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ATCC hek 293t cells
Hek 293t Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 38795 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hek+293t+cells/293T/pm42893758-46-21-23
Average 99 stars, based on 38795 article reviews

hek 293t cells - by Bioz Stars, 2026-11

99/100 stars

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Multiple Displacement Amplification:

Article Title: Targeting PRDX1-G6PD Interaction Promotes a Metabolic Vulnerability and Redox Imbalance in Triple-Negative Breast Cancer.
Article Snippet: 27 Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with 28 Jo urn al Pr e-p roo f

Transfection:

Article Title: Transcriptional rewiring of NF-κB by HBZ and Fra-2 drives inflammatory chemoresistance in Tax-negative adult T-cell leukemia/lymphoma
Article Snippet: ATL-2 (-) (CVCL_A6TF) were cultivated in ImmunoCult-XF T Cell Expansion Medium (STEMCELL Technologies). .. HEK 293T cells (ATCC CRL-3216) were propagated in DMEM with 10% FCS and transfected according to the manufacturer’s protocol using PEIMax (1mg/ml, Polysciences). ..

Produced:

Article Title: Sunitinib induces senolysis associated with modulation of platelet-derived growth factor receptor beta.
Article Snippet: .. Lentiviruses were produced in HEK-293T cells (ATCC, CRL-3216) by co-transfecting the lentiviral expression vector, pCMV-VSV-G envelope plasmid (Addgene, Cambridge, MA), and psPAX2 packaging plasmid with Lipofectamine 2000 (Invitrogen). ..

Expressing:

Article Title: Bone-Targeted Engineered Exosomes Delivering Betaine Alleviate Osteoporosis via Autophagy-Driven Osteogenesis.
Article Snippet: Dysregulated bone remodeling, attenuated endogenous osteogenic capacity, and the lack of bone-targeting capability in therapeutics constitute the core challenges in current clinical interventions for osteoporosis.. In this study, a hybrid nanodelivery system integrating betaine-loaded metal-organic frameworks with engineered exosomes (BZ@Exos) is constructed to restore bone metabolic homeostasis and improve bone microstructure.. The engineered exosomes co-overexpressing CXCR4 and CD47 proteins on the surface exhibit high bone tissue targeting efficiency and evade clearance by the mononuclear phagocyte system, while ZIF8 enables stable encapsulation of betaine.

Plasmid Preparation:

Construct:

Cell Culture:

Article Title: Comparative Analysis of Altered lncRNA and mRNA Expression Profiles in RMI1-Knockdown Cells Following Ionizing Radiation Exposure
Article Snippet: .. HEK 293T cells were obtained from ATCC (Manassas, VA, USA) and cultured in DMEM medium (Hyclone, Logan, UT, USA) supplemented with 10% fetal bovine serum (Gibco, Carlsbad, CA, USA), and incubated at 37 °C in 5% CO2. .. In November 2017, the cells were transduced with lentiviruses (GeneChem, Shanghai, China) containing short hairpin RNA (shRNA) targeting the human RMI1 gene.

Article Title: An opioid efficacy switch for reversible optical control of analgesia.
Article Snippet: In brief Azo-morphine-3 (AM-3) is a photoswitchable ligand that toggles between low and high efficacy states to control mu-opioid receptor activity in vitro and in vivo both in the brain and periphery.. AM-3 provides a powerful tool to probe the structural basis of opioid efficacy and enables spatiotemporally precise control of analgesia across pain models with reduced side effects compared with systemic drugs.

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( A to C and G ) eGFP reporter assay to assess the silencing efficiency of 3-nt tiled Psp Cas13b crRNAs targeting the breakpoint region of fusion transcripts BCR::ABL1-p190 (A), SNX2::ABL1 (B), SFPQ::ABL1 (C), and BCR::ABL1-p210 (G). Data points in the graphs are averages of mean fluorescence; N = 3. The data are represented in arbitrary units (A.U.). Errors are SEM, and P values of the one-way analysis of variance (ANOVA) test with Dunnett’s multiple comparisons are indicated (95% confidence interval). ( D to F ) RT-PCR assays measuring silencing efficiency of tiled Psp Cas13b crRNAs (3-nt resolution) targeting the breakpoint regions of fusion transcripts (D) BCR::ABL1-p190, (E) SNX2::ABL1, and (F) SFPQ::ABL1; N = 3. Data are normalized means and errors are SEM. Results are analyzed by one-way ANOVA test (Dunnett’s multiple comparisons) with P values indicated (95% confidence interval). ( H ) Representative Western blot analysis to examine the expression level of BCR::ABL1-p190 protein in HEK 293T cells expressing tiled crRNAs targeting BCR::ABL1-p190 transcripts 24 hours posttransfection, with quantification from three independent experiments; N = 3. n.s., not significant. ( I ) Schematic of BCR::ABL1-dependent phosphorylation of ERK and STAT proteins, and inhibition of BCR::ABL1 oncogenic activity with imatinib, a potent competitor of adenosine 5′-triphosphate (ATP) binding to ABL kinase. ( J ) Representative Western blot analysis examining the suppression of BCR::ABL1 expression and the subsequent inhibition of STAT5 and ERK phosphorylation in HEK 293T cells expressing BCR::ABL1-p190, Psp Cas13b, and either NT or crRNA targeting the BCR::ABL1 24 hours posttransfection. HEK 293T cells expressing BCR::ABL1-p190 and Psp Cas13b treated with 1 μM imatinib for 4 hours were used as a positive control. Parental cells are HEK 293T cells transfected with Psp Cas13b, NT, and a control plasmid; N = 3. N is the number of independent biological experiments.

Journal: Science Advances

Article Title: Programmable and selective silencing of oncogenic fusion transcripts by CRISPR-Cas13b via breakpoint sequence recognition

doi: 10.1126/sciadv.ady0296

Figure Lengend Snippet: ( A to C and G ) eGFP reporter assay to assess the silencing efficiency of 3-nt tiled Psp Cas13b crRNAs targeting the breakpoint region of fusion transcripts BCR::ABL1-p190 (A), SNX2::ABL1 (B), SFPQ::ABL1 (C), and BCR::ABL1-p210 (G). Data points in the graphs are averages of mean fluorescence; N = 3. The data are represented in arbitrary units (A.U.). Errors are SEM, and P values of the one-way analysis of variance (ANOVA) test with Dunnett’s multiple comparisons are indicated (95% confidence interval). ( D to F ) RT-PCR assays measuring silencing efficiency of tiled Psp Cas13b crRNAs (3-nt resolution) targeting the breakpoint regions of fusion transcripts (D) BCR::ABL1-p190, (E) SNX2::ABL1, and (F) SFPQ::ABL1; N = 3. Data are normalized means and errors are SEM. Results are analyzed by one-way ANOVA test (Dunnett’s multiple comparisons) with P values indicated (95% confidence interval). ( H ) Representative Western blot analysis to examine the expression level of BCR::ABL1-p190 protein in HEK 293T cells expressing tiled crRNAs targeting BCR::ABL1-p190 transcripts 24 hours posttransfection, with quantification from three independent experiments; N = 3. n.s., not significant. ( I ) Schematic of BCR::ABL1-dependent phosphorylation of ERK and STAT proteins, and inhibition of BCR::ABL1 oncogenic activity with imatinib, a potent competitor of adenosine 5′-triphosphate (ATP) binding to ABL kinase. ( J ) Representative Western blot analysis examining the suppression of BCR::ABL1 expression and the subsequent inhibition of STAT5 and ERK phosphorylation in HEK 293T cells expressing BCR::ABL1-p190, Psp Cas13b, and either NT or crRNA targeting the BCR::ABL1 24 hours posttransfection. HEK 293T cells expressing BCR::ABL1-p190 and Psp Cas13b treated with 1 μM imatinib for 4 hours were used as a positive control. Parental cells are HEK 293T cells transfected with Psp Cas13b, NT, and a control plasmid; N = 3. N is the number of independent biological experiments.

Article Snippet: The HEK 293T cell line [American Type Culture Collection (ATCC), CRL-3216] was cultured in Dulbecco’s modified Eagle’s medium high-glucose medium (Thermo Fisher Scientific, 11965092) containing 10% heat-inactivated fetal bovine serum (Thermo Fisher Scientific, 10100147), Penicillin-Streptomycin (100 mg/ml; Thermo Fisher Scientific, 151401220), and 2 mM GlutaMAX (Thermo Fisher Scientific, A1286001).

Techniques: Reporter Assay, Fluorescence, Analysis, Reverse Transcription Polymerase Chain Reaction, Western Blot, Expressing, Phospho-proteomics, Inhibition, Activity Assay, Binding Assay, Positive Control, Transfection, Control, Plasmid Preparation

( A and B ) Comprehensive analysis of spacer-target interaction examining specificity and mismatch tolerance of Psp Cas13b crRNAs targeting the breakpoint region of BCR::ABL1-p190 transcript. The nucleotides in red highlight various mismatch positions in the spacer sequence. Data points in the graph are averages of mean fluorescence from four representative fields of views per condition imaged; N = 4. The data are represented in A.U. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval). ( C ) Western blot analysis examining the expression level of BCR::ABL1-p190 protein and phosphorylation status of STAT5 and ERK in HEK 293T cells expressing crRNAs with various mismatches 24 hours posttransfection; N = 3 (uncropped blots and protein quantifications are available in the Supplementary Materials.). ( D to F ) Three-color fluorescence-based reporter assays to assess the specificity of crRNA targeting the breakpoint region of BCR::ABL1 in HEK 293T cells 48 hours posttransfection. The schematics show (D) BCR::ABL1-mCherry mRNA, (E) ABL1-eGFP mRNA, and (F) BCR-TagBFP mRNA and their interaction with crBCR, crBCR::ABL1, and crABL1 crRNAs through full, partial, or no spacer-target base pairing. The quantifications of the silencing of (E) BCR::ABL1-mCherry, (F) ABL1-eGFP, and ( G ) BCR-TagBFP. Data points are averages of normalized mean fluorescence from four representative fields of view per condition imaged. The data are represented in A.U. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval); N = 3. The right panels show representative Western blot analyses to examine the expression levels of ΔBCR::ABL, ΔABL1, and ΔBCR proteins from data in (D) to (F); N = 3 (see uncropped blots in the Supplementary Materials). N represents the number of biological replicates. See Dryad for source data.

Journal: Science Advances

Article Title: Programmable and selective silencing of oncogenic fusion transcripts by CRISPR-Cas13b via breakpoint sequence recognition

doi: 10.1126/sciadv.ady0296

Figure Lengend Snippet: ( A and B ) Comprehensive analysis of spacer-target interaction examining specificity and mismatch tolerance of Psp Cas13b crRNAs targeting the breakpoint region of BCR::ABL1-p190 transcript. The nucleotides in red highlight various mismatch positions in the spacer sequence. Data points in the graph are averages of mean fluorescence from four representative fields of views per condition imaged; N = 4. The data are represented in A.U. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval). ( C ) Western blot analysis examining the expression level of BCR::ABL1-p190 protein and phosphorylation status of STAT5 and ERK in HEK 293T cells expressing crRNAs with various mismatches 24 hours posttransfection; N = 3 (uncropped blots and protein quantifications are available in the Supplementary Materials.). ( D to F ) Three-color fluorescence-based reporter assays to assess the specificity of crRNA targeting the breakpoint region of BCR::ABL1 in HEK 293T cells 48 hours posttransfection. The schematics show (D) BCR::ABL1-mCherry mRNA, (E) ABL1-eGFP mRNA, and (F) BCR-TagBFP mRNA and their interaction with crBCR, crBCR::ABL1, and crABL1 crRNAs through full, partial, or no spacer-target base pairing. The quantifications of the silencing of (E) BCR::ABL1-mCherry, (F) ABL1-eGFP, and ( G ) BCR-TagBFP. Data points are averages of normalized mean fluorescence from four representative fields of view per condition imaged. The data are represented in A.U. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval); N = 3. The right panels show representative Western blot analyses to examine the expression levels of ΔBCR::ABL, ΔABL1, and ΔBCR proteins from data in (D) to (F); N = 3 (see uncropped blots in the Supplementary Materials). N represents the number of biological replicates. See Dryad for source data.

Techniques: Analysis, Sequencing, Fluorescence, Western Blot, Expressing, Phospho-proteomics

( A and B ) Mean-difference plots showing the log 2 fold change (FC) and average abundance of transcripts. The full-length BCR::ABL1 sequence (A) or a 180-nt-long flanking Psp Cas13b binding site at the breakpoint (B) was included in the reference genome for read alignment and quantification, respectively; N = 3. The histograms depict counts per million (CPM) of reads mapped to the full-length BCR::ABL1 transcript (A) or the BCR::ABL1 breakpoint (B). ( C ) Representative Arriba fusion plots showing read alignments against the BCR::ABL1 transcript. Sashimi plots (bottom) depict the frequency and positions of reads with aberrant junctions. The breakpoint region is highlighted with a dashline box. ( D ) Counts per million (top) and relative frequency (bottom) of aberrant reads exclusively mapped to BCR::ABL1 breakpoint in HEK 293T cells. ( E ) Schematic showing the design of RT-qPCR primers binding different regions on BCR::ABL1-p190-IRES-eGFP transcript (top). RT-qPCR assays (bottom) to measure BCR::ABL1-p190 and eGFP transcript abundance; N = 3. Data are normalized means, and errors are SEM. Results are analyzed by unpaired two-tailed Student’s t test (95% confidence interval). ( F to I ) Detection of BCR::ABL1 aberrant transcripts containing internal deletions in HEK 293T cells obtained using long-read direct RNA-seq (Oxford Nanopore); N = 3. (F) Counts per million of BCR-ABL1 reads. Results are analyzed by unpaired two-tailed Student’s t test (95% confidence interval). (G) Frequency and positions of internal deletions. (H) Length of deletions in BCR::ABL1 aberrant transcripts. Dashed lines indicate the median. (I) Proportions of in-frame and out-of-frame aberrant reads. ( J ) Arriba fusion plots showing the read alignments against PAX3::FOXO1 gene fusion in Rh30 cells following RfxCas13d-mediated cleavage using NT (control), olfactory receptor–targeting (OR; control), and PAX3::FOXO1-targeting crRNA1/crRNA2. The Sashimi plots at the bottom illustrate aberrant read junctions; N = 4. ( K ) Relative frequency of aberrant reads exclusively mapped to PAX3::FOXO1 breakpoint; N = 4. N represents the number of biological replicates.

Journal: Science Advances

Article Title: Programmable and selective silencing of oncogenic fusion transcripts by CRISPR-Cas13b via breakpoint sequence recognition

doi: 10.1126/sciadv.ady0296

Figure Lengend Snippet: ( A and B ) Mean-difference plots showing the log 2 fold change (FC) and average abundance of transcripts. The full-length BCR::ABL1 sequence (A) or a 180-nt-long flanking Psp Cas13b binding site at the breakpoint (B) was included in the reference genome for read alignment and quantification, respectively; N = 3. The histograms depict counts per million (CPM) of reads mapped to the full-length BCR::ABL1 transcript (A) or the BCR::ABL1 breakpoint (B). ( C ) Representative Arriba fusion plots showing read alignments against the BCR::ABL1 transcript. Sashimi plots (bottom) depict the frequency and positions of reads with aberrant junctions. The breakpoint region is highlighted with a dashline box. ( D ) Counts per million (top) and relative frequency (bottom) of aberrant reads exclusively mapped to BCR::ABL1 breakpoint in HEK 293T cells. ( E ) Schematic showing the design of RT-qPCR primers binding different regions on BCR::ABL1-p190-IRES-eGFP transcript (top). RT-qPCR assays (bottom) to measure BCR::ABL1-p190 and eGFP transcript abundance; N = 3. Data are normalized means, and errors are SEM. Results are analyzed by unpaired two-tailed Student’s t test (95% confidence interval). ( F to I ) Detection of BCR::ABL1 aberrant transcripts containing internal deletions in HEK 293T cells obtained using long-read direct RNA-seq (Oxford Nanopore); N = 3. (F) Counts per million of BCR-ABL1 reads. Results are analyzed by unpaired two-tailed Student’s t test (95% confidence interval). (G) Frequency and positions of internal deletions. (H) Length of deletions in BCR::ABL1 aberrant transcripts. Dashed lines indicate the median. (I) Proportions of in-frame and out-of-frame aberrant reads. ( J ) Arriba fusion plots showing the read alignments against PAX3::FOXO1 gene fusion in Rh30 cells following RfxCas13d-mediated cleavage using NT (control), olfactory receptor–targeting (OR; control), and PAX3::FOXO1-targeting crRNA1/crRNA2. The Sashimi plots at the bottom illustrate aberrant read junctions; N = 4. ( K ) Relative frequency of aberrant reads exclusively mapped to PAX3::FOXO1 breakpoint; N = 4. N represents the number of biological replicates.

Techniques: Sequencing, Binding Assay, Quantitative RT-PCR, Two Tailed Test, RNA Sequencing, Control, Olfactory

$( A to C ) Schematic (top) of Psp Cas13b crRNAs targeting the breakpoint sequence of (A) RUNX1-RUNX1T1, (B) NPM-ALK, and (C) SS18-SSX1/2 mRNAs. The bar graphs (middle) quantify the silencing efficiency of crRNAs in HEK 293T cells. Data points in the graph are averages of normalized mean fluorescence from four representative fields of view per experiment imaged; N = 3. The data are represented in A.U. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval). Representative Western blot and quantification analysis (bottom) to examine the expression level of (A) RUNX1-RUNX1T1, (B) NPM-ALK, and (C) SS18-SSX1/2 in HEK 293T cells; N = 3. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval). N is the number of independent biological experiments. ( D ) Design principles for potent, specific, and personalized silencing of various gene fusion mRNAs with Psp Cas13b nuclease. The left panel shows the rational design of crRNAs targeting the breakpoint of gene fusion transcripts, which enables efficient and specific silencing of these oncogenic drivers, as well as drug-resistant fusion mutants. A fraction of cleaved targets harbor internal deletions near PspCas13b cleavage site. The cleavage disrupts the translation of fusion mRNA. This targeting of the breakpoint strategy avoids the off-targeting of untranslocated gene partners that are expressed in normal tissues. The top right panel shows spacer nucleotide positions that are important for the rational design of potent crRNA ( https://cas13target.azurewebsites.net/ ) . The bottom right panel shows the versatility of Psp Cas13b to silence various undruggable gene fusion transcripts and their oncogenic networks in a personalized manner through precise targeting of fusion’s breakpoint sequence that is exclusively expressed in tumor cells.$

Journal: Science Advances

Article Title: Programmable and selective silencing of oncogenic fusion transcripts by CRISPR-Cas13b via breakpoint sequence recognition

doi: 10.1126/sciadv.ady0296

Figure Lengend Snippet: ( A to C ) Schematic (top) of Psp Cas13b crRNAs targeting the breakpoint sequence of (A) RUNX1-RUNX1T1, (B) NPM-ALK, and (C) SS18-SSX1/2 mRNAs. The bar graphs (middle) quantify the silencing efficiency of crRNAs in HEK 293T cells. Data points in the graph are averages of normalized mean fluorescence from four representative fields of view per experiment imaged; N = 3. The data are represented in A.U. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval). Representative Western blot and quantification analysis (bottom) to examine the expression level of (A) RUNX1-RUNX1T1, (B) NPM-ALK, and (C) SS18-SSX1/2 in HEK 293T cells; N = 3. Errors are SEM, and P values of the one-way ANOVA test with Dunnett’s multiple comparisons are indicated (95% confidence interval). N is the number of independent biological experiments. ( D ) Design principles for potent, specific, and personalized silencing of various gene fusion mRNAs with Psp Cas13b nuclease. The left panel shows the rational design of crRNAs targeting the breakpoint of gene fusion transcripts, which enables efficient and specific silencing of these oncogenic drivers, as well as drug-resistant fusion mutants. A fraction of cleaved targets harbor internal deletions near PspCas13b cleavage site. The cleavage disrupts the translation of fusion mRNA. This targeting of the breakpoint strategy avoids the off-targeting of untranslocated gene partners that are expressed in normal tissues. The top right panel shows spacer nucleotide positions that are important for the rational design of potent crRNA ( https://cas13target.azurewebsites.net/ ) . The bottom right panel shows the versatility of Psp Cas13b to silence various undruggable gene fusion transcripts and their oncogenic networks in a personalized manner through precise targeting of fusion’s breakpoint sequence that is exclusively expressed in tumor cells.

Techniques: Sequencing, Fluorescence, Western Blot, Analysis, Expressing

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hek 293t cells (ATCC)

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Multiple Displacement Amplification:

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