) and with 9 healthy control samples from 9 individuals ( P = 0.00017); H3K27ac signal at TFE3 fusion–occupied TFBSs was significantly higher in 27 tRCC samples from 10 patients compared with 12 ccRCC samples from 12 patients ( P = 0.0003) and with 9 healthy control samples from 9 individuals ( P = 0.00042). P values were determined by Wilcoxon’s test. ( D ) Comparison of TIESs of cf-ChIP H3K4me3 and H3K27ac signals at cell line–informed sites (H3K4me3 tRCC-up peaks, H3K27ac tRCC-up peaks, and TFE3 fusion–occupied binding sites) among tRCC, ccRCC, and healthy plasma, with samples color-scaled according to tumor fraction. TIES was significantly higher in 27 tRCC samples from 10 patients compared with 11 ccRCC samples from 11 patients ( P = 0.00035) and with 9 healthy control samples from 9 individuals ( P = 0.000049). HP, healthy plasma. P values were determined by Wilcoxon’s test. The box plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median.$

Journal: The Journal of Clinical Investigation

Article Title: Cell-free DNA epigenomic profiling enables noninvasive detection and monitoring of translocation renal cell carcinoma

doi: 10.1172/JCI195725

Figure Lengend Snippet: ( A ) Epigenomic datasets generated from 51 plasma samples collected from patients with metastatic tRCC ( N = 30; 10 patients), metastatic ccRCC ( N = 12; 12 patients), or those acting as healthy controls ( N = 9; 9 individuals). ( B ) Integrative Genomics Viewer tracks from ChIP-seq profiles for H3K4me3, H3K27ac, and TFE3 in cell lines (tRCC: UOK109, s-TFE; ccRCC: 786-O, A-498) and plasma samples at representative tRCC-selective ( GPR143 ) or ccRCC-selective ( C1Q1L ) loci. ( C ) Aggregated cf-ChIP signal compared among tRCC, ccRCC, and healthy plasma samples for the following marks; the box plots quantify the AUCs for each histone mark (left to right): H3K4me3 signal at cell line–informed H3K4me3 tRCC-up sites was significantly higher in 28 tRCC samples from 10 patients compared with 11 ccRCC samples from 11 patients ( P = 0.0027) and showed a trend when compared with 9 healthy control samples ( P = 0.079); H3K27ac signal at cell line–informed H3K27ac tRCC-up sites was significantly higher in 27 tRCC samples from 10 patients compared with 12 ccRCC samples from 12 patients ( P = 0.0029) and with 9 healthy control samples from 9 individuals ( P = 0.00017); H3K27ac signal at TFE3 fusion–occupied TFBSs was significantly higher in 27 tRCC samples from 10 patients compared with 12 ccRCC samples from 12 patients ( P = 0.0003) and with 9 healthy control samples from 9 individuals ( P = 0.00042). P values were determined by Wilcoxon’s test. ( D ) Comparison of TIESs of cf-ChIP H3K4me3 and H3K27ac signals at cell line–informed sites (H3K4me3 tRCC-up peaks, H3K27ac tRCC-up peaks, and TFE3 fusion–occupied binding sites) among tRCC, ccRCC, and healthy plasma, with samples color-scaled according to tumor fraction. TIES was significantly higher in 27 tRCC samples from 10 patients compared with 11 ccRCC samples from 11 patients ( P = 0.00035) and with 9 healthy control samples from 9 individuals ( P = 0.000049). HP, healthy plasma. P values were determined by Wilcoxon’s test. The box plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median.

Techniques: Generated, Clinical Proteomics, ChIP-sequencing, Control, Comparison, Binding Assay

A) Microscopy images of 786-O cells upon treatment with siGLO MNPs. Red: siGLO; Green: Cell Membrane; Blue: Nucleus. B) Flow cytometry gating strategy. C) Fluorescence signal distribution after treatment with increasing siGLO concentrations encapsulated within MNPs. D) Percent of cells with fluorescence above 0 ng siGLO controls. Scale bar: 300 µm.

Journal: bioRxiv

Article Title: Endocytosis of PEGylated polymeric mesoscale nanoparticles is dynamin- and macropinocytosis-dependent

doi: 10.64898/2026.01.22.701067

Figure Lengend Snippet: A) Microscopy images of 786-O cells upon treatment with siGLO MNPs. Red: siGLO; Green: Cell Membrane; Blue: Nucleus. B) Flow cytometry gating strategy. C) Fluorescence signal distribution after treatment with increasing siGLO concentrations encapsulated within MNPs. D) Percent of cells with fluorescence above 0 ng siGLO controls. Scale bar: 300 µm.

Article Snippet: To evaluate siRNA-MNP endocytosis, we used fluorescently-labeled siRNA mimic siGLO MNPs with renal cell adenocarcinoma 786-O cells (American Type Culture Collection, Cat. No. CRL-1932).

Techniques: Microscopy, Membrane, Flow Cytometry, Fluorescence

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