lipid mediated transfection reagent  (Thermo Fisher)


Bioz Verified Symbol Thermo Fisher is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99
    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
    Buy from Supplier


    Structured Review

    Thermo Fisher lipid mediated transfection reagent
    hSpry2 degradation is impaired in AR-treated cells HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g), GFP–Cbl WT (4 μ g) and FLAG–hSprouty2 (2 μ g). At 48 h <t>post-transfection,</t> cells were serum-starved and incubated without (0 min) or with AR (136 nM) or EGF (17 nM) for 2, 5, 10, 40 or 90 min. ( A ) Immunoblotting results from a representative experiment. A 100 μ g cell lysate protein sample was loaded per lane, gel-resolved, transferred on to PVDF and immunoblotted as indicated. ( B ) Quantitative analysis of three independent degradation experiments, showing the average amount of total cellular hSprouty2 remaining after 90 min of receptor stimulation by ligand. Results are means ± S.D. A two-tailed Student’s t test with α =0.05 determined that a significantly different amount of hSprouty2 degradation was effected by AR compared with EGF (**).
    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 mediated transfection reagent/product/Thermo Fisher
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    lipid mediated transfection reagent - by Bioz Stars, 2020-09
    99/100 stars

    Images

    1) Product Images from "EGF and amphiregulin differentially regulate Cbl recruitment to endosomes and EGF receptor fate"

    Article Title: EGF and amphiregulin differentially regulate Cbl recruitment to endosomes and EGF receptor fate

    Journal: The Biochemical journal

    doi: 10.1042/BJ20071505

    hSpry2 degradation is impaired in AR-treated cells HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g), GFP–Cbl WT (4 μ g) and FLAG–hSprouty2 (2 μ g). At 48 h post-transfection, cells were serum-starved and incubated without (0 min) or with AR (136 nM) or EGF (17 nM) for 2, 5, 10, 40 or 90 min. ( A ) Immunoblotting results from a representative experiment. A 100 μ g cell lysate protein sample was loaded per lane, gel-resolved, transferred on to PVDF and immunoblotted as indicated. ( B ) Quantitative analysis of three independent degradation experiments, showing the average amount of total cellular hSprouty2 remaining after 90 min of receptor stimulation by ligand. Results are means ± S.D. A two-tailed Student’s t test with α =0.05 determined that a significantly different amount of hSprouty2 degradation was effected by AR compared with EGF (**).
    Figure Legend Snippet: hSpry2 degradation is impaired in AR-treated cells HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g), GFP–Cbl WT (4 μ g) and FLAG–hSprouty2 (2 μ g). At 48 h post-transfection, cells were serum-starved and incubated without (0 min) or with AR (136 nM) or EGF (17 nM) for 2, 5, 10, 40 or 90 min. ( A ) Immunoblotting results from a representative experiment. A 100 μ g cell lysate protein sample was loaded per lane, gel-resolved, transferred on to PVDF and immunoblotted as indicated. ( B ) Quantitative analysis of three independent degradation experiments, showing the average amount of total cellular hSprouty2 remaining after 90 min of receptor stimulation by ligand. Results are means ± S.D. A two-tailed Student’s t test with α =0.05 determined that a significantly different amount of hSprouty2 degradation was effected by AR compared with EGF (**).

    Techniques Used: Transfection, Incubation, Two Tailed Test

    AR is a partial agonist for site-specific EGF-R tyrosine phosphorylation HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g) and GFP–Cbl WT (4 μ g) or GFP (3 μ g). At 48 h post-transfection, cells were serum-starved and incubated without (0) or with EGF (17 nM) or AR (17–136 nM) for 10 min. Cell lysate proteins (100 μ g per lane) were gel-resolved, transferred on to PVDF membrane and immunoblotted with the indicated antibodies. ( A ) Immunoblotting results from a representative experiment. ( B , C ) Quantitative analysis of phospho-Tyr 845 and phospho-Tyr 1045 levels in treated cells. In each case, the phosphotyrosine signal was normalized to the corresponding EGF-R level. Results are means ± S.D. for three independent experiments, except in ( C ), ● (two independent experiments).
    Figure Legend Snippet: AR is a partial agonist for site-specific EGF-R tyrosine phosphorylation HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g) and GFP–Cbl WT (4 μ g) or GFP (3 μ g). At 48 h post-transfection, cells were serum-starved and incubated without (0) or with EGF (17 nM) or AR (17–136 nM) for 10 min. Cell lysate proteins (100 μ g per lane) were gel-resolved, transferred on to PVDF membrane and immunoblotted with the indicated antibodies. ( A ) Immunoblotting results from a representative experiment. ( B , C ) Quantitative analysis of phospho-Tyr 845 and phospho-Tyr 1045 levels in treated cells. In each case, the phosphotyrosine signal was normalized to the corresponding EGF-R level. Results are means ± S.D. for three independent experiments, except in ( C ), ● (two independent experiments).

    Techniques Used: Transfection, Incubation

    Relative to EGF treatment, AR treatment impairs EGFR down-regulation and degradation HEK-293 cells were transiently transfected with cDNA encoding EGF-R WT (0.05 μ g) and GFP (3.2 μ g), GFP–Cbl WT (4 μ g) or GFP–Cbl Y371F (4 μ g). ( A ) Down-regulation assay. At 48 h post-transfection, the cells were serum-starved and incubated at 37 °C without (0 min) or with EGF (17 nM) or AR (136 nM) for 10, 40 or 90 min. Cells were harvested intact on ice, plated in triplicate and stained with anti-EGF-R, anti-Syk (isotype-matched negative control) or anti-MHC Class I (isotype-matched positive control) antibodies. This was followed by incubation with phycoerythrin-conjugated secondary antibody and paraformaldehyde fixation. The surface phycoerythrin signals were analysed by flow cytometry for 5000 GFP-positive cells per sample. Surface receptor levels for each sample were determined by subtracting the mean fluorescence index of the anti-Syk-stained cells from the MFI of the matched anti-EGF-R-stained cells. For each transfection condition, the surface EGFR levels are expressed as a percentage of the EGF-R signal of unstimulated, matched transfection plates. Results are means ± S.D. for three independent experiments. ( B ) EGF-R degradation assay. A 100 μ g cell lysate protein sample was loaded per lane, gel-resolved, transferred on to PVDF and immunoblotted as indicated. Results shown are from a representative experiment employing 17 nM EGF and 136 nM AR. ( C ) Quantitative analysis of three independent degradation experiments, showing the average amount of total cellular EGF-R remaining after 90 min of receptor stimulation by ligand. Results are means ± S.D.
    Figure Legend Snippet: Relative to EGF treatment, AR treatment impairs EGFR down-regulation and degradation HEK-293 cells were transiently transfected with cDNA encoding EGF-R WT (0.05 μ g) and GFP (3.2 μ g), GFP–Cbl WT (4 μ g) or GFP–Cbl Y371F (4 μ g). ( A ) Down-regulation assay. At 48 h post-transfection, the cells were serum-starved and incubated at 37 °C without (0 min) or with EGF (17 nM) or AR (136 nM) for 10, 40 or 90 min. Cells were harvested intact on ice, plated in triplicate and stained with anti-EGF-R, anti-Syk (isotype-matched negative control) or anti-MHC Class I (isotype-matched positive control) antibodies. This was followed by incubation with phycoerythrin-conjugated secondary antibody and paraformaldehyde fixation. The surface phycoerythrin signals were analysed by flow cytometry for 5000 GFP-positive cells per sample. Surface receptor levels for each sample were determined by subtracting the mean fluorescence index of the anti-Syk-stained cells from the MFI of the matched anti-EGF-R-stained cells. For each transfection condition, the surface EGFR levels are expressed as a percentage of the EGF-R signal of unstimulated, matched transfection plates. Results are means ± S.D. for three independent experiments. ( B ) EGF-R degradation assay. A 100 μ g cell lysate protein sample was loaded per lane, gel-resolved, transferred on to PVDF and immunoblotted as indicated. Results shown are from a representative experiment employing 17 nM EGF and 136 nM AR. ( C ) Quantitative analysis of three independent degradation experiments, showing the average amount of total cellular EGF-R remaining after 90 min of receptor stimulation by ligand. Results are means ± S.D.

    Techniques Used: Transfection, Incubation, Staining, Negative Control, Positive Control, Flow Cytometry, Cytometry, Fluorescence, Degradation Assay

    AR treatment leads to the formation of EGF-R-positive vesicles that lack associated GFP–Cbl COS-7 cells were transiently transfected with cDNA encoding GFP–Cbl WT (4 μ g). At 48 h post-transfection, cells were serum-starved and incubated without ligand (0 min) or with AR (136 nM) or EGF (17 nM) for 5 or 25 min. Following stimulation, the cells were paraformaldehyde-fixed, permeabilized and stained with anti-EGF-R antibody. Scale bar, 20 μ m. Images shown are representative results from one experiment. Three independent experiments were performed, with evaluation of more than 20 cells per ligand condition per experiment.
    Figure Legend Snippet: AR treatment leads to the formation of EGF-R-positive vesicles that lack associated GFP–Cbl COS-7 cells were transiently transfected with cDNA encoding GFP–Cbl WT (4 μ g). At 48 h post-transfection, cells were serum-starved and incubated without ligand (0 min) or with AR (136 nM) or EGF (17 nM) for 5 or 25 min. Following stimulation, the cells were paraformaldehyde-fixed, permeabilized and stained with anti-EGF-R antibody. Scale bar, 20 μ m. Images shown are representative results from one experiment. Three independent experiments were performed, with evaluation of more than 20 cells per ligand condition per experiment.

    Techniques Used: Transfection, Incubation, Staining

    Equimolar concentrations of AR and EGF induce different levels of EGF-R ubiquitination, phosphorylation and degradation HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g) and either GFP (3 μ g) or GFP–Cbl WT (4 μ g). At 48 h post-transfection, cells were serum-starved and incubated without (0 nM) or with AR (17 nM), BTC (8.5 nM) or EGF (17 nM) for 10, 40 or 90 min. Cell lysate proteins and immunoprecipitates (IP) were gel-resolved, transferred on to PVDF and immunoblotted (IB) with the antibodies indicated. ( A ) Immunoblotting results from a representative experiment. Top arrow: ubiquitinated EGF-R; middle arrow, non-ubiquitinated EGF-R; bottom arrow, GFP–Cbl; *, phosphorylated Hrs, a marker for EGF-R complex trafficking to early endosomes. ( B ) Quantitative analysis of three independent experiments, showing the amount of total cellular EGF-R remaining after receptor stimulation by the ligands (Amphi, amphiregulin). Results are means ± S.D. A two-tailed Student’s t test with α =0.05 determined that GFP–Cbl expression significantly affected EGF-R degradation only in the case of receptors activated by EGF (**).
    Figure Legend Snippet: Equimolar concentrations of AR and EGF induce different levels of EGF-R ubiquitination, phosphorylation and degradation HEK-293 cells were transiently transfected with cDNA encoding EGF-R (0.05 μ g) and either GFP (3 μ g) or GFP–Cbl WT (4 μ g). At 48 h post-transfection, cells were serum-starved and incubated without (0 nM) or with AR (17 nM), BTC (8.5 nM) or EGF (17 nM) for 10, 40 or 90 min. Cell lysate proteins and immunoprecipitates (IP) were gel-resolved, transferred on to PVDF and immunoblotted (IB) with the antibodies indicated. ( A ) Immunoblotting results from a representative experiment. Top arrow: ubiquitinated EGF-R; middle arrow, non-ubiquitinated EGF-R; bottom arrow, GFP–Cbl; *, phosphorylated Hrs, a marker for EGF-R complex trafficking to early endosomes. ( B ) Quantitative analysis of three independent experiments, showing the amount of total cellular EGF-R remaining after receptor stimulation by the ligands (Amphi, amphiregulin). Results are means ± S.D. A two-tailed Student’s t test with α =0.05 determined that GFP–Cbl expression significantly affected EGF-R degradation only in the case of receptors activated by EGF (**).

    Techniques Used: Transfection, Incubation, Marker, Two Tailed Test, Expressing

    Related Articles

    Electroporation:

    Article Title: An Efficient Method for Electroporation of Small Interfering RNAs into ENCODE Project Tier 1 GM12878 and K562 Cell Lines
    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
    Article Snippet: .. Exponentially growing human lung cancer cells (106 ) were plated for 18 h, and then constitutively active AKT (AKT-CA), which harbored a consensus myristylation domain that replaced the 4–129 amino acids of wild-type AKT, were transfected into cells using Lipofectamine (Invitrogen). .. The sense-strand sequences of small interfering RNA (siRNA) duplexes used for ERCC1 and scrambled (as a control) were 5′-GGAGCUGGCUAAGAUGUGU-3′ and 5′-GCGCGCUUUGUAGGATTCG-3′ (Dharmacon Research, Lafayette, CO).

    Article Title: NOTCH-1 and NOTCH-4 are novel gene targets of PEA3 in breast cancer: novel therapeutic implications
    Article Snippet: .. Transfection reagents used were Lipofectamine 2000 and Lipofectamine RNAiMAX, which were purchased from Invitrogen (Carlsbad, CA, USA), and FuGENE 6 was purchased from Roche Diagnostics Corporation (Indianapolis, IN, USA). .. Antibodies Notch-1 (antibody clone C-20), Notch-4 (antibody clone H-225), PEA3 [ ] (product number sc-113), c-JUN (antibody clone G-4) were purchased from Santa Cruz Biotechnology. β-actin (antibody clone AC-15) was purchased from Sigma-Aldrich and used as the loading 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′.

    Article Title: An Efficient Method for Electroporation of Small Interfering RNAs into ENCODE Project Tier 1 GM12878 and K562 Cell Lines
    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).

    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 ( ).

    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). ..

    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 ( ).

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 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 34 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 34 article reviews
    Price from $9.99 to $1999.99
    cationic lipid transfections - by Bioz Stars, 2020-09
    99/100 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

    Copy number analysis. a Copy number profiles of each tumor. Differences in color intensity depend on copy number amplitude and tumor purity. b Broad copy number changes enriched in the metastases ( n = 32) compared with TCGA tumors ( n = 80). Two-tailed Fisher’s exact tests with adjustment for multiple testing using the Benjamini–Hochberg method. c Two primary tumors compared with matched metastases. d Focal deletions of CDKN2A in two samples. e RNA-seq from the UM9 metastasis and corresponding PDX showing the region with focal CDKN2A deletion. f Genes in recurrent arm-level copy number aberrations ranked by associations between gene expression and copy number that were consistent in this cohort and TCGA tumors, and further ranked by protein–protein interaction network degree from the Human Protein Reference Database (HPRD), and additionally by presence of any associations with worse survival. The top three candidates are shown in each region. Connecting lines represent protein interactions of the highest ranked gene per region. Blue represents regions of loss and red regions of gain. Summarized representations of copy number profiles per region show the relative numbers of gain and loss events, with the inner circle representing TCGA samples and the outer our cohort. For the metastatic cohort, n = 28 samples with matching DNA and RNA data were included. g Pathways enriched among the combined set of the top 10 genes per region of gain or loss. h Functional interrogation by siRNA of main candidate genes whose expression is elevated due to copy number alteration. Cells were counted or viability was measured at 72 h, 96 h and 96 h for the cell lines UM22, MP-41, and 92-1, respectively, after transfection of the siRNA pools. n = 3 samples were transfected independently, for each cell line. Data are presented as mean values ± standard error of the mean (SEM). Two-way ANOVA was used to estimate differences, taking into account both cell line and target gene as variables. q values were calculated using Benjamini–Hochberg correction, taking into account all genes in h as well as those in Supplementary Fig. 3c , which shows other candidates of interest investigated. Dotted lines indicate q = 0.05.

    Journal: Nature Communications

    Article Title: Molecular profiling of driver events in metastatic uveal melanoma

    doi: 10.1038/s41467-020-15606-0

    Figure Lengend Snippet: Copy number analysis. a Copy number profiles of each tumor. Differences in color intensity depend on copy number amplitude and tumor purity. b Broad copy number changes enriched in the metastases ( n = 32) compared with TCGA tumors ( n = 80). Two-tailed Fisher’s exact tests with adjustment for multiple testing using the Benjamini–Hochberg method. c Two primary tumors compared with matched metastases. d Focal deletions of CDKN2A in two samples. e RNA-seq from the UM9 metastasis and corresponding PDX showing the region with focal CDKN2A deletion. f Genes in recurrent arm-level copy number aberrations ranked by associations between gene expression and copy number that were consistent in this cohort and TCGA tumors, and further ranked by protein–protein interaction network degree from the Human Protein Reference Database (HPRD), and additionally by presence of any associations with worse survival. The top three candidates are shown in each region. Connecting lines represent protein interactions of the highest ranked gene per region. Blue represents regions of loss and red regions of gain. Summarized representations of copy number profiles per region show the relative numbers of gain and loss events, with the inner circle representing TCGA samples and the outer our cohort. For the metastatic cohort, n = 28 samples with matching DNA and RNA data were included. g Pathways enriched among the combined set of the top 10 genes per region of gain or loss. h Functional interrogation by siRNA of main candidate genes whose expression is elevated due to copy number alteration. Cells were counted or viability was measured at 72 h, 96 h and 96 h for the cell lines UM22, MP-41, and 92-1, respectively, after transfection of the siRNA pools. n = 3 samples were transfected independently, for each cell line. Data are presented as mean values ± standard error of the mean (SEM). Two-way ANOVA was used to estimate differences, taking into account both cell line and target gene as variables. q values were calculated using Benjamini–Hochberg correction, taking into account all genes in h as well as those in Supplementary Fig. 3c , which shows other candidates of interest investigated. Dotted lines indicate q = 0.05.

    Article Snippet: The siRNA duplexes were purchased from Dharmacon (Thermo Fisher Scientific, Waltham, MA, USA) and the lipid based transfection was performed with Lipofectamine-RNAiMAX (Thermo Fisher Scientific, Waltham, MA, USA) using 1 pmol of siRNA per well of a 96-well plate as per the guidelines provided by manufacturer.

    Techniques: Two Tailed Test, RNA Sequencing Assay, Expressing, Functional Assay, Transfection