Interferin reagent

Manufactured by Polyplus Transfection

Sourced in France, United States

INTERFERin is a lipid-based transfection reagent designed for the efficient delivery of small interfering RNA (siRNA) into a wide range of mammalian cell lines. The reagent facilitates the uptake of siRNA into cells, enabling effective gene silencing.

Automatically generated - may contain errors

Lab products found in correlation

Lipofectamine 2000 reagent, by Thermo Fisher Scientific (4 mentions) Jetprime reagent, by Polyplus Transfection (4 mentions) Dual luciferase reporter assay system, by Promega (3 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (3 mentions) Prl tk, by Promega (3 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (3 mentions) Rna oligonucleotides, by GenePharma (2 mentions) Kod plus mutagenesis kit, by Toyobo (2 mentions) On targetplus sirna reagents, by Horizon Discovery (2 mentions) Rneasy mini kit, by Qiagen (2 mentions) Jetpei, by Polyplus Transfection (2 mentions) Fugene 6, by Promega (2 mentions) Pcdna3.1 eukaryotic expression vector, by Thermo Fisher Scientific (2 mentions) Transit lt1 transfection reagent, by Mirus Bio (2 mentions) Arnt targeted and non silencing sirna, by Santa Cruz Biotechnology (2 mentions) Jetpei dna transfection reagent, by Polyplus Transfection (2 mentions) Jetpei reagent, by Polyplus Transfection (2 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (2 mentions) Lipofectamine 3000, by Polyplus Transfection (1 mentions) Small interfering rna, by GenePharma (1 mentions)

Close spelling variants of this product

INTERFERin (472 citations) INTERFERin transfection reagent (142 citations) INTERFERin siRNA transfection reagent (65 citations) INTERFERin in vitro siRNA transfection reagent (8 citations) INTERFERin® siRNA/miRNA transfection reagent (4 citations) INTERFERin in vitro siRNA miRNA transfection reagent (2 citations) INTERFERin® siRNA and miRNA transfection reagent (2 citations)

91 protocols using interferin reagent

Overexpression of miR-320b in c-MYC

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RNA oligos were chemically synthesized and purified by (Genepharma, China). Sense sequence of human miR-320b mimics was 5’- AAA GCU GGG UUG AGA GGG CAA -3’ and antisense sequence was 5’- UUG CCC UCU CAA CCC AGC UUU U-3’. Negative control oligonucleotides were 5’-AAU UCU CCG AAC GUG UCA CTT-3’ and 5’-GUG ACA CGU UCG GAG AAU UTT-3’. The transfections were performed with INTERFERin reagent (Polyplus-transfection). The final concentration of miRNA was found to be 50 nM.
To generate pGL3-c-MYC constructs, the coding DNA sequence fragment of c-MYC was amplified and inserted into the KpnI and XhoI sites of the pGL3 construct. All constructs were verified by direct sequencing. Finally, the transfections were conducted using INTERFERin reagent (Polyplus-transfection, France). The final concentration of plasmids was diluted to 100 ng.

Wang H., Cao F., Li X., Miao H., E J., Xing J, & Fu C.G. (2015). miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells. BMC Cancer, 15, 748.

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miRNA-mediated VDAC1 regulation study

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All miRNA sequences were got from miRBase (http://www.mirbase.org). RNA oligos were chemically synthesized and purified by Genepharma Co. Ltd., (Shanghai, China). Sequence of human miR-320a mimics was 5′-AAA AGC UGG GUU GAG AGG GCG A-3′. Negative control oligonucleotides for miRNA was 5′-CAG UAC UUU UGU GUA GUA CAA-3′. The transfections were performed with INTERFERin reagent (Polyplus-transfection). The final concentration of miRNA was 50 nM. To generate pGL3-VDAC1 constructs, the sequence of VDAC1 mRNA was amplified by the primers listed in Table 2. The fragments were inserted into pGL3 with the designed cutting sites: KpnI and XhoI. The transfections were performed with INTERFERin reagent (Polyplus-transfection). The final concentration of plasmids was 100 ng.

Zhang G., Jiang G., Wang C., Zhong K., Zhang J., Xue Q., Li X., Jin H, & Li B. (2016). Decreased expression of microRNA-320a promotes proliferation and invasion of non-small cell lung cancer cells by increasing VDAC1 expression. Oncotarget, 7(31), 49470-49480.

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RNA Oligo Transfection and Luciferase Assay

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RNA oligos were chemically synthesized and purified by GenePharma Co., Ltd. (Shanghai, China). The sequences of lncRNA 1308 siRNA were as follows: 5′-CGG AGA GGU CAG AGG UAG ATT-3′ (sense) and 5′- UCU ACC UCU GAC CUC UCC GTT-3′ (antisense). The sequences of control siRNA were as follows: 5′-UUC UCC GAA CGU GUC ACG UTT-3′ (sense) and 5′-ACG UGA CAC GUU CGU AGA ATT-3′ (antisense). The sequence of human miR-124 mimics was 5′- UAA GGC ACG CGG UGA AUG CC-3′. The sequence of negative control oligonucleotides for miRNA was 5′-CAG UAC UUU UGU GUA GUA CAA-3′. The sequence of human miR-124 inhibitors was 5′- GGC AUU CAC CGC GUG CCU UA-3′. The sequence of negative control oligonucleotides for miRNA was 5′-CAG UAC UUU UGU GUA GUA CAA-3′. The transfections were performed with INTERFERin reagent (Polyplus-transfection). The final concentration of miRNA mimics was 50 nmol/L, the final concentration of miRNA inhibitors was 100 nmol/L, and the final concentration of siRNAs was 20 nmol/L.
To generate pGL3-lncRNA 1308 constructs, the sequence of lncRNA 1308 mRNA was amplified by the primers listed in Table S1. The fragments were inserted into pGL3 with the designed cutting sites KpnI and XhoI. The transfections were performed with INTERFERin reagent (Polyplus-transfection). The final concentration of plasmids was 100 ng.

Li H., Guo X., Li Q., Ran P., Xiang X., Yuan Y., Dong T., Zhu B., Wang L., Li F., Yang C., Mu D., Wang D., Xiao C, & Zheng S. (2018). Long non-coding RNA 1308 promotes cell invasion by regulating the miR-124/ADAM 15 axis in non-small-cell lung cancer cells. Cancer Management and Research, 10, 6599-6609.

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LINC00240 and DDX21 Plasmid Construction

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The human full-length LINC00240 (NR_026775.2) cDNA and truncated versions of LINC00240 cDNA were directly synthesized and cloned after the CMV promoter of pCDH-CMV-MCS-EF1-Puro. The full-length LINC00240 cDNA plasmid was named as LINC00240. After one HA-tag sequence was inserted after ATG of the CDS region of DDX21 (NM_004728.4), the cDNA was cloned into the pcDNA3.1 vector to generate the HA-tagged DDX21 plasmid (WT). Five truncated DDX21 plasmids (ΔDEADc, Δ1-398, Δ617-783, ΔGUCT, and ΔAdoMet) were mutants of the HA-tagged DDX21 plasmid with CDS region after deletion of the DEADc domain, 1-398aa, 329-1283aa, the GUCT domain, or the AdoMet domain, separately. Two shRNA hairpins targeting human LINC00240 (sh240-1 or sh240-2) or the control shRNA (Supplementary Table 2) were cloned into the pLKO.1 vector. The resultant plasmids were designated sh240-1, sh240-2, or shNC. All the plasmids were synthesized by Genewiz (Suzhou, China) and sequenced to confirm the orientation and integrity. Transient transfection of plasmid constructs or small interfering RNAs (GenePharma, Shanghai, China) (Supplementary Table 2) was performed with Lipofectamine 3000 or the INTERFERin reagent (Polyplus, 409–10).

Zhang N., Wang B., Ma C., Zeng J., Wang T., Han L, & Yang M. (2023). LINC00240 in the 6p22.1 risk locus promotes gastric cancer progression through USP10-mediated DDX21 stabilization. Journal of Experimental & Clinical Cancer Research : CR, 42, 89.

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siRNA Library Screening and Validation

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The custom library (ON-TARGETplus siRNAs with 4 siRNAs per gene) was purchased from Thermo Fisher Scientific. For the screen, the 4 siRNA sequences were pooled to a final siRNA concentration of 30 nM. For validation experiments the 4 single siRNAs for each target were tested individually at a concentration of 20 nM. Reverse transfection was performed using the INTERFERin® reagent (Polyplus-Transfection SA) according to the manufacturer's instructions. For all validation assays, RT-PCR was performed to check for RNA interference at mRNA level of the targeted genes.

Boutter J., Huang Y., Marovca B., Vonderheit A., Grotzer M.A., Eckert C., Cario G., Wollscheid B., Horvath P., Bornhauser B.C, & Bourquin J.P. (2014). Image-based RNA interference screening reveals an individual dependence of acute lymphoblastic leukemia on stromal cysteine support. Oncotarget, 5(22), 11501-11512.

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RNA Oligonucleotides for MiRNA and siRNA Transfection

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RNA oligonucleotides were chemically synthesized and purified by Genepharma Co. Ltd., (Shanghai, China). Sequence of human miR-30b mimics was 5′- UGU AAA CAUC CUA CAC UCA GCU -3′ and human miR-30c mimics was 5′- UGU AAA CAU CCU ACA CUC UCA GC -3′. Negative control oligonucleotides for miRNA mimics was 5′-CAG UAC UUU UGU GUA GUA CAA-3′. The sequences of Rab18 siRNA was: 5′- GAA ACA UAC UGU ACA AGA ATT -3′ (sense) and 5′-UUC UUG UAC AGU AUG UUU CTT-3′ (antisense), Control siRNA was: 5′-UUC UCC GAA CGU GUC ACG UTT-3′ (sense), 5′-ACG UGA CAC GUU CGU AGA ATT-3′ (antisense). The transfections were performed with INTERFERin reagent (Polyplus-transfection). The final concentration of miRNA was 50 nM. The final concentration of siRNA was 20 nM.

Zhong K., Chen K., Han L, & Li B. (2014). microRNA-30b/c inhibits non-small cell lung cancer cell proliferation by targeting Rab18. BMC Cancer, 14, 703.

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Plasmid and siRNA Transfection in HEK 293T Cells

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The plasmids SELENOK-GFP, SELENOK-FLAG, SELENOK-GFP N42, SELENOK-GFP C43, and STING-MYC C88/91S were procured from Biosune Biotechnology (Shanghai, China). The IFN-β reporter plasmid and expression plasmids for cGAS, STING, and TBK1 have been described before [22 (link)]. The STING-HA C139 mutants were generated using the KOD-Plus-Mutagenesis kit (Toyobo). All plasmids were verified by DNA sequencing. These plasmids were transfected into HEK 293T cells using Lipofectamine 2000 reagent (Invitrogen). The siRNA duplexes were transfected into cells with the INTERFERin reagent (Polyplus-transfection) according to the manufacturer’s protocol. The siRNA sequences are listed in S1 Table. When it came to knocking down the genes with multiple siRNA sequences in S1 Table, the multiple siRNAs were mixed for use.

Lv L., Chai L., Wang J., Wang M., Qin D., Song H., Fu Y., Zhao C., Jia J., Zhao W, & Jia M. (2023). Selenoprotein K enhances STING oligomerization to facilitate antiviral response. PLOS Pathogens, 19(4), e1011314.

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Knockdown of SOCS3 in Keratinocytes

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SOCS3 was knocked-down by using a pool of 4 small short interfering (si)RNA ON-TARGET plus SMARTpool (L-004299-00-0005, Dharmacon RNA Technology, Lafayette, CO, USA). In parallel, a pool of 4 non-targeting siRNA was used as negative control (L-011511-00-0005). Primary cultures of keratinocytes were transfected with SOCS3 or control siRNA at 50 nM final concentration, using Interferin reagent (Polyplus Transfection, New York, NY, USA). After 2 days of transfection, keratinocytes were treated with IL-22 for the indicated time periods.

Madonna S., Scarponi C., Morelli M., Sestito R., Scognamiglio P.L., Marasco D, & Albanesi C. (2017). SOCS3 inhibits the pathological effects of IL-22 in non-melanoma skin tumor-derived keratinocytes. Oncotarget, 8(15), 24652-24667.

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Downregulation of CPT1C and Cell Viability

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Panc-1 cells (400,000) were plated in 6-well plates in DMEM with 10% FBS. The day after, four CPT1C siRNA (L-008824-01-0010, ON-TARGETplus siRNA Reagents, Dharmacon) were transfected at a final concentration of 20 nM using INTERFERin reagent (Polyplus-transfection) with Opti-MEM (Gibco) medium according to the manufacturer’s protocol. A control siRNA pool (Scramble siRNA) was used as the negative control (D-001810-10-05, ON-TARGETplus Non-targeting Pool, Dharmacon). The medium was replaced with DMEM 10% FBS 6h after the start of transfection. To check the downregulation of CPT1C expression after 24h, cells were detached with pre-warmed accutase (Gibco), triplicates were pooled and processed for RT-qPCR as described above. For the viability test, cells were treated the day after transfection with 7μM of perhexiline in triplicates. Cells were detached 72h later and viability was assessed via Trypan blue exclusion using a cell viability analyzer (Vi-cell XR, Beckman Coulter).

Reyes-Castellanos G., Abdel Hadi N., Gallardo-Arriaga S., Masoud R., Garcia J., Lac S., El Kaoutari A., Gicquel T., Planque M., Fendt S.M., Linares L.K., Gayet O., Guillaumond F., Dusetti N., Iovanna J, & Carrier A. (2023). Combining the antianginal drug perhexiline with chemotherapy induces complete pancreatic cancer regression in vivo. iScience, 26(6), 106899.

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Nupr1 Silencing in Cell Culture

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Cells were plated at 70% confluence and INTERFErin™ reagent (Polyplus-transfection) was used to perform siRNA transfections, following manufacturer’s protocol. Scrambled siRNA that targets no known gene sequence was used as a negative control. The sequence of Nupr1-specific siRNA was r(GGAGGACCCAGGACAGGAU)dTdT.

Huang C., Santofimia-Castaño P., Liu X., Xia Y., Peng L., Gotorbe C., Neira J.L., Tang D., Pouyssegur J, & Iovanna J. (2021). NUPR1 inhibitor ZZW-115 induces ferroptosis in a mitochondria-dependent manner. Cell Death Discovery, 7, 269.

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