lipid transfections  (Thermo Fisher)


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    Name:
    Lipofectamine Transfection Reagent
    Description:
    Lipofectamine Transfection Reagent is one of our first generation cationic lipid transfection reagents formulated for the transfection of DNA into eukaryotic cells Lipofectamine Transfection Reagent is a trusted value reagent with many years of cited use in thousands of publications and with many cell lines With Lipofectamine Transfection Reagent you ll get • A reagent proven to work in high throughput applications• A reliable reagent for establishing stable cell lines• A reagent that works well with PLUS Reagent for higher protein expressionA proven technologyOur Lipofectamine brand reagents have been recognized as the most cited transfection reagent family with tens of thousands of citations since launch in 1993 Lipofectamine Transfection Reagent is no exception as a trusted reagent for a wide range of cell lines When used in combination with PLUS Reagent Lipofectamine Transfection Reagent has been shown to work well with cells such as BHK 21 NIH 3T3 COS 1 fibroblasts keratinocytes HT 29 MRC 5 and SK BR3 A value alternative for plasmid DNAWith such a legacy comes a commitment to providing the best reagents for all scientists and labs regardless of their funding capabilities Lipofectamine Transfection Reagent is a value alternative for transfection of plasmid DNA into eukaryotic cells with a simplified protocol For optimal results in a wider range of plasmid DNA transfection conditions we recommend Lipofectamine LTX Reagent due to its optimal balance of potency low cytotoxicity Lipofectamine 2000 Transfection Reagent is recommended if you are transfecting a broad range of cell lines or want to transfect RNA
    Catalog Number:
    18324010
    Price:
    None
    Applications:
    Cell Culture|Plasmid Transfection|Stem Cell & Primary Cell Transfections|Transfection
    Category:
    Cell Culture Transfection Reagents
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    Structured Review

    Thermo Fisher lipid transfections
    Activation of FXN expression and comparison to wild-type cells. ( A ) Time course showing activation of FXN mRNA expression starting 48 h <t>post-transfection</t> in FRDA patient-derived NPCs F4259 (5 µM, n = 2, Optimization 4). ( B ) Expression levels of FXN mRNA in FRDA patient-derived NPCs F4259 and wild-type NPCs C7522 ( n = 4). ( C ) Activation in FRDA patient-derived NPCs F4259. ( D ) Effect of adding anti-AAG ASOs to wild-type NPCs C7522. Relative FXN mRNA levels were measured by RT-qPCR when transfected with oligonucleotides using Optimization 4 ( n = 4) post 72 h transfection. EP(−) is non-oligo treatment, no electroporation control. All data are presented as ±STDEV. (*) P
    Lipofectamine Transfection Reagent is one of our first generation cationic lipid transfection reagents formulated for the transfection of DNA into eukaryotic cells Lipofectamine Transfection Reagent is a trusted value reagent with many years of cited use in thousands of publications and with many cell lines With Lipofectamine Transfection Reagent you ll get • A reagent proven to work in high throughput applications• A reliable reagent for establishing stable cell lines• A reagent that works well with PLUS Reagent for higher protein expressionA proven technologyOur Lipofectamine brand reagents have been recognized as the most cited transfection reagent family with tens of thousands of citations since launch in 1993 Lipofectamine Transfection Reagent is no exception as a trusted reagent for a wide range of cell lines When used in combination with PLUS Reagent Lipofectamine Transfection Reagent has been shown to work well with cells such as BHK 21 NIH 3T3 COS 1 fibroblasts keratinocytes HT 29 MRC 5 and SK BR3 A value alternative for plasmid DNAWith such a legacy comes a commitment to providing the best reagents for all scientists and labs regardless of their funding capabilities Lipofectamine Transfection Reagent is a value alternative for transfection of plasmid DNA into eukaryotic cells with a simplified protocol For optimal results in a wider range of plasmid DNA transfection conditions we recommend Lipofectamine LTX Reagent due to its optimal balance of potency low cytotoxicity Lipofectamine 2000 Transfection Reagent is recommended if you are transfecting a broad range of cell lines or want to transfect RNA
    https://www.bioz.com/result/lipid transfections/product/Thermo Fisher
    Average 99 stars, based on 7 article reviews
    Price from $9.99 to $1999.99
    lipid transfections - by Bioz Stars, 2020-09
    99/100 stars

    Images

    1) Product Images from "Efficient electroporation of neuronal cells using synthetic oligonucleotides: identifying duplex RNA and antisense oligonucleotide activators of human frataxin expression"

    Article Title: Efficient electroporation of neuronal cells using synthetic oligonucleotides: identifying duplex RNA and antisense oligonucleotide activators of human frataxin expression

    Journal: RNA

    doi: 10.1261/rna.071290.119

    Activation of FXN expression and comparison to wild-type cells. ( A ) Time course showing activation of FXN mRNA expression starting 48 h post-transfection in FRDA patient-derived NPCs F4259 (5 µM, n = 2, Optimization 4). ( B ) Expression levels of FXN mRNA in FRDA patient-derived NPCs F4259 and wild-type NPCs C7522 ( n = 4). ( C ) Activation in FRDA patient-derived NPCs F4259. ( D ) Effect of adding anti-AAG ASOs to wild-type NPCs C7522. Relative FXN mRNA levels were measured by RT-qPCR when transfected with oligonucleotides using Optimization 4 ( n = 4) post 72 h transfection. EP(−) is non-oligo treatment, no electroporation control. All data are presented as ±STDEV. (*) P
    Figure Legend Snippet: Activation of FXN expression and comparison to wild-type cells. ( A ) Time course showing activation of FXN mRNA expression starting 48 h post-transfection in FRDA patient-derived NPCs F4259 (5 µM, n = 2, Optimization 4). ( B ) Expression levels of FXN mRNA in FRDA patient-derived NPCs F4259 and wild-type NPCs C7522 ( n = 4). ( C ) Activation in FRDA patient-derived NPCs F4259. ( D ) Effect of adding anti-AAG ASOs to wild-type NPCs C7522. Relative FXN mRNA levels were measured by RT-qPCR when transfected with oligonucleotides using Optimization 4 ( n = 4) post 72 h transfection. EP(−) is non-oligo treatment, no electroporation control. All data are presented as ±STDEV. (*) P

    Techniques Used: Activation Assay, Expressing, Transfection, Derivative Assay, Quantitative RT-PCR, Electroporation

    Identifying an electroporation protocol using iXCells human motor neurons (HMNs). ( A, left ) Relative MALAT-1 RNA levels measured by q RT-PCR when transfected with control gapmer ctrl-gap (1 µM) and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 and 6 ( n = 2) post 24 h transfection. ( Right ) Cell viability post 24 h transfection measured by trypan blue staining ( n = 2) using 1× trypsin as detachment reagent. ( B, left ) Relative MALAT1 RNA levels measured by q RT-PCR when transfected with control gapmer ctrl-gap (1 µM) and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 ( n = 2) compared with Lipofectamine stem transfection reagent or gymnotic delivery post 24 h transfection. ( Right ) Cell viability post 24 h transfection measured by trypan blue staining ( n = 2) using accutase + 10 µM Y27632. EP(−) is non-oligo treatment, no electroporation control. All data are presented as ±STDEV.
    Figure Legend Snippet: Identifying an electroporation protocol using iXCells human motor neurons (HMNs). ( A, left ) Relative MALAT-1 RNA levels measured by q RT-PCR when transfected with control gapmer ctrl-gap (1 µM) and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 and 6 ( n = 2) post 24 h transfection. ( Right ) Cell viability post 24 h transfection measured by trypan blue staining ( n = 2) using 1× trypsin as detachment reagent. ( B, left ) Relative MALAT1 RNA levels measured by q RT-PCR when transfected with control gapmer ctrl-gap (1 µM) and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 ( n = 2) compared with Lipofectamine stem transfection reagent or gymnotic delivery post 24 h transfection. ( Right ) Cell viability post 24 h transfection measured by trypan blue staining ( n = 2) using accutase + 10 µM Y27632. EP(−) is non-oligo treatment, no electroporation control. All data are presented as ±STDEV.

    Techniques Used: Electroporation, Reverse Transcription Polymerase Chain Reaction, Transfection, Staining

    Activation of FXN protein expression, western analysis. ( A ) FXN protein in FRDA patient-derived NPCs F4259 and wild-type NPCs C7522 ( n = 3) with different confluency. ( B ) FXN protein expression in FRDA patient-derived NPCs F4259 when transfected with oligonucleotides (5 µM) using Optimization 4 ( n = 3) post 96 h transfection. All data are presented as ±STDEV. (*) P
    Figure Legend Snippet: Activation of FXN protein expression, western analysis. ( A ) FXN protein in FRDA patient-derived NPCs F4259 and wild-type NPCs C7522 ( n = 3) with different confluency. ( B ) FXN protein expression in FRDA patient-derived NPCs F4259 when transfected with oligonucleotides (5 µM) using Optimization 4 ( n = 3) post 96 h transfection. All data are presented as ±STDEV. (*) P

    Techniques Used: Activation Assay, Expressing, Western Blot, Derivative Assay, Transfection

    Identifying an electroporation protocol for FRDA patient-derived F4259 iPSC-NPCs. ( A, left ) Relative MALAT1 RNA levels measured by RT-qPCR when transfected with control gapmer ctrl-gap and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 ( n = 2) compared with Lipofectamine stem transfection reagent and gymnotic delivery post 24 h transfection. ( Right ) Cell viability post 24 h transfection measured by trypan blue staining ( n = 2). ( B, left ) Relative MALAT1 RNA levels measured by qRT-PCR when transfected with control gapmer ctrl-gap and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 ( n = 4) post 48 h transfection. ( Right ) Cell viability post 48 h transfection measured by trypan blue staining ( n = 4). ( C ) Time course experiments showing inhibition of MALAT1 RNA expression (1 µM, n = 2, Optimization 4). EP(−) is non-oligo treatment, no electroporation control. All data are presented as ± STDEV.
    Figure Legend Snippet: Identifying an electroporation protocol for FRDA patient-derived F4259 iPSC-NPCs. ( A, left ) Relative MALAT1 RNA levels measured by RT-qPCR when transfected with control gapmer ctrl-gap and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 ( n = 2) compared with Lipofectamine stem transfection reagent and gymnotic delivery post 24 h transfection. ( Right ) Cell viability post 24 h transfection measured by trypan blue staining ( n = 2). ( B, left ) Relative MALAT1 RNA levels measured by qRT-PCR when transfected with control gapmer ctrl-gap and anti-MALAT1 gapmer anti-MALAT1 using Optimization 4 ( n = 4) post 48 h transfection. ( Right ) Cell viability post 48 h transfection measured by trypan blue staining ( n = 4). ( C ) Time course experiments showing inhibition of MALAT1 RNA expression (1 µM, n = 2, Optimization 4). EP(−) is non-oligo treatment, no electroporation control. All data are presented as ± STDEV.

    Techniques Used: Electroporation, Derivative Assay, Quantitative RT-PCR, Transfection, Staining, Inhibition, RNA Expression

    2) Product Images from "Localization and Sub-Cellular Shuttling of HTLV-1 Tax with the miRNA Machinery"

    Article Title: Localization and Sub-Cellular Shuttling of HTLV-1 Tax with the miRNA Machinery

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0040662

    Suppression of endogenous miRNAs dysregulated by HTLV-1. A ) 293Ts were transfected with pACH.Tax (5 µg) and 24 hours later were transfected with pGFP-Drosha (10 µg). Cells were collected 48 hours post transfection and were western blotted (50 µg) for IKK-β, BRM and β-Actin. B ) 293T cells were transfected with Tax (5 µg) or antagomiRs (100 nM) targeting miR-199a-3p, miR-132, or Let7i. Cells were collected 72 hours post transfection, and western blotted (50 µg) for IKK-β, p65, p50, GSK-3β, BRM, and β-Actin. Densitometry counts of western blots for each indicated protein normalized to β-Actin, plotted as a percent change (measured as arbitrary counts) between antagomiR treated cells and 293T cells alone. Densitometry counts were calculated using ImageJ.
    Figure Legend Snippet: Suppression of endogenous miRNAs dysregulated by HTLV-1. A ) 293Ts were transfected with pACH.Tax (5 µg) and 24 hours later were transfected with pGFP-Drosha (10 µg). Cells were collected 48 hours post transfection and were western blotted (50 µg) for IKK-β, BRM and β-Actin. B ) 293T cells were transfected with Tax (5 µg) or antagomiRs (100 nM) targeting miR-199a-3p, miR-132, or Let7i. Cells were collected 72 hours post transfection, and western blotted (50 µg) for IKK-β, p65, p50, GSK-3β, BRM, and β-Actin. Densitometry counts of western blots for each indicated protein normalized to β-Actin, plotted as a percent change (measured as arbitrary counts) between antagomiR treated cells and 293T cells alone. Densitometry counts were calculated using ImageJ.

    Techniques Used: Transfection, Western Blot

    Tax prevents primary miRNA cleavage by Drosha. 293T cells were transfected with Tax expression vectors (1 µg): Tax WT, TD1 (Δ1–37), TD55 (Δ55–92), TD99 (Δ99–142), TD150 (Δ150–198), TD254 (Δ254–287), or TD319 (Δ319–353). A ) Forty-eight hours post transfection, total RNA was isolated by TRIzol extraction and expression of miR326 was determined by quantiMiR PCR kit using primers specific to miR326. Values shown are normalized to U6 and shown relative to control. B ) Primary transcripts encoding miR326 were detected by RT-qPCR against a region upstream of the miRNA hairpin. Quantities were normalized to GAPDH and efficiency of Drosha processing was determined by charting the expression of mature miRNA over the expression of the primary transcript. Data is shown with the efficiency in the control cells set to 100%. C ) A graphical depiction of the Tax mutant constructs TD1 and TD55 with deleted regions and the corresponding domains and motifs of full length Tax. The function of each domain is indicated in brackets and arrows, as well as the associated interacting cellular proteins below each region. The proposed Drosha binding region is indicated by the grey shaded box.
    Figure Legend Snippet: Tax prevents primary miRNA cleavage by Drosha. 293T cells were transfected with Tax expression vectors (1 µg): Tax WT, TD1 (Δ1–37), TD55 (Δ55–92), TD99 (Δ99–142), TD150 (Δ150–198), TD254 (Δ254–287), or TD319 (Δ319–353). A ) Forty-eight hours post transfection, total RNA was isolated by TRIzol extraction and expression of miR326 was determined by quantiMiR PCR kit using primers specific to miR326. Values shown are normalized to U6 and shown relative to control. B ) Primary transcripts encoding miR326 were detected by RT-qPCR against a region upstream of the miRNA hairpin. Quantities were normalized to GAPDH and efficiency of Drosha processing was determined by charting the expression of mature miRNA over the expression of the primary transcript. Data is shown with the efficiency in the control cells set to 100%. C ) A graphical depiction of the Tax mutant constructs TD1 and TD55 with deleted regions and the corresponding domains and motifs of full length Tax. The function of each domain is indicated in brackets and arrows, as well as the associated interacting cellular proteins below each region. The proposed Drosha binding region is indicated by the grey shaded box.

    Techniques Used: Transfection, Expressing, Isolation, Polymerase Chain Reaction, Quantitative RT-PCR, Mutagenesis, Construct, Binding Assay

    Loss of Drosha increases viral replication. A ) 293T cells were transfected with HTLV-1 pACH (5 µg) and 24 hours later were transfected with siRNAs against Luciferase (150 nM), Drosha (50, 150, and 300 nM), DGCR8 (50, 150, 300 nM), and Ago2 (50, 150, 300 nM) or were treated with 0.1, 1.0, or 2.5 µM Acriflavine (ACF). At 72 hours post-transfection, supernatants were collected and assessed for viral replication by RT (reverse transcriptase) assay. Data was collected in triplicate from at least 2 independent experiments. B ) 293T cells from panel A were assayed by western blot for the efficiency of siRNA knockdown of the target proteins. β-Actin serves as a positive loading control.
    Figure Legend Snippet: Loss of Drosha increases viral replication. A ) 293T cells were transfected with HTLV-1 pACH (5 µg) and 24 hours later were transfected with siRNAs against Luciferase (150 nM), Drosha (50, 150, and 300 nM), DGCR8 (50, 150, 300 nM), and Ago2 (50, 150, 300 nM) or were treated with 0.1, 1.0, or 2.5 µM Acriflavine (ACF). At 72 hours post-transfection, supernatants were collected and assessed for viral replication by RT (reverse transcriptase) assay. Data was collected in triplicate from at least 2 independent experiments. B ) 293T cells from panel A were assayed by western blot for the efficiency of siRNA knockdown of the target proteins. β-Actin serves as a positive loading control.

    Techniques Used: Transfection, Luciferase, Reverse Transcriptase Assay, Western Blot

    Nuclear colocalization of HTLV-1 Tax with cellular proteins. HeLa cells were grown on coverslips in the presence or absence of HTLV-1 Tax. Forty-eight hours post transfection of pcTax (5 µg), cells were stained for BRG1 ( A ), Drosha ( B, C ), Rb ( D ), and GIT2 ( E ) and were visualized with confocal microscopy. Cellular protein staining is represented in green, Tax staining in red, and yellow foci represent colocalization of dual stained cells. Nuclei were stained with DAPI (blue). GIT2 serves as a cytoplasmic protein control.
    Figure Legend Snippet: Nuclear colocalization of HTLV-1 Tax with cellular proteins. HeLa cells were grown on coverslips in the presence or absence of HTLV-1 Tax. Forty-eight hours post transfection of pcTax (5 µg), cells were stained for BRG1 ( A ), Drosha ( B, C ), Rb ( D ), and GIT2 ( E ) and were visualized with confocal microscopy. Cellular protein staining is represented in green, Tax staining in red, and yellow foci represent colocalization of dual stained cells. Nuclei were stained with DAPI (blue). GIT2 serves as a cytoplasmic protein control.

    Techniques Used: Transfection, Staining, Confocal Microscopy

    3) Product Images from "Localization and Sub-Cellular Shuttling of HTLV-1 Tax with the miRNA Machinery"

    Article Title: Localization and Sub-Cellular Shuttling of HTLV-1 Tax with the miRNA Machinery

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0040662

    Suppression of endogenous miRNAs dysregulated by HTLV-1. A ) 293Ts were transfected with pACH.Tax (5 µg) and 24 hours later were transfected with pGFP-Drosha (10 µg). Cells were collected 48 hours post transfection and were western blotted (50 µg) for IKK-β, BRM and β-Actin. B ) 293T cells were transfected with Tax (5 µg) or antagomiRs (100 nM) targeting miR-199a-3p, miR-132, or Let7i. Cells were collected 72 hours post transfection, and western blotted (50 µg) for IKK-β, p65, p50, GSK-3β, BRM, and β-Actin. Densitometry counts of western blots for each indicated protein normalized to β-Actin, plotted as a percent change (measured as arbitrary counts) between antagomiR treated cells and 293T cells alone. Densitometry counts were calculated using ImageJ.
    Figure Legend Snippet: Suppression of endogenous miRNAs dysregulated by HTLV-1. A ) 293Ts were transfected with pACH.Tax (5 µg) and 24 hours later were transfected with pGFP-Drosha (10 µg). Cells were collected 48 hours post transfection and were western blotted (50 µg) for IKK-β, BRM and β-Actin. B ) 293T cells were transfected with Tax (5 µg) or antagomiRs (100 nM) targeting miR-199a-3p, miR-132, or Let7i. Cells were collected 72 hours post transfection, and western blotted (50 µg) for IKK-β, p65, p50, GSK-3β, BRM, and β-Actin. Densitometry counts of western blots for each indicated protein normalized to β-Actin, plotted as a percent change (measured as arbitrary counts) between antagomiR treated cells and 293T cells alone. Densitometry counts were calculated using ImageJ.

    Techniques Used: Transfection, Western Blot

    Tax prevents primary miRNA cleavage by Drosha. 293T cells were transfected with Tax expression vectors (1 µg): Tax WT, TD1 (Δ1–37), TD55 (Δ55–92), TD99 (Δ99–142), TD150 (Δ150–198), TD254 (Δ254–287), or TD319 (Δ319–353). A ) Forty-eight hours post transfection, total RNA was isolated by TRIzol extraction and expression of miR326 was determined by quantiMiR PCR kit using primers specific to miR326. Values shown are normalized to U6 and shown relative to control. B ) Primary transcripts encoding miR326 were detected by RT-qPCR against a region upstream of the miRNA hairpin. Quantities were normalized to GAPDH and efficiency of Drosha processing was determined by charting the expression of mature miRNA over the expression of the primary transcript. Data is shown with the efficiency in the control cells set to 100%. C ) A graphical depiction of the Tax mutant constructs TD1 and TD55 with deleted regions and the corresponding domains and motifs of full length Tax. The function of each domain is indicated in brackets and arrows, as well as the associated interacting cellular proteins below each region. The proposed Drosha binding region is indicated by the grey shaded box.
    Figure Legend Snippet: Tax prevents primary miRNA cleavage by Drosha. 293T cells were transfected with Tax expression vectors (1 µg): Tax WT, TD1 (Δ1–37), TD55 (Δ55–92), TD99 (Δ99–142), TD150 (Δ150–198), TD254 (Δ254–287), or TD319 (Δ319–353). A ) Forty-eight hours post transfection, total RNA was isolated by TRIzol extraction and expression of miR326 was determined by quantiMiR PCR kit using primers specific to miR326. Values shown are normalized to U6 and shown relative to control. B ) Primary transcripts encoding miR326 were detected by RT-qPCR against a region upstream of the miRNA hairpin. Quantities were normalized to GAPDH and efficiency of Drosha processing was determined by charting the expression of mature miRNA over the expression of the primary transcript. Data is shown with the efficiency in the control cells set to 100%. C ) A graphical depiction of the Tax mutant constructs TD1 and TD55 with deleted regions and the corresponding domains and motifs of full length Tax. The function of each domain is indicated in brackets and arrows, as well as the associated interacting cellular proteins below each region. The proposed Drosha binding region is indicated by the grey shaded box.

    Techniques Used: Transfection, Expressing, Isolation, Polymerase Chain Reaction, Quantitative RT-PCR, Mutagenesis, Construct, Binding Assay

    Loss of Drosha increases viral replication. A ) 293T cells were transfected with HTLV-1 pACH (5 µg) and 24 hours later were transfected with siRNAs against Luciferase (150 nM), Drosha (50, 150, and 300 nM), DGCR8 (50, 150, 300 nM), and Ago2 (50, 150, 300 nM) or were treated with 0.1, 1.0, or 2.5 µM Acriflavine (ACF). At 72 hours post-transfection, supernatants were collected and assessed for viral replication by RT (reverse transcriptase) assay. Data was collected in triplicate from at least 2 independent experiments. B ) 293T cells from panel A were assayed by western blot for the efficiency of siRNA knockdown of the target proteins. β-Actin serves as a positive loading control.
    Figure Legend Snippet: Loss of Drosha increases viral replication. A ) 293T cells were transfected with HTLV-1 pACH (5 µg) and 24 hours later were transfected with siRNAs against Luciferase (150 nM), Drosha (50, 150, and 300 nM), DGCR8 (50, 150, 300 nM), and Ago2 (50, 150, 300 nM) or were treated with 0.1, 1.0, or 2.5 µM Acriflavine (ACF). At 72 hours post-transfection, supernatants were collected and assessed for viral replication by RT (reverse transcriptase) assay. Data was collected in triplicate from at least 2 independent experiments. B ) 293T cells from panel A were assayed by western blot for the efficiency of siRNA knockdown of the target proteins. β-Actin serves as a positive loading control.

    Techniques Used: Transfection, Luciferase, Reverse Transcriptase Assay, Western Blot

    Nuclear colocalization of HTLV-1 Tax with cellular proteins. HeLa cells were grown on coverslips in the presence or absence of HTLV-1 Tax. Forty-eight hours post transfection of pcTax (5 µg), cells were stained for BRG1 ( A ), Drosha ( B, C ), Rb ( D ), and GIT2 ( E ) and were visualized with confocal microscopy. Cellular protein staining is represented in green, Tax staining in red, and yellow foci represent colocalization of dual stained cells. Nuclei were stained with DAPI (blue). GIT2 serves as a cytoplasmic protein control.
    Figure Legend Snippet: Nuclear colocalization of HTLV-1 Tax with cellular proteins. HeLa cells were grown on coverslips in the presence or absence of HTLV-1 Tax. Forty-eight hours post transfection of pcTax (5 µg), cells were stained for BRG1 ( A ), Drosha ( B, C ), Rb ( D ), and GIT2 ( E ) and were visualized with confocal microscopy. Cellular protein staining is represented in green, Tax staining in red, and yellow foci represent colocalization of dual stained cells. Nuclei were stained with DAPI (blue). GIT2 serves as a cytoplasmic protein control.

    Techniques Used: Transfection, Staining, Confocal Microscopy

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    Article Snippet: .. K562 cells, a myelogenous leukemia cell line that also belongs to Tier 1 of the ENCODE cell line, are readily transfectable via cationic, lipid-based transfection reagents, , such as Lipofectamine 2000 or RNAiMax (Invitrogen, Life Technologies), as well as electroporation. .. In contrast, numerous lipid-based transfection reagents and conditions tested in GM12878 cells were not successful at different cell densities (5 × 105 , 1 × 106 –4 × 106 GM12878 cells) by use of 150 pmol DDX5 or hnRNP A1 siRNAs (data not shown).

    Transfection:

    Article Title: Manganese superoxide dismutase induces migration and invasion of tongue squamous cell carcinoma via H2O2-dependent Snail signaling
    Article Snippet: .. The constructed plasmids were transiently transfected into UM1 cells using Lipofectamine Plus reagent (Invitrogen, CA, USA), according to the manufacturer's instructions[ ]. .. SOD2 activity was determined by measuring the ability of SOD to inhibit xanthine/xanthine oxidase-induced cytochrome c reduction in the presence of 5 mmol/L potassium cyanide (KCN), which inhibits SOD1 and SOD3 activities[ ].

    Article Title: Capsaicin enhances erlotinib-induced cytotoxicity via AKT inactivation and excision repair cross-complementary 1 (ERCC1) down-regulation in human lung cancer cells
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    Negative Control:

    Article Title: Lysophosphatidylcholine acyltransferase 2-mediated lipid droplet production supports colorectal cancer chemoresistance
    Article Snippet: .. For small-interfering RNA (siRNA)-mediated knockdown of the LPCAT2 , PLIN2 and EPAS1 (gene encoding HIF2α protein), the cells were reverse-transfected with 10 nM of either the targeting siRNA Silencer® Select or negative control siRNA (Ambion) using Lipofectamine RNAiMax as the transfection reagent (Invitrogen) for 24 h. Fresh or chemotherapy-containing media were then added to cells for 48 or 72 h before subsequent analysis. .. The sequence of siRNA targeting human LPCAT2 , PLIN2 and EPAS1 are as follows: LPCAT2 sense 5′-CAACAUACCUAGACCUCCAtt-3′; antisense 5′-UGGAGGUCUAGGUAUGUUGta-3′; PLIN2 sense 5′-GGGUUAAAGAAGCUAAGCAtt-3′; antisense 5′-UGCUUAGCUUCUUUAACCCtg-3′; EPAS1 sense 5′-CACCUACUGUGAUGACAGAtt -3′; antisense 5′-UCUGUCAUCACAGUAGGUGaa -3′.

    Construct:

    Article Title: Manganese superoxide dismutase induces migration and invasion of tongue squamous cell carcinoma via H2O2-dependent Snail signaling
    Article Snippet: .. The constructed plasmids were transiently transfected into UM1 cells using Lipofectamine Plus reagent (Invitrogen, CA, USA), according to the manufacturer's instructions[ ]. .. SOD2 activity was determined by measuring the ability of SOD to inhibit xanthine/xanthine oxidase-induced cytochrome c reduction in the presence of 5 mmol/L potassium cyanide (KCN), which inhibits SOD1 and SOD3 activities[ ].

    Concentration Assay:

    Article Title: LRIG1 Enhances Chemosensitivity by Modulating BCL-2 Expression and Receptor Tyrosine Kinase Signaling in Glioma Cells
    Article Snippet: .. According to the manufacturer's instructions, cells at 30-50% confluence were transfected with a final concentration of 40 nM siRNA using the Lipofectamine 2000 transfection reagent (Invitrogen, Carlsbad, CA, USA). ..

    Small Interfering RNA:

    Article Title: Lysophosphatidylcholine acyltransferase 2-mediated lipid droplet production supports colorectal cancer chemoresistance
    Article Snippet: .. For small-interfering RNA (siRNA)-mediated knockdown of the LPCAT2 , PLIN2 and EPAS1 (gene encoding HIF2α protein), the cells were reverse-transfected with 10 nM of either the targeting siRNA Silencer® Select or negative control siRNA (Ambion) using Lipofectamine RNAiMax as the transfection reagent (Invitrogen) for 24 h. Fresh or chemotherapy-containing media were then added to cells for 48 or 72 h before subsequent analysis. .. The sequence of siRNA targeting human LPCAT2 , PLIN2 and EPAS1 are as follows: LPCAT2 sense 5′-CAACAUACCUAGACCUCCAtt-3′; antisense 5′-UGGAGGUCUAGGUAUGUUGta-3′; PLIN2 sense 5′-GGGUUAAAGAAGCUAAGCAtt-3′; antisense 5′-UGCUUAGCUUCUUUAACCCtg-3′; EPAS1 sense 5′-CACCUACUGUGAUGACAGAtt -3′; antisense 5′-UCUGUCAUCACAGUAGGUGaa -3′.

    Plasmid Preparation:

    Article Title: Improved isolation of murine hepatocytes for in vitro malaria liver stage studies
    Article Snippet: .. Briefly, 0.5 mg of an EGFP-tagged DNA vector (Invitrogen) was mixed with 2.5 μl of Lipofectamine and 200 μl of Optimem (Invitrogen) or 1 mg of an EGFP-tagged DNA vector was mixed with 5 μl of Fugene6 and 200 μl of Optimem, mixtures were allowed to rest for 15 minutes at room temperature and added to cells. .. Cells were left in transfection mixture for three hours at 37°C before the medium was changed to normal growth medium.

    Article Title: Transcription Factor YY1 and Its Associated Acetyltransferases CBP and p300 Interact with Hepatitis Delta Antigens and Modulate Hepatitis Delta Virus RNA Replication
    Article Snippet: .. For transient DNA transfection experiments, plasmid DNAs were transfected into HuH-7 cells by Lipofectamine 2000 transfection reagent (Invitrogen) according to the instructions provided by the supplier. .. For transient RNA transfection experiments, in vitro transcribed HDV genomic RNA (15 μg) and SHDAg mRNA (5 μg) were cotransfected into HuH-7 cells by DMRIE-C (1,2-dimyristyloxypropyl-3-dimethyl-hydroxy ethyl ammonium bromide and cholesterol) transfection reagent (Invitrogen) according to the manufacturer's instructions ( ).

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  • 99
    Thermo Fisher cationic lipid transfections
    SPC25 knockdown inhibits the proliferation of PC-3 cells. (A) Expression of SPC25 mRNA following <t>transfection</t> with the indicated shRNAs in PC-3 cells. (B) An MTT assay demonstrated that knockdown of SPC25 inhibited cell proliferation in PC-3 cells. (C) The Celigo ® system revealed that knockdown of SPC25 inhibited cell proliferation in PC-3 cells. (D) Cell number of shCtrl or shSPC25 group in each day was calculated using the Celigo ® system. P
    Cationic Lipid Transfections, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cationic lipid transfections/product/Thermo Fisher
    Average 99 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    cationic lipid transfections - by Bioz Stars, 2020-09
    99/100 stars
      Buy from Supplier

    85
    Thermo Fisher lipid based transient transfection
    Measurements of PKA activation using the AKAR FRET biosensor for RI α −/− cells expressing the various RI α constructs. (A, B) Examples of RI α −/− cells expressing the indicated constructs stimulated with 8-CPT-cAMP or 8-CPT-cGMP at t = 0 (minutes). Cell images as shown were pseudocolored according to the calculated YFP/CFP FRET ratios, with the range displayed indicated on the color bars at right. Left panels show the tracings of the FRET ratios as % change over time. Scale bars: 10 μ M. (C) Box plots of the data showing all 8-CPT-cAMP and 8-CPT-cGMP cell stimulations plotted as % change of the normalized FRET ratios. Total number of individual cells analyzed for each condition is between 20 and 26, encompassing multiple independently conducted stimulations and <t>transfections.</t>
    Lipid Based Transient Transfection, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lipid based transient transfection/product/Thermo Fisher
    Average 85 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    lipid based transient transfection - by Bioz Stars, 2020-09
    85/100 stars
      Buy from Supplier

    Image Search Results


    SPC25 knockdown inhibits the proliferation of PC-3 cells. (A) Expression of SPC25 mRNA following transfection with the indicated shRNAs in PC-3 cells. (B) An MTT assay demonstrated that knockdown of SPC25 inhibited cell proliferation in PC-3 cells. (C) The Celigo ® system revealed that knockdown of SPC25 inhibited cell proliferation in PC-3 cells. (D) Cell number of shCtrl or shSPC25 group in each day was calculated using the Celigo ® system. P

    Journal: Oncology Letters

    Article Title: Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer

    doi: 10.3892/ol.2018.8003

    Figure Lengend Snippet: SPC25 knockdown inhibits the proliferation of PC-3 cells. (A) Expression of SPC25 mRNA following transfection with the indicated shRNAs in PC-3 cells. (B) An MTT assay demonstrated that knockdown of SPC25 inhibited cell proliferation in PC-3 cells. (C) The Celigo ® system revealed that knockdown of SPC25 inhibited cell proliferation in PC-3 cells. (D) Cell number of shCtrl or shSPC25 group in each day was calculated using the Celigo ® system. P

    Article Snippet: Opti-modified Eagle's medium (Opti-MEM) which was ideal for use during cationic lipid transfections especially Lipofectamine 2000 transfection reagents was purchased from Thermo Fisher Scientific, Inc (cat. no. 31985062).

    Techniques: Expressing, Transfection, MTT Assay

    MCM10 knockdown inhibits its expression levels in DU145 and PC‐3 cells. A‐C, Real‐time reverse transcription PCR analysis showed expression of MCM10 mRNA was reduced after transfection with the indicated shRNAs in DU145 (A) PC‐3 (B) and LNCaP (C) cells. D‐F, Western blot analysis showed protein expression of MCM10 was reduced after transfection with the indicated shRNAs in DU145 (D), PC‐3 (E), and LNCaP (F) cells. Data are represented as the mean ± SD (* P

    Journal: The Prostate

    Article Title: Overexpression of MCM10 promotes cell proliferation and predicts poor prognosis in prostate cancer. Overexpression of MCM10 promotes cell proliferation and predicts poor prognosis in prostate cancer

    doi: 10.1002/pros.23703

    Figure Lengend Snippet: MCM10 knockdown inhibits its expression levels in DU145 and PC‐3 cells. A‐C, Real‐time reverse transcription PCR analysis showed expression of MCM10 mRNA was reduced after transfection with the indicated shRNAs in DU145 (A) PC‐3 (B) and LNCaP (C) cells. D‐F, Western blot analysis showed protein expression of MCM10 was reduced after transfection with the indicated shRNAs in DU145 (D), PC‐3 (E), and LNCaP (F) cells. Data are represented as the mean ± SD (* P

    Article Snippet: Opti‐modified Eagle's medium (Opti‐MEM) which was ideal for use during cationic lipid transfections especially Lipofectamine™ transfection reagents was purchased from Thermo Fisher Scientific, Inc. (Catalog number: 31985062).

    Techniques: Expressing, Polymerase Chain Reaction, Transfection, Western Blot

    MCM10 knockdown inhibits its expression levels in DU145 and PC‐3 cells. A‐C, Real‐time reverse transcription PCR analysis showed expression of MCM10 mRNA was reduced after transfection with the indicated shRNAs in DU145 (A) PC‐3 (B) and LNCaP (C) cells. D‐F, Western blot analysis showed protein expression of MCM10 was reduced after transfection with the indicated shRNAs in DU145 (D), PC‐3 (E), and LNCaP (F) cells. Data are represented as the mean ± SD (* P

    Journal: The Prostate

    Article Title: Overexpression of MCM10 promotes cell proliferation and predicts poor prognosis in prostate cancer. Overexpression of MCM10 promotes cell proliferation and predicts poor prognosis in prostate cancer

    doi: 10.1002/pros.23703

    Figure Lengend Snippet: MCM10 knockdown inhibits its expression levels in DU145 and PC‐3 cells. A‐C, Real‐time reverse transcription PCR analysis showed expression of MCM10 mRNA was reduced after transfection with the indicated shRNAs in DU145 (A) PC‐3 (B) and LNCaP (C) cells. D‐F, Western blot analysis showed protein expression of MCM10 was reduced after transfection with the indicated shRNAs in DU145 (D), PC‐3 (E), and LNCaP (F) cells. Data are represented as the mean ± SD (* P

    Article Snippet: Opti‐modified Eagle's medium (Opti‐MEM) which was ideal for use during cationic lipid transfections especially Lipofectamine™ transfection reagents was purchased from Thermo Fisher Scientific, Inc. (Catalog number: 31985062).

    Techniques: Expressing, Polymerase Chain Reaction, Transfection, Western Blot

    Measurements of PKA activation using the AKAR FRET biosensor for RI α −/− cells expressing the various RI α constructs. (A, B) Examples of RI α −/− cells expressing the indicated constructs stimulated with 8-CPT-cAMP or 8-CPT-cGMP at t = 0 (minutes). Cell images as shown were pseudocolored according to the calculated YFP/CFP FRET ratios, with the range displayed indicated on the color bars at right. Left panels show the tracings of the FRET ratios as % change over time. Scale bars: 10 μ M. (C) Box plots of the data showing all 8-CPT-cAMP and 8-CPT-cGMP cell stimulations plotted as % change of the normalized FRET ratios. Total number of individual cells analyzed for each condition is between 20 and 26, encompassing multiple independently conducted stimulations and transfections.

    Journal: ACS chemical biology

    Article Title: Switching Cyclic Nucleotide-Selective Activation of Cyclic Adenosine Monophosphate-Dependent Protein Kinase Holoenzyme Reveals Distinct Roles of Tandem Cyclic Nucleotide-Binding Domains

    doi: 10.1021/acschembio.7b00732

    Figure Lengend Snippet: Measurements of PKA activation using the AKAR FRET biosensor for RI α −/− cells expressing the various RI α constructs. (A, B) Examples of RI α −/− cells expressing the indicated constructs stimulated with 8-CPT-cAMP or 8-CPT-cGMP at t = 0 (minutes). Cell images as shown were pseudocolored according to the calculated YFP/CFP FRET ratios, with the range displayed indicated on the color bars at right. Left panels show the tracings of the FRET ratios as % change over time. Scale bars: 10 μ M. (C) Box plots of the data showing all 8-CPT-cAMP and 8-CPT-cGMP cell stimulations plotted as % change of the normalized FRET ratios. Total number of individual cells analyzed for each condition is between 20 and 26, encompassing multiple independently conducted stimulations and transfections.

    Article Snippet: In additional experiments, lipid-based transient transfection was carried out using Lipofectamine 2000 (Thermo-Fisher).

    Techniques: Activation Assay, Expressing, Construct, Cycling Probe Technology, Transfection