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pce mp53dd 41856  (Addgene inc)


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    Addgene inc pce mp53dd 41856
    Pce Mp53dd 41856, supplied by Addgene inc, used in various techniques. Bioz Stars score: 95/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pce-mp53dd/pCE-mp53DD+(Plasmid+%2341856)/pm41850000-45-16-19
    Average 95 stars, based on 81 article reviews
    pce mp53dd 41856 - by Bioz Stars, 2026-11
    95/100 stars

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    Related Articles

    Transfection:

    Article Title: A Mutant Methionyl-tRNA Synthetase-Based toolkit to assess induced-Mesenchymal Stromal Cell secretome in mixed-culture disease models
    Article Snippet: 500ng donor plasmid, CLYBL-Puro-(NLS)eGFP-CAG-MetRS L274G or CLYBL-BSD-mApple-CAG-MetRS L274G , and 100ng dominant negative p53 plasmid (pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ; RRID:Addgene_41856) to increase survival in cells undergoing double-strand breaks, were added to the RNP complex and mixed with 10μL Lipofectamine 2000 (Invitrogen, #11668–019) in 125μL OptiMEM per well for a total transfection mix volume of 250μL per well.

    Article Title: MSH2 is not required for either maintenance of DNA methylation or repeat contraction at the FMR1 locus in fragile X syndrome or the FXN locus in Friedreich’s ataxia
    Article Snippet: Cells were transfected with pX462-MSH2-dual-gRNA and pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ) [ ] using Lipofectamine STEM (Thermo Fisher Scientific, STEM00008) according to the manufacturer’s guidelines. pCE-mp53DD was used to improve cell survival after CRISPR editing.

    Plasmid Preparation:

    Article Title: A Mutant Methionyl-tRNA Synthetase-Based toolkit to assess induced-Mesenchymal Stromal Cell secretome in mixed-culture disease models
    Article Snippet: 500ng donor plasmid, CLYBL-Puro-(NLS)eGFP-CAG-MetRS L274G or CLYBL-BSD-mApple-CAG-MetRS L274G , and 100ng dominant negative p53 plasmid (pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ; RRID:Addgene_41856) to increase survival in cells undergoing double-strand breaks, were added to the RNP complex and mixed with 10μL Lipofectamine 2000 (Invitrogen, #11668–019) in 125μL OptiMEM per well for a total transfection mix volume of 250μL per well.

    Article Title: MSH2 is not required for either maintenance of DNA methylation or repeat contraction at the FMR1 locus in fragile X syndrome or the FXN locus in Friedreich’s ataxia
    Article Snippet: Cells were transfected with pX462-MSH2-dual-gRNA and pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ) [ ] using Lipofectamine STEM (Thermo Fisher Scientific, STEM00008) according to the manufacturer’s guidelines. pCE-mp53DD was used to improve cell survival after CRISPR editing.

    CRISPR:

    Article Title: A Mutant Methionyl-tRNA Synthetase-Based toolkit to assess induced-Mesenchymal Stromal Cell secretome in mixed-culture disease models
    Article Snippet: 500ng donor plasmid, CLYBL-Puro-(NLS)eGFP-CAG-MetRS L274G or CLYBL-BSD-mApple-CAG-MetRS L274G , and 100ng dominant negative p53 plasmid (pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ; RRID:Addgene_41856) to increase survival in cells undergoing double-strand breaks, were added to the RNP complex and mixed with 10μL Lipofectamine 2000 (Invitrogen, #11668–019) in 125μL OptiMEM per well for a total transfection mix volume of 250μL per well.

    Article Title: MSH2 is not required for either maintenance of DNA methylation or repeat contraction at the FMR1 locus in fragile X syndrome or the FXN locus in Friedreich’s ataxia
    Article Snippet: Cells were transfected with pX462-MSH2-dual-gRNA and pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ) [ ] using Lipofectamine STEM (Thermo Fisher Scientific, STEM00008) according to the manufacturer’s guidelines. pCE-mp53DD was used to improve cell survival after CRISPR editing.

    Dominant Negative Mutation:

    Article Title: A Mutant Methionyl-tRNA Synthetase-Based toolkit to assess induced-Mesenchymal Stromal Cell secretome in mixed-culture disease models
    Article Snippet: 500ng donor plasmid, CLYBL-Puro-(NLS)eGFP-CAG-MetRS L274G or CLYBL-BSD-mApple-CAG-MetRS L274G , and 100ng dominant negative p53 plasmid (pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ; RRID:Addgene_41856) to increase survival in cells undergoing double-strand breaks, were added to the RNP complex and mixed with 10μL Lipofectamine 2000 (Invitrogen, #11668–019) in 125μL OptiMEM per well for a total transfection mix volume of 250μL per well.

    Article Title: MSH2 is not required for either maintenance of DNA methylation or repeat contraction at the FMR1 locus in fragile X syndrome or the FXN locus in Friedreich’s ataxia
    Article Snippet: Cells were transfected with pX462-MSH2-dual-gRNA and pCE-mp53DD, a gift from Shinya Yamanaka (Addgene plasmid # 41856; http://n2t.net/addgene:41856 ) [ ] using Lipofectamine STEM (Thermo Fisher Scientific, STEM00008) according to the manufacturer’s guidelines. pCE-mp53DD was used to improve cell survival after CRISPR editing.



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    ATRX LoF neuroblastoma cells have an impaired chromatin response to RA compared to their wild-type counterparts. (A) Time course experiment showing expression of CYP26A , normalized to GAPDH following exposure of <t>p53(2)</t> ( ATRX wildtype) and E6 ( ATRX LoF) cells to retinoic acid (RA). Data represented as mean ± SEM of n = 3 ( t test, * P <0.05). (B) HOXA1 and HOXA4 expression by RT-qPCR following 72 hours treatment with RA, compared to vehicle control. Inverse log delta CT is indicated. Where no expression was seen, this is indicated as 0. Mean ± SEM of n = 3; t test, * P < 0.05. (C) Clonogenic assay results for p53(2) and E6 cell lines following treatment with 10μM RA versus control (mean ± SEM of n = 3; t test, *** P < 0.001). (D-E) Volcano plots showing differentially accessible regions in E6 versus p53(2) cell lines following (D) vehicle control treatment conditions and (E) RA treatment. (F) Venn diagrams comparing differentially accessible transcription factor binding motifs following RA treatment in p53(2) and E6 cell lines. (G-J) Gene ontology analysis, comparing differential accessibility at gene promoters between E6 and p53(2) lines in (G) vehicle control conditions and (H) following treatment with RA. Displayed terms have been selected using REVIGO which eliminates redundant GO terms. (I-J) List of pathways grouped under the term “regionalization” and “embryonic skeletal system development” by Revigo for (I) vehicle control and (J) RA treated samples, respectively.
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    Image Search Results


    ATRX LoF neuroblastoma cells have an impaired chromatin response to RA compared to their wild-type counterparts. (A) Time course experiment showing expression of CYP26A , normalized to GAPDH following exposure of p53(2) ( ATRX wildtype) and E6 ( ATRX LoF) cells to retinoic acid (RA). Data represented as mean ± SEM of n = 3 ( t test, * P <0.05). (B) HOXA1 and HOXA4 expression by RT-qPCR following 72 hours treatment with RA, compared to vehicle control. Inverse log delta CT is indicated. Where no expression was seen, this is indicated as 0. Mean ± SEM of n = 3; t test, * P < 0.05. (C) Clonogenic assay results for p53(2) and E6 cell lines following treatment with 10μM RA versus control (mean ± SEM of n = 3; t test, *** P < 0.001). (D-E) Volcano plots showing differentially accessible regions in E6 versus p53(2) cell lines following (D) vehicle control treatment conditions and (E) RA treatment. (F) Venn diagrams comparing differentially accessible transcription factor binding motifs following RA treatment in p53(2) and E6 cell lines. (G-J) Gene ontology analysis, comparing differential accessibility at gene promoters between E6 and p53(2) lines in (G) vehicle control conditions and (H) following treatment with RA. Displayed terms have been selected using REVIGO which eliminates redundant GO terms. (I-J) List of pathways grouped under the term “regionalization” and “embryonic skeletal system development” by Revigo for (I) vehicle control and (J) RA treated samples, respectively.

    Journal: Neoplasia (New York, N.Y.)

    Article Title: Differential chromatin accessibility response to retinoic acid in neuroblastoma with ATRX in-frame-deletions versus ATRX loss-of-function

    doi: 10.1016/j.neo.2025.101263

    Figure Lengend Snippet: ATRX LoF neuroblastoma cells have an impaired chromatin response to RA compared to their wild-type counterparts. (A) Time course experiment showing expression of CYP26A , normalized to GAPDH following exposure of p53(2) ( ATRX wildtype) and E6 ( ATRX LoF) cells to retinoic acid (RA). Data represented as mean ± SEM of n = 3 ( t test, * P <0.05). (B) HOXA1 and HOXA4 expression by RT-qPCR following 72 hours treatment with RA, compared to vehicle control. Inverse log delta CT is indicated. Where no expression was seen, this is indicated as 0. Mean ± SEM of n = 3; t test, * P < 0.05. (C) Clonogenic assay results for p53(2) and E6 cell lines following treatment with 10μM RA versus control (mean ± SEM of n = 3; t test, *** P < 0.001). (D-E) Volcano plots showing differentially accessible regions in E6 versus p53(2) cell lines following (D) vehicle control treatment conditions and (E) RA treatment. (F) Venn diagrams comparing differentially accessible transcription factor binding motifs following RA treatment in p53(2) and E6 cell lines. (G-J) Gene ontology analysis, comparing differential accessibility at gene promoters between E6 and p53(2) lines in (G) vehicle control conditions and (H) following treatment with RA. Displayed terms have been selected using REVIGO which eliminates redundant GO terms. (I-J) List of pathways grouped under the term “regionalization” and “embryonic skeletal system development” by Revigo for (I) vehicle control and (J) RA treated samples, respectively.

    Article Snippet: SH-SY5Y cells were subsequently electroporated with plasmids containing sgRNA for targeting Intron 1 and Intron 10 of ATRX as well as a pCE-mp53-DD plasmid (p53-DD) (Addgene Plasmid #41856) for transient inhibition of p53 [ , ] using the 4D-Nucleofector® X Unit with the SF Cell Line 4D-Nucleofector® X Kit L (Lonza, Cat# V4XC-2024), following the manufacturer’s protocol.

    Techniques: Expressing, Quantitative RT-PCR, Control, Clonogenic Assay, Binding Assay