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pmcherry c1 plasmid  (Addgene inc)


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    Structured Review

    Addgene inc pmcherry c1 plasmid
    Pmcherry C1 Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pmcherry+c1/pmCherry-Akt1(WT)+(Plasmid+%2386631)/bio_rxiv__64898__2026__03__31__715582-184-76-78
    Average 91 stars, based on 5 article reviews
    pmcherry c1 plasmid - by Bioz Stars, 2026-09
    91/100 stars

    Images

    Related Articles

    Construct:

    Article Title: A single-component optogenetic toolkit for programmable control of microtubule
    Article Snippet: .. Opto-αTAT1 (αTAT1-mCh-CIBN-NLS-LEXY) was constructed by using the HiFi DNA assembly method. αTAT1, mCherry, CIBN and LEXY (LOV2-NES) were amplified by standard PCR from pEF5B-FRT-GFP-αTAT1 (Addgene, #27099), pmCherry-C1, CIB1-CreC(N1) (Addgene, #75367) and NLS-mCherry-LEXY (Addgene, #72655), respectively. .. αTAT1, mCherry, CIBN and LEXY (LOV2-NES) were amplified by standard PCR from pEF5B-FRT-GFP-αTAT1 (Addgene, #27099), pmCherry-C1, CIB1-CreC(N1) (Addgene, #75367) and NLS-mCherry-LEXY (Addgene, #72655), respectively.

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene). ..

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect.
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene, USA). ..

    Amplification:

    Article Title: A single-component optogenetic toolkit for programmable control of microtubule
    Article Snippet: .. Opto-αTAT1 (αTAT1-mCh-CIBN-NLS-LEXY) was constructed by using the HiFi DNA assembly method. αTAT1, mCherry, CIBN and LEXY (LOV2-NES) were amplified by standard PCR from pEF5B-FRT-GFP-αTAT1 (Addgene, #27099), pmCherry-C1, CIB1-CreC(N1) (Addgene, #75367) and NLS-mCherry-LEXY (Addgene, #72655), respectively. .. αTAT1, mCherry, CIBN and LEXY (LOV2-NES) were amplified by standard PCR from pEF5B-FRT-GFP-αTAT1 (Addgene, #27099), pmCherry-C1, CIB1-CreC(N1) (Addgene, #75367) and NLS-mCherry-LEXY (Addgene, #72655), respectively.

    Polymerase Chain Reaction:

    Article Title: A single-component optogenetic toolkit for programmable control of microtubule
    Article Snippet: .. Opto-αTAT1 (αTAT1-mCh-CIBN-NLS-LEXY) was constructed by using the HiFi DNA assembly method. αTAT1, mCherry, CIBN and LEXY (LOV2-NES) were amplified by standard PCR from pEF5B-FRT-GFP-αTAT1 (Addgene, #27099), pmCherry-C1, CIB1-CreC(N1) (Addgene, #75367) and NLS-mCherry-LEXY (Addgene, #72655), respectively. .. αTAT1, mCherry, CIBN and LEXY (LOV2-NES) were amplified by standard PCR from pEF5B-FRT-GFP-αTAT1 (Addgene, #27099), pmCherry-C1, CIB1-CreC(N1) (Addgene, #75367) and NLS-mCherry-LEXY (Addgene, #72655), respectively.

    Expressing:

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene). ..

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect.
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene, USA). ..

    Mutagenesis:

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene). ..

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect.
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene, USA). ..

    Clone Assay:

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene). ..

    Article Title: Tau destabilization in a familial deletion mutant K280 accelerates its fibrillization and enhances the seeding effect.
    Article Snippet: .. For mammalian expression constructs, WT tau, mutant tau, and mCherry-eGFP tandem protein were cloned into mammalian expressing vector pEGFP-C1 and pmCherry-C1 (Addgene, USA). ..

    Article Title: CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance
    Article Snippet: 2 As the third most common cause of cancer-related mortality, hepatocellular carcinoma 36 (HCC) is a global health concern.. Despite its prevalence, treatment options are limited, 37 underscoring the need to identify potential therapeutic targets and strategies.. Here, we 38 identified amplification of CRTC2, situated in the 1q21.3 region, due to copy number 39 alterations in HCC.

    Fluorescence:

    Article Title: CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance
    Article Snippet: 2 As the third most common cause of cancer-related mortality, hepatocellular carcinoma 36 (HCC) is a global health concern.. Despite its prevalence, treatment options are limited, 37 underscoring the need to identify potential therapeutic targets and strategies.. Here, we 38 identified amplification of CRTC2, situated in the 1q21.3 region, due to copy number 39 alterations in HCC.

    other:

    Article Title: Plasma membrane nanodeformations promote actin polymerization through CIP4/CDC42 recruitment and regulate type II IFN signaling
    Article Snippet: FBP17 , Human , pmCherry-C1 , CMV , N-ter mCherry , Addgene #27688 , .

    Article Title: Plasma membrane nanodeformations promote actin polymerization through CIP4/CDC42 recruitment and regulate type II IFN signaling
    Article Snippet: FCHo2 , Mouse , pmCherry-C1 , CMV , N-ter mCherry , Addgene #27686 , .

    Article Title: Plasma membrane nanodeformations promote actin polymerization through CIP4/CDC42 recruitment and regulate type II IFN signaling
    Article Snippet: FCHo1 , Mouse , pmCherry-C1 , CMV , N-ter mCherry , Addgene #27690 , .

    Plasmid Preparation:

    Article Title: UVSSA facilitates transcription-coupled repair of DNA interstrand crosslinks.
    Article Snippet: DNA interstrand crosslinks (ICLs) are covalent bonds between bases on opposing strands of the DNA helix which prevent DNA melting and subsequent DNA replication or RNA transcription.. Here, we show that Ultraviolet Stimulated Scaffold Protein A (UVSSA) is critical for ICL repair in human cells, at least in part via the transcription coupled ICL repair (TC-ICR) pathway.. Inactivation of UVSSA sensitizes human cells to ICL-inducing drugs, and delays ICL repair.



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    Image Search Results


    a, BFP channel of cytosolic condensates formed by 3×SH3 FBP17 –BFP, GFP–Nck1, N-WASP, and WIP, which fail to recruit Src(SH3–SH2) or Src(ΔSH4, Y530F). Scale bar, 10 µm. Related to . b, BFP channel of cytosolic condensates formed by 3×SH3 FBP17 –BFP, GFP–Nck1, N-WASP, and WIP, which recruit cortactin. Scale bar, 10 µm. Related to . c, BFP channel of cytosolic condensates formed by cortactin together with 3×SH3 FBP17 –BFP, GFP–Nck1, N-WASP, and WIP, which recruit Src(SH3–SH2) or Src(ΔSH4, Y530F). Scale bar, 10 µm. Related to . d, FRAP analysis of GFP–Nck1 and Src(ΔSH4, Y530F)–RFP in cytosolic condensates reveals rapid fluorescence recovery, indicating liquid-like dynamics. Nck1 recovers slightly faster than Src(ΔSH4, Y530F). Scale bars, 10 µm; 5 µm (montages). See also Supplementary Video 4. e, Sequences of the SH2- and SH3-binding motifs in adaptor proteins known to engage Src in a bipartite manner. Adaptor proteins include cortactin, Tks5, Tks4, AFAP1, FAK, Sam68, and p130Cas. f and g, Representative images of GFP-tagged adaptor proteins on nanobar substrates. Cortactin, Tks4, Tks5, and AFAP1 accumulate at nanobar ends, whereas FAK, Sam68, and p130Cas do not. Scale bars, 10 µm. h , Quantification of curvature enrichment (nanobar end-to-side ratios) for adaptor proteins shown in (e-g). Cortactin, Tks4, Tks5, and AFAP1 show significant enrichment, while FAK, Sam68, and p130Cas do not. n = 12 cells per condition, from two independent experiments; data are mean ± SD.

    Journal: bioRxiv

    Article Title: Membrane Curvature Activates Src kinase and Promotes Metastatic Cancer Cell Survival

    doi: 10.64898/2026.03.03.709279

    Figure Lengend Snippet: a, BFP channel of cytosolic condensates formed by 3×SH3 FBP17 –BFP, GFP–Nck1, N-WASP, and WIP, which fail to recruit Src(SH3–SH2) or Src(ΔSH4, Y530F). Scale bar, 10 µm. Related to . b, BFP channel of cytosolic condensates formed by 3×SH3 FBP17 –BFP, GFP–Nck1, N-WASP, and WIP, which recruit cortactin. Scale bar, 10 µm. Related to . c, BFP channel of cytosolic condensates formed by cortactin together with 3×SH3 FBP17 –BFP, GFP–Nck1, N-WASP, and WIP, which recruit Src(SH3–SH2) or Src(ΔSH4, Y530F). Scale bar, 10 µm. Related to . d, FRAP analysis of GFP–Nck1 and Src(ΔSH4, Y530F)–RFP in cytosolic condensates reveals rapid fluorescence recovery, indicating liquid-like dynamics. Nck1 recovers slightly faster than Src(ΔSH4, Y530F). Scale bars, 10 µm; 5 µm (montages). See also Supplementary Video 4. e, Sequences of the SH2- and SH3-binding motifs in adaptor proteins known to engage Src in a bipartite manner. Adaptor proteins include cortactin, Tks5, Tks4, AFAP1, FAK, Sam68, and p130Cas. f and g, Representative images of GFP-tagged adaptor proteins on nanobar substrates. Cortactin, Tks4, Tks5, and AFAP1 accumulate at nanobar ends, whereas FAK, Sam68, and p130Cas do not. Scale bars, 10 µm. h , Quantification of curvature enrichment (nanobar end-to-side ratios) for adaptor proteins shown in (e-g). Cortactin, Tks4, Tks5, and AFAP1 show significant enrichment, while FAK, Sam68, and p130Cas do not. n = 12 cells per condition, from two independent experiments; data are mean ± SD.

    Article Snippet: These DNA fragments were used to replace the EGFP in pEGFP-N1 for mammalian expression, or inserted into pEGFP-N1, pEGFP-C1, pmCherry-N1 or pmCherry-C1 vector (Clontech) for the expression of GFP- or RFP-tagged constructs.

    Techniques: Fluorescence, Binding Assay

    a, Schematic illustrating curvature-induced Src activation: condensates formed at membrane curvature enrich open-conformation Src, promoting local trans-autophosphorylation at Y419. b, Ratiometric imaging of Src(pY419)/Src–GFP and Src(pY419)/Src(Y530F)–GFP reveals enhanced Y419 phosphorylation at nanopillars. Scale bar, 10 µm. c, Quantification confirms that Src autophosphorylation (pY419) is significantly elevated at nanopillars compared to flat regions or focal adhesions. n = 12 (Src–GFP) and 15 (Src(Y530F)–GFP) cells, from two independent experiments; data are mean ± SD; p values from one-way ANOVA with Dunnett’s T3 multiple comparisons. d, Immunostaining for total Src, open conformation Src(Y530), and active Src(pY419) shows different degrees of enrichment at nanopillars. Scale bar, 10 µm. e, Quantification reveals highest curvature enrichment for Src(pY419), intermediate for Src(Y530), and minimal for total Src. n = 22, 19, 21 cells from two independent experiments; mean ± SD; p values from one-way ANOVA with Dunnett’s T3 multiple comparisons. f, At nanopillars, Src(Y530F)–RFP colocalizes with N-WASP/WIP/GFP–Nck1 condensates, while Csk–RFP (a negative regulator of Src) is excluded. Scale bar, 10 µm. g, Schematic illustrating PI3K/Akt signaling downstream of curvature-induced Src activation. h, PI3K regulatory subunit alpha (p85α–GFP) accumulates at nanopillars, colocalizing with Src(pY419). Scale bar, 10 µm. i, Live-cell imaging showing Akt–PH–GFP, a PI(3,4,5)P3 sensor, enriched at nanopillars together with Src(Y530F)–RFP. Scale bar, 10 µm. j, Treatment with Src inhibitor dasatinib abolishes p85α–GFP and Src(pY419) enrichment at nanopillars. Scale bar, 10 µm. k, Dasatinib treatment eliminates p85α–GFP enrichment at nanopillars, while Src(Y530F)–RFP enrichment remains, indicating that curvature localization of Src(Y530F) does not rely on its kinase activity. Scale bar, 10 µm. l, PI3K inhibition (ZSTK474) does not affect Src(pY419) or p85α–GFP enrichment at nanopillars. Scale bar, 10 µm. m, Enrichment of Akt–PH–GFP at nanopillars is abolished by either Src or PI3K inhibition, indicating that both kinases are required for Akt signaling at curvature. Scale bar, 10 µm. n, Quantification of curvature enrichment for p85α-GFP, Src(pY419), and Akt–PH–GFP under the indicated inhibitor treatments. n = 19, 18, 21, 17, and 16 cells (p85α-GFP co-stained with Src(pY419)); 20, 15, 17, 19, and 19 cells (Akt–PH–GFP), from two independent experiments; data are mean ± SD; p -values from Kruskal-Wallis tests with Dunn’s multiple comparisons.

    Journal: bioRxiv

    Article Title: Membrane Curvature Activates Src kinase and Promotes Metastatic Cancer Cell Survival

    doi: 10.64898/2026.03.03.709279

    Figure Lengend Snippet: a, Schematic illustrating curvature-induced Src activation: condensates formed at membrane curvature enrich open-conformation Src, promoting local trans-autophosphorylation at Y419. b, Ratiometric imaging of Src(pY419)/Src–GFP and Src(pY419)/Src(Y530F)–GFP reveals enhanced Y419 phosphorylation at nanopillars. Scale bar, 10 µm. c, Quantification confirms that Src autophosphorylation (pY419) is significantly elevated at nanopillars compared to flat regions or focal adhesions. n = 12 (Src–GFP) and 15 (Src(Y530F)–GFP) cells, from two independent experiments; data are mean ± SD; p values from one-way ANOVA with Dunnett’s T3 multiple comparisons. d, Immunostaining for total Src, open conformation Src(Y530), and active Src(pY419) shows different degrees of enrichment at nanopillars. Scale bar, 10 µm. e, Quantification reveals highest curvature enrichment for Src(pY419), intermediate for Src(Y530), and minimal for total Src. n = 22, 19, 21 cells from two independent experiments; mean ± SD; p values from one-way ANOVA with Dunnett’s T3 multiple comparisons. f, At nanopillars, Src(Y530F)–RFP colocalizes with N-WASP/WIP/GFP–Nck1 condensates, while Csk–RFP (a negative regulator of Src) is excluded. Scale bar, 10 µm. g, Schematic illustrating PI3K/Akt signaling downstream of curvature-induced Src activation. h, PI3K regulatory subunit alpha (p85α–GFP) accumulates at nanopillars, colocalizing with Src(pY419). Scale bar, 10 µm. i, Live-cell imaging showing Akt–PH–GFP, a PI(3,4,5)P3 sensor, enriched at nanopillars together with Src(Y530F)–RFP. Scale bar, 10 µm. j, Treatment with Src inhibitor dasatinib abolishes p85α–GFP and Src(pY419) enrichment at nanopillars. Scale bar, 10 µm. k, Dasatinib treatment eliminates p85α–GFP enrichment at nanopillars, while Src(Y530F)–RFP enrichment remains, indicating that curvature localization of Src(Y530F) does not rely on its kinase activity. Scale bar, 10 µm. l, PI3K inhibition (ZSTK474) does not affect Src(pY419) or p85α–GFP enrichment at nanopillars. Scale bar, 10 µm. m, Enrichment of Akt–PH–GFP at nanopillars is abolished by either Src or PI3K inhibition, indicating that both kinases are required for Akt signaling at curvature. Scale bar, 10 µm. n, Quantification of curvature enrichment for p85α-GFP, Src(pY419), and Akt–PH–GFP under the indicated inhibitor treatments. n = 19, 18, 21, 17, and 16 cells (p85α-GFP co-stained with Src(pY419)); 20, 15, 17, 19, and 19 cells (Akt–PH–GFP), from two independent experiments; data are mean ± SD; p -values from Kruskal-Wallis tests with Dunn’s multiple comparisons.

    Article Snippet: These DNA fragments were used to replace the EGFP in pEGFP-N1 for mammalian expression, or inserted into pEGFP-N1, pEGFP-C1, pmCherry-N1 or pmCherry-C1 vector (Clontech) for the expression of GFP- or RFP-tagged constructs.

    Techniques: Activation Assay, Membrane, Imaging, Phospho-proteomics, Immunostaining, Live Cell Imaging, Activity Assay, Inhibition, Staining

    a , GFP-tagged nSH2–cSH2 fragment of p85α accumulates at nanopillars and colocalizes with Src(pY419). Scale bar, 10 µm. b, Immunostaining of p85α(pY467) showing its strong curvature-dependent enrichment at nanopillars, colocalizing with Src(pY419). Scale bar, 10 µm. c , Treatment with Src inhibitor saracatinib abolishes the enrichment of p85α–GFP and Src(pY419) at nanopillars, similar to the effect of dasatinib. Scale bar, 10 µm. d, Despite saracatinib treatment, Src(Y530F)–RFP remains enriched at nanopillars, while p85α–GFP enrichment is abolished, indicating that Src kinase activity is necessary for PI3K but not Src recruitment to curvature. Scale bar, 10 µm. e, Immunostaining confirms that both dasatinib and saracatinib eliminate nanopillar enrichment of Src(pY419) and p85α(pY467). Scale bar, 10 µm.

    Journal: bioRxiv

    Article Title: Membrane Curvature Activates Src kinase and Promotes Metastatic Cancer Cell Survival

    doi: 10.64898/2026.03.03.709279

    Figure Lengend Snippet: a , GFP-tagged nSH2–cSH2 fragment of p85α accumulates at nanopillars and colocalizes with Src(pY419). Scale bar, 10 µm. b, Immunostaining of p85α(pY467) showing its strong curvature-dependent enrichment at nanopillars, colocalizing with Src(pY419). Scale bar, 10 µm. c , Treatment with Src inhibitor saracatinib abolishes the enrichment of p85α–GFP and Src(pY419) at nanopillars, similar to the effect of dasatinib. Scale bar, 10 µm. d, Despite saracatinib treatment, Src(Y530F)–RFP remains enriched at nanopillars, while p85α–GFP enrichment is abolished, indicating that Src kinase activity is necessary for PI3K but not Src recruitment to curvature. Scale bar, 10 µm. e, Immunostaining confirms that both dasatinib and saracatinib eliminate nanopillar enrichment of Src(pY419) and p85α(pY467). Scale bar, 10 µm.

    Article Snippet: These DNA fragments were used to replace the EGFP in pEGFP-N1 for mammalian expression, or inserted into pEGFP-N1, pEGFP-C1, pmCherry-N1 or pmCherry-C1 vector (Clontech) for the expression of GFP- or RFP-tagged constructs.

    Techniques: Immunostaining, Activity Assay