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Nonspecific sirna

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Nonspecific siRNA is a laboratory tool used for gene silencing experiments. It is designed to target and degrade multiple mRNA transcripts in a non-specific manner, allowing researchers to study the effects of gene knockdown on cellular processes. The core function of nonspecific siRNA is to facilitate the investigation of gene function without targeting a specific gene of interest.

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Lab products found in correlation

Lipofectamine 2000, by Thermo Fisher Scientific (7 mentions) Lipofectamine rnaimax, by Thermo Fisher Scientific (4 mentions) Upar sirna, by Santa Cruz Biotechnology (2 mentions) Sall4 sirna, by Santa Cruz Biotechnology (2 mentions) Dharmafect transfection reagent, by Horizon Discovery (1 mentions) Pten sirna, by Santa Cruz Biotechnology (1 mentions) Opti mem 1 medium, by Thermo Fisher Scientific (1 mentions) Runx1 sirna, by Santa Cruz Biotechnology (1 mentions)

Close spelling variants of this product

SiRNAs (95 citations) Control nonspecific siRNA (3 citations) Nonspecific siRNA (si-NS) (2 citations) Control nonspecific siRNA (sc-37007) (2 citations) Nonspecific control siRNA oligonucleotide (2 citations) Scramble nonspecific siRNA (2 citations) Control nonspecific siRNA oligonucleotides (2 citations)

12 protocols using nonspecific sirna

1

Knockdown of AMPKα2 and Sirt1 in BMMCs

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Knockdown experiments were carried out as described previously8 (link). Mouse AMPKα2 siRNA and Sirt1 siRNA in the SMARTpool were obtained from Dharmacon, and non-specific siRNA and mouse PTP1B shRNA were obtained from Santa Cruz Biotechnology. BMMCs were cultured for 16 h in serum-free medium and transfected with a DharmaFECT transfection reagent (Dharmacon) containing siRNA (100 nM per well) or shRNA lentiviral particles (5 × 104 IFU per well) according to the manufacturer’s protocol in 12-well plates. After 24 h, BMMCs were sensitized with IgE in the presence or absence of resveratrol and then stimulated with DNP-HSA as above.
Li X., Lee Y.J., Jin F., Park Y.N., Deng Y., Kang Y., Yang J.H., Chang J.H., Kim D.Y., Kim J.A., Chang Y.C., Ko H.J., Kim C.H., Murakami M, & Chang H.W. (2017). Sirt1 negatively regulates FcεRI-mediated mast cell activation through AMPK- and PTP1B-dependent processes. Scientific Reports, 7, 6444.
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2

Notch3 Silencing Impacts Cell Proliferation

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Small interfering RNA (siRNA) against Notch3 or nonspecific siRNA (Santa Cruz Biotechnology) were transfected into TT cells using Lipofectamine RNAiMAX (Invitrogen) according to manufacturer’s instruction. After 24h incubation, cells were treated with DMSO or AB3 (1.5µM) for additional 48 hours followed by mRNA isolation for qRT-PCR analyses. For the MTT cell proliferation analyses (as described above) TT cells were incubated for 24, 48 and 72h after AB3 treatment and viable cells were calculated at each timpoint. Additionally, to confirm that increased proliferation is due to Notch3 silencing, qRT-PCR was performed to detect Notch3 expression at each time point.
Jaskula-Sztul R., Eide J., Tesfazghi S., Dammalapati A., Harrison A.D., Yu X.M., Scheinebeck C., Winston-McPherson G., Kupcho K.R., Robers M.B., Hundal A.K., Tang W, & Chen H. (2014). Tumor suppressor role of Notch3 in Medullary Thyroid Carcinoma revealed by genetic and pharmacological induction. Molecular cancer therapeutics, 14(2), 499-512.
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3

Knockdown of Cathepsin D, G, and PARP-1

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Knock down of cathepsin D, cathepsin G, and PARP-1 mRNA was performed using pre-designed cathepsin D or G siRNA (final concentration 10 nM, Santa Cruz, Dallas, TX, USA), or PARP-1 siRNA (final concentration 10 nM, Cell Signaling Technology). Non-specific siRNA (10 nM, Santa Cruz, Santa Cruz, Dallas, TX, USA) was used as a negative control. Cells were seeded in 35 mm Petri dishes and transfected with siRNA using Lipofectamine RNAiMAX (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s protocol, then treated with the relevant drugs as indicated 24 h post transfection and incubated for 3 days before cell harvest.
Xie Y., Wang L., Khan M.A., Hamburger A.W., Guang W., Passaniti A., Munir K., Ross D.D., Dean M, & Hussain A. (2021). Metformin and Androgen Receptor-Axis-Targeted (ARAT) Agents Induce Two PARP-1-Dependent Cell Death Pathways in Androgen-Sensitive Human Prostate Cancer Cells. Cancers, 13(4), 633.
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4

uPA and uPAR Silencing in RAW 264.7 Cells

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RAW 264.7 cells were transfected with uPA or uPAR siRNA (Santa Cruz Biotechnology, Santa Cruz, CA) using Lipofectamine 2000 (Invitrogen, Carlsbad, CA) according to the manufacturer's instructions. A nonspecific siRNA (Santa Cruz Biotechnology) was employed as the control.
Kanno Y., Maruyama C., Matsuda A, & Ishisaki A. (2017). uPA‐derived peptide, Å6 is involved in the suppression of lipopolysaccaride‐promoted inflammatory osteoclastogenesis and the resultant bone loss. Immunity, Inflammation and Disease, 5(3), 289-299.
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5

SALL4 Knockdown Transfection Protocol

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Cells were cultured into 70% confluence. Lipofectamine 2000 (Life Technologies) was used to perform transfection according to the manufacture’s instruction. Briefly, SALL4 siRNA (Santa Cruz), non-specific siRNA (Santa Cruz), or Lipofectamine 2000 was diluted with serum-free medium, respectively. The diluted Lipofectamine 2000 was then added into the diluted siRNA, and incubated for 20 minutes at room temperature, and then added into the cell medium. Then, cells were incubated at 37°C, 5% CO2 for 6 hours. After that, the medium in each well was replaced by the normal serum-containing medium, and cultured for 24 hours before the following assays.
Deng G., Zhu L., Huang F., Nie W., Huang W., Xu H., Zheng S., Yi Z, & Wan T. (2015). SALL4 is a novel therapeutic target in intrahepatic cholangiocarcinoma. Oncotarget, 6(29), 27416-27426.
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6

Knockdown and Overexpression in ICC-9810 Cells

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In order to knock down Sall4 or PTEN, or to overexpress Bmi-1, we transfected the siRNA or expressed vector into ICC-9810 cells by using lipofectamine 2000 (Thermo Fisher Scientific) according to the manufacturer’s instruction. Sall4 siRNA, PTEN siRNA, and nonspecific siRNA were purchased from Santa Cruz Biotechnology Inc. (Dallas, TX, USA); Bmi-1 expressed vector was purchased from Qiagen NV (Venlo, the Netherlands). The transfected cells were used for further analysis.
Zhu L., Huang F., Deng G., Nie W., Huang W., Xu H., Zheng S., Yi Z, & Wan T. (2016). Knockdown of Sall4 inhibits intrahepatic cholangiocarcinoma cell migration and invasion in ICC-9810 cells. OncoTargets and therapy, 9, 5297-5305.
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7

PARP-1 Silencing in Myotubes

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Myotubes were transfected with PARP‐1 siRNA as we published before.21 Briefly, myotubes were grown in Opti‐MEM I medium (Invitrogen) for 24 hours before transfection with 500 pmol of siRNA specific for mouse PARP‐1 or nonspecific siRNA (Santa Cruz Biotechnology). siRNA transfection was performed with Lipofectamine RNAi MAX as per the manufacturer's guidelines (Thermo Fisher Scientific). The transfection medium was replaced with DM after 8 hours. Subsequent assays were conducted 24‐48 hours after transfection.
Tuntevski K., Hajira A., Nichols A., Alway S.E, & Mohamed J.S. (2020). Muscle‐specific sirtuin1 gain‐of‐function ameliorates skeletal muscle atrophy in a pre‐clinical mouse model of cerebral ischemic stroke. FASEB BioAdvances, 2(7), 387-397.
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8

RAB22A Modulation in Cell Culture

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Cells were cultured into 70% confluence. RAB22A siRNA (Santa Cruz, USA), non-specific siRNA (Santa Cruz), pcDNA3.1-RAB22A ORF plasmid, blank pcDNA3.1 vector, miR-203 mimic, scramble miR-203, anti-miR-203 (5′-TAGTGGTCCTAAACATTTCA-3′) or Lipofectamine 2000 (Thermo Fisher, USA) was diluted with serum-free medium, respectively. The diluted Lipofectamine 2000 was then added into the diluted siRNA, plasmid or miR at a final concentration of 50 nM, and incubated for 20 min at room temperature, and then added into the cell medium. Then, cells were incubated at 37°C, 5% CO2 for 6 h. After that, the medium was replaced by the DMEM with 10% FBS, and cultured for 24 h before the following assays for expression.
Su F., Chen Y., Zhu S., Li F., Zhao S., Wu L., Chen X, & Su J. (2016). RAB22A overexpression promotes the tumor growth of melanoma. Oncotarget, 7(44), 71744-71753.
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9

Sensitizing 4T1 Cells to Doxorubicin

Cited 2 times
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We seeded 4T1 cells at a density of 5 × 103 cells/well in 96-well plates and after 24 h we transfected the cells with two different concentrations of uPAR siRNA or nonspecific siRNA (Santa Cruz Biotechnology, Santa Cruz, CA) using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instructions. After uPAR-siRNA treatment, we added the eEVs-(ScuPA) PLGA-antimiRNA-21-Cy5 or eEVs-(uPA) PLGA-antimiRNA-21-Cy5 (1×107 EVs/well) to the cell culture and acquired fluorescence imaging using Celigo, as described previously.[33 (link)] To investigate the chemosensitizing functional effect of 4T1-eEVs-PNCs, we seeded the 4T1 cells at a density of 1 × 105 cells/well in 12-well plates. We then treated the cells with eEV-NPs (5×107 EVs/well) for 24 h and treated them with doxorubicin 0.5 μM for a further 48 h. We investigated the synergistic cytotoxicity effect of 4T1-eEVs-PNCs independently loaded with either antisense miRNAs-21 or antisense miRNAs-10b + DOX cells using the Cell titer blue (CTB) assay, as described previously with minor modifications.[34 (link)]
Bose R.J., Kumar U.S., Garcia-Marques F., Zeng Y., Habte F., McCarthy J.R., Pitteri S., Massoud T.F, & Paulmurugan R. (2021). Engineered Cell-Derived Vesicles Displaying Targeting Peptide and Functionalized with Nanocarriers for Therapeutic microRNA Delivery to Triple-Negative Breast Cancer in Mice. Advanced healthcare materials, 11(5), e2101387.
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10

Knockdown of PARP-1 in myotubes

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For siRNA-mediated knockdown studies, myotubes were transfected with 500 pmol of siRNA specific for mouse PARP-1 or nonspecific siRNA (Santa Cruz Biotechnology). RNA transfection studies were performed with Lipofectamine RNAi MAX (Invitrogen) according to the manufacturer's instructions. After 8 h, the transfection medium was replaced with DM. Subsequent assays were conducted 24 to 48 h after transfection.
Mohamed J.S., Wilson J.C., Myers M.J., Sisson K.J, & Alway S.E. (2014). Dysregulation of SIRT-1 in aging mice increases skeletal muscle fatigue by a PARP-1-dependent mechanism. Aging (Albany NY), 6(10), 820-834.
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