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control shrna shc001  (Addgene inc)


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    Addgene inc control shrna shc001
    Control Shrna Shc001, supplied by Addgene inc, 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/control+shrna+shc001/control+shrna+shc001/pmc10874890-207-8-18
    Average 90 stars, based on 1 article reviews
    control shrna shc001 - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    Construct:

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR.
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [18].

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [ ].

    Functional Assay:

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR.
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [18].

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [ ].

    Control:

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR.
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [18].

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [ ].

    shRNA:

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR.
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [18].

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [ ].

    Over Expression:

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR.
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [18].

    Article Title: CASC4/GOLM2 drives high grade serous carcinoma anoikis resistance through the recycling of EGFR
    Article Snippet: All constructs were obtained from the University of Colorado Functional Genomics Facility (control shRNA: SHC001, pLKO.1-puro Empty Vector; RRID:Addgene_8453; shCASC4 #1: TRCN0000133832; shCASC4 #2: TRCN0000136384; empty vector: pLX304 control; CASC4 overexpression: ccsbBroad304_13019) and packaged using 293FT cells as previously described [ ].



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    Image Search Results


    (A) WT and Gpx4−/− BMDMs were pretreated with or without vitamin E (100 μM) for three hours, and then transfected with GSDMD-N. Protein expression was assayed using western blot. (B) Analysis of GSDMD-N-mediated cytotoxicity, DAG, IP3, and calcium production at 24 hours in WT and Gpx4−/− BMDMs in the absence or presence of Plcg1-shRNA, U73122 (10 μM), or BAPTA-AM (10 μM) (n=3 wells/group; data expressed as means ± SD, *, P<0.05 versus GSDMD-N group, t test). (C) Analysis of GSDMD-N-mediated cytotoxicity at 24 hours in THP1, HL-60, and HeLa cell lines (n=3 wells/group; data expressed as means ± SD, *, P<0.05, t test). (D) WT BMDMs were pretreated with indicated lipid components (20 μM) for three hours, and then transfected with GSDMD-N for 24 hours. Protein expression was assayed using western blot. (E) Analysis of GSDMD-N/PI4P- or GSDMD-N/PI(4,5)P2-mediated cytotoxicity at 24 hours in BMDMs in the absence or presence of Plcg1-shRNA, U73122 (10 μM), or BAPTA-AM (10 μM) (n=3 wells/group; data expressed as means ± SD, *, P<0.05 versus control group, t test). (F) Analysis of LPS electroporation- or E. coli (MOI=25) infection-mediated cytotoxicity at 16 hours in BMDMs in the absence or presence of Plcg1-shRNA or U73122 (10 μM) (n=3 wells/group; data expressed as means ± SD, *, P<0.05 versus control group, t test). (G) Analysis of LPS electroporation- or E. coli (MOI=25) infection-mediated protein expression at 16 hours in BMDMs in the absence or presence of Plcg1-shRNA or U73122 (10 μM).

    Journal: Cell host & microbe

    Article Title: Lipid Peroxidation Drives Gasdermin D-mediated Pyroptosis in Lethal Polymicrobial Sepsis

    doi: 10.1016/j.chom.2018.05.009

    Figure Lengend Snippet: (A) WT and Gpx4−/− BMDMs were pretreated with or without vitamin E (100 μM) for three hours, and then transfected with GSDMD-N. Protein expression was assayed using western blot. (B) Analysis of GSDMD-N-mediated cytotoxicity, DAG, IP3, and calcium production at 24 hours in WT and Gpx4−/− BMDMs in the absence or presence of Plcg1-shRNA, U73122 (10 μM), or BAPTA-AM (10 μM) (n=3 wells/group; data expressed as means ± SD, *, P<0.05 versus GSDMD-N group, t test). (C) Analysis of GSDMD-N-mediated cytotoxicity at 24 hours in THP1, HL-60, and HeLa cell lines (n=3 wells/group; data expressed as means ± SD, *, P<0.05, t test). (D) WT BMDMs were pretreated with indicated lipid components (20 μM) for three hours, and then transfected with GSDMD-N for 24 hours. Protein expression was assayed using western blot. (E) Analysis of GSDMD-N/PI4P- or GSDMD-N/PI(4,5)P2-mediated cytotoxicity at 24 hours in BMDMs in the absence or presence of Plcg1-shRNA, U73122 (10 μM), or BAPTA-AM (10 μM) (n=3 wells/group; data expressed as means ± SD, *, P<0.05 versus control group, t test). (F) Analysis of LPS electroporation- or E. coli (MOI=25) infection-mediated cytotoxicity at 16 hours in BMDMs in the absence or presence of Plcg1-shRNA or U73122 (10 μM) (n=3 wells/group; data expressed as means ± SD, *, P<0.05 versus control group, t test). (G) Analysis of LPS electroporation- or E. coli (MOI=25) infection-mediated protein expression at 16 hours in BMDMs in the absence or presence of Plcg1-shRNA or U73122 (10 μM).

    Article Snippet: RNAi and gene transfection Mouse PLCG1-shRNA (#TRCN0000024974 and #TRCN0000024976), human PLCG1-shRNA (#TRCN0000218478), and control-shRNA (#SHC001) were obtained from Sigma (St. Louis, MO, USA).

    Techniques: Transfection, Expressing, Western Blot, shRNA, Electroporation, Infection

    KEY RESOURCES TABLE

    Journal: Cell host & microbe

    Article Title: Lipid Peroxidation Drives Gasdermin D-mediated Pyroptosis in Lethal Polymicrobial Sepsis

    doi: 10.1016/j.chom.2018.05.009

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: RNAi and gene transfection Mouse PLCG1-shRNA (#TRCN0000024974 and #TRCN0000024976), human PLCG1-shRNA (#TRCN0000218478), and control-shRNA (#SHC001) were obtained from Sigma (St. Louis, MO, USA).

    Techniques: Recombinant, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Lactate Dehydrogenase Assay, Multiple Displacement Amplification, Mouse Assay, shRNA, Sequencing, Software