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  • 99
    Thermo Fisher rnaimax
    Full-length UBE2O and the CR2 truncation rescue the effect of UBE2O knockdown on BMAL1 protein level. HEK293T cells ( A ) or N2a cells ( B ) were first transfected with the control or UBE2O ( Ube2o )-specific siRNAs using <t>RNAiMAX.</t> At 24 h post-transfection, cells were further transfected with pcDNA3.1, Myc-UBE2O, or Myc-CR2 plasmid. Cells were lysed 48 h after the second transfection, and cell lysates were immunoblotted with the indicated antibodies. Asterisks on the right indicate the full-length UBE2O or the CR2 truncation. Quantification was performed for data from three biological replicates, and data are presented as mean ± S.D. ( error bars ). Student's t test was used for statistical analyses. ns , not significant; *, p
    Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 22634 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Fisher Scientific rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Rnaimax, supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 91/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Thermo Fisher lipofetamine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
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    91
    Thermo Fisher liptofectamine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Liptofectamine Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Thermo Fisher oligofectamine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Oligofectamine Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Thermo Fisher liopfectamine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Liopfectamine Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Thermo Fisher lipid rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Lipid Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 61 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Thermo Fisher lipofactamine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Lipofactamine Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 47 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Thermo Fisher lipofectaimine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Lipofectaimine Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 89/100, based on 104 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher lipofectam rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Lipofectam Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Thermo Fisher lipofectaminer rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    Lipofectaminer Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher by rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
    By Rnaimax, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Millipore rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
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    Thermo Fisher lipifectamine rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
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    Thermo Fisher lipofectamina rnaimax
    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with <t>RNAiMAX</t> serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).
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    Image Search Results


    Full-length UBE2O and the CR2 truncation rescue the effect of UBE2O knockdown on BMAL1 protein level. HEK293T cells ( A ) or N2a cells ( B ) were first transfected with the control or UBE2O ( Ube2o )-specific siRNAs using RNAiMAX. At 24 h post-transfection, cells were further transfected with pcDNA3.1, Myc-UBE2O, or Myc-CR2 plasmid. Cells were lysed 48 h after the second transfection, and cell lysates were immunoblotted with the indicated antibodies. Asterisks on the right indicate the full-length UBE2O or the CR2 truncation. Quantification was performed for data from three biological replicates, and data are presented as mean ± S.D. ( error bars ). Student's t test was used for statistical analyses. ns , not significant; *, p

    Journal: The Journal of Biological Chemistry

    Article Title: Ubiquitin-conjugating enzyme UBE2O regulates cellular clock function by promoting the degradation of the transcription factor BMAL1

    doi: 10.1074/jbc.RA117.001432

    Figure Lengend Snippet: Full-length UBE2O and the CR2 truncation rescue the effect of UBE2O knockdown on BMAL1 protein level. HEK293T cells ( A ) or N2a cells ( B ) were first transfected with the control or UBE2O ( Ube2o )-specific siRNAs using RNAiMAX. At 24 h post-transfection, cells were further transfected with pcDNA3.1, Myc-UBE2O, or Myc-CR2 plasmid. Cells were lysed 48 h after the second transfection, and cell lysates were immunoblotted with the indicated antibodies. Asterisks on the right indicate the full-length UBE2O or the CR2 truncation. Quantification was performed for data from three biological replicates, and data are presented as mean ± S.D. ( error bars ). Student's t test was used for statistical analyses. ns , not significant; *, p

    Article Snippet: Cells were transfected with the indicated plasmids or siRNAs using polyethyleneimine (PEI; Sigma), Lipofectamine 2000 (Life Technologies, Inc.), or RNAiMAX (Life Technologies) transfection reagents according to the manufacturer's instructions, and growth medium was changed 6 h after transfection.

    Techniques: Transfection, Plasmid Preparation

    Knockdown of neogenin suppresses BMP4-induced hepcidin expression. A, knockdown of neogenin decreases pSmad1/5/8. Control-, HJV-, and G99V HJV-HepG2 cells in 12-well plates were transfected with either control ( Ctrl ) or neogenin ( Neo ) siRNA using RNAiMAX

    Journal: The Journal of Biological Chemistry

    Article Title: Hemojuvelin-Neogenin Interaction Is Required for Bone Morphogenic Protein-4-induced Hepcidin Expression *

    doi: 10.1074/jbc.M109.027318

    Figure Lengend Snippet: Knockdown of neogenin suppresses BMP4-induced hepcidin expression. A, knockdown of neogenin decreases pSmad1/5/8. Control-, HJV-, and G99V HJV-HepG2 cells in 12-well plates were transfected with either control ( Ctrl ) or neogenin ( Neo ) siRNA using RNAiMAX

    Article Snippet: RNAiMAX reagent (Invitrogen) was used for the transfection.

    Techniques: Expressing, Transfection

    Effect of the charge ratio on the gene silencing activity of Luc-HeLa cells transfected with Luc-siRNA. siRNA was transfected for 4 h at 37 °C or 42 °C using liposomes and lipofectamine RNAiMAX. The data are mean ± standard deviation (SD) ( n = 3 or 4, ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Effect of Polymer Phase Transition Behavior on Temperature-Responsive Polymer-Modified Liposomes for siRNA Transfection

    doi: 10.3390/ijms20020430

    Figure Lengend Snippet: Effect of the charge ratio on the gene silencing activity of Luc-HeLa cells transfected with Luc-siRNA. siRNA was transfected for 4 h at 37 °C or 42 °C using liposomes and lipofectamine RNAiMAX. The data are mean ± standard deviation (SD) ( n = 3 or 4, ** p

    Article Snippet: Lipofectamine RNAiMAX (RNAiMAX) (Invitrogen, Corp., Carlsbad, CA, USA) was used for comparison, and transfection procedures were performed in accordance with the manufacturer’s instructions.

    Techniques: Activity Assay, Transfection, Standard Deviation

    Effect of temperature on gene silencing activity of Luc-HeLa cells transfected with Luc-siRNA. siRNA was transfected for 4 h at 37 °C or 42 °C using liposomes and lipofectamine RNAiMAX. The charge ratio (+/−) was 5:1 and the siRNA concentration was 25 nM. The data are mean ± standard deviation (SD). ( n = 3 or 4, ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Effect of Polymer Phase Transition Behavior on Temperature-Responsive Polymer-Modified Liposomes for siRNA Transfection

    doi: 10.3390/ijms20020430

    Figure Lengend Snippet: Effect of temperature on gene silencing activity of Luc-HeLa cells transfected with Luc-siRNA. siRNA was transfected for 4 h at 37 °C or 42 °C using liposomes and lipofectamine RNAiMAX. The charge ratio (+/−) was 5:1 and the siRNA concentration was 25 nM. The data are mean ± standard deviation (SD). ( n = 3 or 4, ** p

    Article Snippet: Lipofectamine RNAiMAX (RNAiMAX) (Invitrogen, Corp., Carlsbad, CA, USA) was used for comparison, and transfection procedures were performed in accordance with the manufacturer’s instructions.

    Techniques: Activity Assay, Transfection, Concentration Assay, Standard Deviation

    microRNAs 146a, 146b, and 155 are down-regulated in statin-treated Mac. a microRNA array. Total RNA was isolated from macrophages differentiated in the absence or presence of statin (25 cm 2 flasks, 100,000 cells/cm 2 ) with the “RNeasy Plus Mini Kit”. Deep sequencing was performed by the “Core Unit DNA”, Universität Leipzig, using the “TruSeq™Small RNA sample prepkit v2” (illumina, San Diego, USA). The mean of the normalized data of macrophages pretreated without statin and macrophages pretreated with statin was calculated and data of samples with a mean > 100 counts (192 samples; compare Supplementary Table 2 ) were included into the analysis and blotted against each other. The orange line indicates unchanged expression. The red dots mark three selected miRs, which were down-regulated in statin-pretreated macrophages, as compared to Mac prepared in the absence of statin (compare Supplementary Table 2 ). A second array showed a similar result. b Blockade of miR-146a and miR-155 reverses the hypo-responsiveness in macrophages only to some degree. Macrophages were incubated as described in Fig. 1a (6-well plate; 100,000 cells/cm 2 ). The respective “miRCURY LNA™” anti-miR (Exiqon, Qiagen, Vedbaek, Denmark) were prepared in “Lipofectamine RNAiMax” and 250 µl of this solution was added to 2750 µl of culture medium in the absence (−) or presence (+) of statin. After 24 h LPS was added. After further 24 h, the supernatants were harvested and analyzed in ELISA. Four experiments with similar results were performed. Data analysis and color code as in Fig. 1c (“Ctrl” vs. “anti-miR”).

    Journal: Cell Death & Disease

    Article Title: The differential statin effect on cytokine production of monocytes or macrophages is mediated by differential geranylgeranylation-dependent Rac1 activation

    doi: 10.1038/s41419-019-2109-9

    Figure Lengend Snippet: microRNAs 146a, 146b, and 155 are down-regulated in statin-treated Mac. a microRNA array. Total RNA was isolated from macrophages differentiated in the absence or presence of statin (25 cm 2 flasks, 100,000 cells/cm 2 ) with the “RNeasy Plus Mini Kit”. Deep sequencing was performed by the “Core Unit DNA”, Universität Leipzig, using the “TruSeq™Small RNA sample prepkit v2” (illumina, San Diego, USA). The mean of the normalized data of macrophages pretreated without statin and macrophages pretreated with statin was calculated and data of samples with a mean > 100 counts (192 samples; compare Supplementary Table 2 ) were included into the analysis and blotted against each other. The orange line indicates unchanged expression. The red dots mark three selected miRs, which were down-regulated in statin-pretreated macrophages, as compared to Mac prepared in the absence of statin (compare Supplementary Table 2 ). A second array showed a similar result. b Blockade of miR-146a and miR-155 reverses the hypo-responsiveness in macrophages only to some degree. Macrophages were incubated as described in Fig. 1a (6-well plate; 100,000 cells/cm 2 ). The respective “miRCURY LNA™” anti-miR (Exiqon, Qiagen, Vedbaek, Denmark) were prepared in “Lipofectamine RNAiMax” and 250 µl of this solution was added to 2750 µl of culture medium in the absence (−) or presence (+) of statin. After 24 h LPS was added. After further 24 h, the supernatants were harvested and analyzed in ELISA. Four experiments with similar results were performed. Data analysis and color code as in Fig. 1c (“Ctrl” vs. “anti-miR”).

    Article Snippet: “Lipofectamine® RNAiMAX” (9 µl; ambion™) was added to 150 µl of “OptiMEM®” and 3 µl of the anti-miR (10 µM) was added to another volume of 150 µl “Optimem®”.

    Techniques: Isolation, Sequencing, Expressing, Incubation, Enzyme-linked Immunosorbent Assay

    Occludin knockdown attenuates serine protease-induced increase in TER. A : SCBN cells were treated with 50, 100, or 300 nM occludin siRNA for 48 h and knockdown assessed by Western blotting. B and C : representative tracings of SCBN cells transfected with 300 nM occludin siRNA for 48 h, and treated with trypsin ( B , n = 6–9) or matriptase ( C , n = 4). Controls include untransfected cells, and RNAiMAX Lipofectamine with or without scrambled siRNA. Baseline TER ( n = 10–14) ( D ) and change in TER 15 min post serine protease treatment ( E and F ) were assessed. Occludin siRNA induced a significant reduction in baseline TER and attenuated the trypsin- and matriptase-induced increase in TER. * P

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    Article Title: The serine protease-mediated increase in intestinal epithelial barrier function is dependent on occludin and requires an intact tight junction

    doi: 10.1152/ajpgi.00441.2015

    Figure Lengend Snippet: Occludin knockdown attenuates serine protease-induced increase in TER. A : SCBN cells were treated with 50, 100, or 300 nM occludin siRNA for 48 h and knockdown assessed by Western blotting. B and C : representative tracings of SCBN cells transfected with 300 nM occludin siRNA for 48 h, and treated with trypsin ( B , n = 6–9) or matriptase ( C , n = 4). Controls include untransfected cells, and RNAiMAX Lipofectamine with or without scrambled siRNA. Baseline TER ( n = 10–14) ( D ) and change in TER 15 min post serine protease treatment ( E and F ) were assessed. Occludin siRNA induced a significant reduction in baseline TER and attenuated the trypsin- and matriptase-induced increase in TER. * P

    Article Snippet: Cells were transfected using RNAiMAX Lipofectamine (Invitrogen) in media without antibiotics.

    Techniques: Western Blot, Transfection

    U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with RNAiMAX serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).

    Journal: Molecular cancer therapeutics

    Article Title: U1 Adaptors suppress the KRAS-MYC oncogenic axis in human pancreatic cancer xenografts

    doi: 10.1158/1535-7163.MCT-16-0867

    Figure Lengend Snippet: U1 Adaptors targeting KRAS are effective in vitro and in vivo A , Cell growth inhibition assay of human pancreatic cancer cell lines MIA PaCa-2, PANC-1, and BxPC-3, after transfection with U1 KRAS1B every 72 hours over 9 days compared to U1 Control adaptor and si KRAS . B , (Top) Schematic of the U1 KRAS1B mutant adaptor. Nucleotides underlined in the KRAS domain have been LNA-modified. Red lowercase nucleotides represent the mutated nucleotides of the U1 domain. (Bottom) Apoptosis assay using Annexin V staining following transfection of MIA PaCa-2 cells with 10 μM U1 Control, U1 KRAS1B, U1 KRAS1B mutant, or si KRAS . after 72 hours ( P =0.0001), with RNAiMAX serving as an additional negative control. C , Western blots for KRAS, MYC, p-AKT, AKT, p-ERK, and ERK, 72 hours following transfection of MIA PaCa-2 cells as in B . Actin serves as a loading control. D , Schematic of the peptide (cRGD)-dendrimer (PPI) linked to the U1 KRAS3 adaptor (Top) used for in vivo delivery of the KRAS adaptor. (Bottom) MIA PaCa-2 xenograft mice (n=9) were treated with cRGD-PAMAM-KRAS3 complex (2 μg KRAS3 Adaptor, 7.5 μg cRGD-PAMAM complex per dose) by tail vein injection twice weekly starting when tumors reached 40–50mm 3 . 68% growth inhibition observed when compared with vehicle control ( p =0.0002).

    Article Snippet: All transfections used 10 nM of adaptor or siRNA in complex with RNAiMax (FisherSci) or PAMAM.

    Techniques: In Vitro, In Vivo, Growth Inhibition Assay, Transfection, Mutagenesis, Modification, Apoptosis Assay, Staining, Negative Control, Western Blot, Mouse Assay, Injection, Inhibition