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profection mammalian transfection kit  (Promega)

 
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    Promega profection mammalian transfection kit
    Profection Mammalian Transfection Kit, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/profections+mammalian+transfection+kit/profection+mammalian+transfection+system/bio_rxiv__2025__03__17__643667-215-18-24
    Average 90 stars, based on 1 article reviews
    profection mammalian transfection kit - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    Plasmid Preparation:

    Article Title: Sustained wash-resistant receptor activation responses of GPR119 agonists.
    Article Snippet: Assay plates were from Greiner Bio-One. .. GloSensor 22F plasmid DNA, GloSensor cAMP reagent, and Profections mammalian transfection kit were from Promega. .. GLP-1 ELISA was from Millipore.

    Transfection:

    Article Title: Sustained wash-resistant receptor activation responses of GPR119 agonists.
    Article Snippet: Assay plates were from Greiner Bio-One. .. GloSensor 22F plasmid DNA, GloSensor cAMP reagent, and Profections mammalian transfection kit were from Promega. .. GLP-1 ELISA was from Millipore.



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    A Timeless SH7A ADP-ribosylation mutant does not restore PARGi-resistance. ( A ) Schematic of Timeless showing locations of the PARP1 binding site (dark blue), seven ADP-ribosylation sites (orange), siRNAs (si1/3, purple), sgRNAs (sg3/5/015, orange) and the anti-Timeless antibody binding site (Ab, light blue). The green box highlights the region analysed by Amplicon-EZ sequencing, showing the location of six RKO-specific nucleotide variants (purple), an allele-specific SNV (light blue), four of the mutated ADP-ribosylation sites (S/H:A, orange). The grey box indicates the location of the Δ4 deletion and overlapping sg5 sequence, with the amino acid sequence expanded below, highlighting the four amino acids deleted in Δ4 (RALQ, orange), the highly conserved MCM-plugin anchor (blue) and two adjacent ADP-ribosylation sites (green). ( B ) Bar graphs comparing TIMELESS cDNA read counts in WT and SH7A lines, with and without transgene-induction (500 ng/ml tetracycline (tet), 48 h). Annotations as in ( A ). ( C ) Timeline of RNAi complementation assay used in panels ( D–F ). RKO cells harbouring tet-inducible, RNAi-resistant, GFP-tagged Timeless transgenes (WT or SH7A) were transfected with siRNA #3, or a non-targeting control (N), exposed to 500 ng/ml tetracycline, treated with 1 μM PARGi then analysed. ( D ) Immunoblots showing expression of endogenous and GFP-tagged Timeless following siRNA <t>transfections</t> and tet-induction as indicated. Arrowhead points to Timeless degradation products. BUB3 is used as a loading control. ( E ) Column scatter plots quantitating pan-nuclear pKAP1 signal. Each symbol represents a single cell, with 827–1000 cells analysed per condition. Bars represent the mean ± SD. Representative experiment of the three biological replicates shown in ( F ). Bar graphs quantitating pan-nuclear pKAP1 and γH2AX signal. Values represent the mean ± SD from three biological replicates. One-way ANOVA with Šídák's multiple comparisons test, * P < 0.03, *** P < 0.0002, **** P < 0.0001, ns: P > 0.03.
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    A Timeless SH7A ADP-ribosylation mutant does not restore PARGi-resistance. ( A ) Schematic of Timeless showing locations of the PARP1 binding site (dark blue), seven ADP-ribosylation sites (orange), siRNAs (si1/3, purple), sgRNAs (sg3/5/015, orange) and the anti-Timeless antibody binding site (Ab, light blue). The green box highlights the region analysed by Amplicon-EZ sequencing, showing the location of six RKO-specific nucleotide variants (purple), an allele-specific SNV (light blue), four of the mutated ADP-ribosylation sites (S/H:A, orange). The grey box indicates the location of the Δ4 deletion and overlapping sg5 sequence, with the amino acid sequence expanded below, highlighting the four amino acids deleted in Δ4 (RALQ, orange), the highly conserved MCM-plugin anchor (blue) and two adjacent ADP-ribosylation sites (green). ( B ) Bar graphs comparing TIMELESS cDNA read counts in WT and SH7A lines, with and without transgene-induction (500 ng/ml tetracycline (tet), 48 h). Annotations as in ( A ). ( C ) Timeline of RNAi complementation assay used in panels ( D–F ). RKO cells harbouring tet-inducible, RNAi-resistant, GFP-tagged Timeless transgenes (WT or SH7A) were transfected with siRNA #3, or a non-targeting control (N), exposed to 500 ng/ml tetracycline, treated with 1 μM PARGi then analysed. ( D ) Immunoblots showing expression of endogenous and GFP-tagged Timeless following siRNA <t>transfections</t> and tet-induction as indicated. Arrowhead points to Timeless degradation products. BUB3 is used as a loading control. ( E ) Column scatter plots quantitating pan-nuclear pKAP1 signal. Each symbol represents a single cell, with 827–1000 cells analysed per condition. Bars represent the mean ± SD. Representative experiment of the three biological replicates shown in ( F ). Bar graphs quantitating pan-nuclear pKAP1 and γH2AX signal. Values represent the mean ± SD from three biological replicates. One-way ANOVA with Šídák's multiple comparisons test, * P < 0.03, *** P < 0.0002, **** P < 0.0001, ns: P > 0.03.
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    A Timeless SH7A ADP-ribosylation mutant does not restore PARGi-resistance. ( A ) Schematic of Timeless showing locations of the PARP1 binding site (dark blue), seven ADP-ribosylation sites (orange), siRNAs (si1/3, purple), sgRNAs (sg3/5/015, orange) and the anti-Timeless antibody binding site (Ab, light blue). The green box highlights the region analysed by Amplicon-EZ sequencing, showing the location of six RKO-specific nucleotide variants (purple), an allele-specific SNV (light blue), four of the mutated ADP-ribosylation sites (S/H:A, orange). The grey box indicates the location of the Δ4 deletion and overlapping sg5 sequence, with the amino acid sequence expanded below, highlighting the four amino acids deleted in Δ4 (RALQ, orange), the highly conserved MCM-plugin anchor (blue) and two adjacent ADP-ribosylation sites (green). ( B ) Bar graphs comparing TIMELESS cDNA read counts in WT and SH7A lines, with and without transgene-induction (500 ng/ml tetracycline (tet), 48 h). Annotations as in ( A ). ( C ) Timeline of RNAi complementation assay used in panels ( D–F ). RKO cells harbouring tet-inducible, RNAi-resistant, GFP-tagged Timeless transgenes (WT or SH7A) were transfected with siRNA #3, or a non-targeting control (N), exposed to 500 ng/ml tetracycline, treated with 1 μM PARGi then analysed. ( D ) Immunoblots showing expression of endogenous and GFP-tagged Timeless following siRNA <t>transfections</t> and tet-induction as indicated. Arrowhead points to Timeless degradation products. BUB3 is used as a loading control. ( E ) Column scatter plots quantitating pan-nuclear pKAP1 signal. Each symbol represents a single cell, with 827–1000 cells analysed per condition. Bars represent the mean ± SD. Representative experiment of the three biological replicates shown in ( F ). Bar graphs quantitating pan-nuclear pKAP1 and γH2AX signal. Values represent the mean ± SD from three biological replicates. One-way ANOVA with Šídák's multiple comparisons test, * P < 0.03, *** P < 0.0002, **** P < 0.0001, ns: P > 0.03.
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    A Timeless SH7A ADP-ribosylation mutant does not restore PARGi-resistance. ( A ) Schematic of Timeless showing locations of the PARP1 binding site (dark blue), seven ADP-ribosylation sites (orange), siRNAs (si1/3, purple), sgRNAs (sg3/5/015, orange) and the anti-Timeless antibody binding site (Ab, light blue). The green box highlights the region analysed by Amplicon-EZ sequencing, showing the location of six RKO-specific nucleotide variants (purple), an allele-specific SNV (light blue), four of the mutated ADP-ribosylation sites (S/H:A, orange). The grey box indicates the location of the Δ4 deletion and overlapping sg5 sequence, with the amino acid sequence expanded below, highlighting the four amino acids deleted in Δ4 (RALQ, orange), the highly conserved MCM-plugin anchor (blue) and two adjacent ADP-ribosylation sites (green). ( B ) Bar graphs comparing TIMELESS cDNA read counts in WT and SH7A lines, with and without transgene-induction (500 ng/ml tetracycline (tet), 48 h). Annotations as in ( A ). ( C ) Timeline of RNAi complementation assay used in panels ( D–F ). RKO cells harbouring tet-inducible, RNAi-resistant, GFP-tagged Timeless transgenes (WT or SH7A) were transfected with siRNA #3, or a non-targeting control (N), exposed to 500 ng/ml tetracycline, treated with 1 μM PARGi then analysed. ( D ) Immunoblots showing expression of endogenous and GFP-tagged Timeless following siRNA <t>transfections</t> and tet-induction as indicated. Arrowhead points to Timeless degradation products. BUB3 is used as a loading control. ( E ) Column scatter plots quantitating pan-nuclear pKAP1 signal. Each symbol represents a single cell, with 827–1000 cells analysed per condition. Bars represent the mean ± SD. Representative experiment of the three biological replicates shown in ( F ). Bar graphs quantitating pan-nuclear pKAP1 and γH2AX signal. Values represent the mean ± SD from three biological replicates. One-way ANOVA with Šídák's multiple comparisons test, * P < 0.03, *** P < 0.0002, **** P < 0.0001, ns: P > 0.03.
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    Average 90 stars, based on 1 article reviews
    profection mammalian transfection system kit #e1200 - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    A Timeless SH7A ADP-ribosylation mutant does not restore PARGi-resistance. ( A ) Schematic of Timeless showing locations of the PARP1 binding site (dark blue), seven ADP-ribosylation sites (orange), siRNAs (si1/3, purple), sgRNAs (sg3/5/015, orange) and the anti-Timeless antibody binding site (Ab, light blue). The green box highlights the region analysed by Amplicon-EZ sequencing, showing the location of six RKO-specific nucleotide variants (purple), an allele-specific SNV (light blue), four of the mutated ADP-ribosylation sites (S/H:A, orange). The grey box indicates the location of the Δ4 deletion and overlapping sg5 sequence, with the amino acid sequence expanded below, highlighting the four amino acids deleted in Δ4 (RALQ, orange), the highly conserved MCM-plugin anchor (blue) and two adjacent ADP-ribosylation sites (green). ( B ) Bar graphs comparing TIMELESS cDNA read counts in WT and SH7A lines, with and without transgene-induction (500 ng/ml tetracycline (tet), 48 h). Annotations as in ( A ). ( C ) Timeline of RNAi complementation assay used in panels ( D–F ). RKO cells harbouring tet-inducible, RNAi-resistant, GFP-tagged Timeless transgenes (WT or SH7A) were transfected with siRNA #3, or a non-targeting control (N), exposed to 500 ng/ml tetracycline, treated with 1 μM PARGi then analysed. ( D ) Immunoblots showing expression of endogenous and GFP-tagged Timeless following siRNA transfections and tet-induction as indicated. Arrowhead points to Timeless degradation products. BUB3 is used as a loading control. ( E ) Column scatter plots quantitating pan-nuclear pKAP1 signal. Each symbol represents a single cell, with 827–1000 cells analysed per condition. Bars represent the mean ± SD. Representative experiment of the three biological replicates shown in ( F ). Bar graphs quantitating pan-nuclear pKAP1 and γH2AX signal. Values represent the mean ± SD from three biological replicates. One-way ANOVA with Šídák's multiple comparisons test, * P < 0.03, *** P < 0.0002, **** P < 0.0001, ns: P > 0.03.

    Journal: NAR Cancer

    Article Title: Intrinsic PARG inhibitor sensitivity is mimicked by TIMELESS haploinsufficiency and rescued by nucleoside supplementation

    doi: 10.1093/narcan/zcae030

    Figure Lengend Snippet: A Timeless SH7A ADP-ribosylation mutant does not restore PARGi-resistance. ( A ) Schematic of Timeless showing locations of the PARP1 binding site (dark blue), seven ADP-ribosylation sites (orange), siRNAs (si1/3, purple), sgRNAs (sg3/5/015, orange) and the anti-Timeless antibody binding site (Ab, light blue). The green box highlights the region analysed by Amplicon-EZ sequencing, showing the location of six RKO-specific nucleotide variants (purple), an allele-specific SNV (light blue), four of the mutated ADP-ribosylation sites (S/H:A, orange). The grey box indicates the location of the Δ4 deletion and overlapping sg5 sequence, with the amino acid sequence expanded below, highlighting the four amino acids deleted in Δ4 (RALQ, orange), the highly conserved MCM-plugin anchor (blue) and two adjacent ADP-ribosylation sites (green). ( B ) Bar graphs comparing TIMELESS cDNA read counts in WT and SH7A lines, with and without transgene-induction (500 ng/ml tetracycline (tet), 48 h). Annotations as in ( A ). ( C ) Timeline of RNAi complementation assay used in panels ( D–F ). RKO cells harbouring tet-inducible, RNAi-resistant, GFP-tagged Timeless transgenes (WT or SH7A) were transfected with siRNA #3, or a non-targeting control (N), exposed to 500 ng/ml tetracycline, treated with 1 μM PARGi then analysed. ( D ) Immunoblots showing expression of endogenous and GFP-tagged Timeless following siRNA transfections and tet-induction as indicated. Arrowhead points to Timeless degradation products. BUB3 is used as a loading control. ( E ) Column scatter plots quantitating pan-nuclear pKAP1 signal. Each symbol represents a single cell, with 827–1000 cells analysed per condition. Bars represent the mean ± SD. Representative experiment of the three biological replicates shown in ( F ). Bar graphs quantitating pan-nuclear pKAP1 and γH2AX signal. Values represent the mean ± SD from three biological replicates. One-way ANOVA with Šídák's multiple comparisons test, * P < 0.03, *** P < 0.0002, **** P < 0.0001, ns: P > 0.03.

    Article Snippet: Lentiviruses were produced by co-transfection of AAV293T cells at 1.2 × 10 6 cells/well in a 6-well microplate, using a Promega ProFection Mammalian Transfection System kit.

    Techniques: Mutagenesis, Binding Assay, Amplification, Sequencing, Transfection, Control, Western Blot, Expressing