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phic31 recombinase  (Genetic Services Inc)

 
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    Genetic Services Inc phic31 recombinase
    Phic31 Recombinase, supplied by Genetic Services 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/phic31+recombinase/phic31+integrase+system/pmc06320681-371-9-11
    Average 90 stars, based on 1 article reviews
    phic31 recombinase - by Bioz Stars, 2026-10
    90/100 stars

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    other:

    Article Title: Abolishment of spontaneous flight turns in visually responsive Drosophila
    Article Snippet: This R83H12-Gal80 vector was then integrated into VK00027 using PhiC31 recombinase (Genetic Services, Inc), and transformants selected as in [ 58 ].



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    The domain organization of the human TFAM and GeneSwap approach. ( A ) The domain structure of human TFAM. The bold upward vertical arrow designates a crossover point in chimeras (between residues 154 and 155 of the hTFAM). Here, we refer to the TFAM portion preceding the crossover point as the N-terminal domain (NTD) and the following portion C-terminal domain (CTD). Subdomain boundaries are given in aa coordinates. MTS, matrix targeting sequence. ( B ) Derivation of the hTFAM GeneSwap cell line 143B#6. In 143B osteosarcoma cells, TFAM was inactivated with CRISPR/Cas9 and replaced with a retrovirus-encoded, loxP-site-flanked wt TFAM cDNA. To reintroduce mtDNA, the resulting cells were fused with chemically enucleated MDA-MB-231 cells, resulting in the 143B#6 cell line (9). ( C ) Schematics of the GeneSwap approach. To implement GeneSwap, 143B#6 cells (top panel) were co-transduced with retroviruses encoding Cre recombinase and altered TFAM (TFAMvar, central panel). This results in the excision of the wtTFAM cDNA and simultaneous re-expression of TFAMvar. In the resulting cotransductants, mtDNA is retained only if TFAMvar is functional in hmtDNA replication. In that case, the functionality is further validated by transducing cells with <t>PhiC31</t> recombinase, which affects the loss of TFAMvar and hmtDNA (the bottom panel).
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    Image Search Results


    The domain organization of the human TFAM and GeneSwap approach. ( A ) The domain structure of human TFAM. The bold upward vertical arrow designates a crossover point in chimeras (between residues 154 and 155 of the hTFAM). Here, we refer to the TFAM portion preceding the crossover point as the N-terminal domain (NTD) and the following portion C-terminal domain (CTD). Subdomain boundaries are given in aa coordinates. MTS, matrix targeting sequence. ( B ) Derivation of the hTFAM GeneSwap cell line 143B#6. In 143B osteosarcoma cells, TFAM was inactivated with CRISPR/Cas9 and replaced with a retrovirus-encoded, loxP-site-flanked wt TFAM cDNA. To reintroduce mtDNA, the resulting cells were fused with chemically enucleated MDA-MB-231 cells, resulting in the 143B#6 cell line (9). ( C ) Schematics of the GeneSwap approach. To implement GeneSwap, 143B#6 cells (top panel) were co-transduced with retroviruses encoding Cre recombinase and altered TFAM (TFAMvar, central panel). This results in the excision of the wtTFAM cDNA and simultaneous re-expression of TFAMvar. In the resulting cotransductants, mtDNA is retained only if TFAMvar is functional in hmtDNA replication. In that case, the functionality is further validated by transducing cells with PhiC31 recombinase, which affects the loss of TFAMvar and hmtDNA (the bottom panel).

    Journal: Cells

    Article Title: TFAM’s Contributions to mtDNA Replication and OXPHOS Biogenesis Are Genetically Separable

    doi: 10.3390/cells11233754

    Figure Lengend Snippet: The domain organization of the human TFAM and GeneSwap approach. ( A ) The domain structure of human TFAM. The bold upward vertical arrow designates a crossover point in chimeras (between residues 154 and 155 of the hTFAM). Here, we refer to the TFAM portion preceding the crossover point as the N-terminal domain (NTD) and the following portion C-terminal domain (CTD). Subdomain boundaries are given in aa coordinates. MTS, matrix targeting sequence. ( B ) Derivation of the hTFAM GeneSwap cell line 143B#6. In 143B osteosarcoma cells, TFAM was inactivated with CRISPR/Cas9 and replaced with a retrovirus-encoded, loxP-site-flanked wt TFAM cDNA. To reintroduce mtDNA, the resulting cells were fused with chemically enucleated MDA-MB-231 cells, resulting in the 143B#6 cell line (9). ( C ) Schematics of the GeneSwap approach. To implement GeneSwap, 143B#6 cells (top panel) were co-transduced with retroviruses encoding Cre recombinase and altered TFAM (TFAMvar, central panel). This results in the excision of the wtTFAM cDNA and simultaneous re-expression of TFAMvar. In the resulting cotransductants, mtDNA is retained only if TFAMvar is functional in hmtDNA replication. In that case, the functionality is further validated by transducing cells with PhiC31 recombinase, which affects the loss of TFAMvar and hmtDNA (the bottom panel).

    Article Snippet: PhiC31 recombinase for excision of chTFAM variants was delivered with rv.5136, which also encodes hygromycin resistance ( , Addgene no. 184853).

    Techniques: Sequencing, CRISPR, Transduction, Expressing, Functional Assay

    TFAM residues making DNA contacts are critical for mtDNA replication. ( A–C ) PCR genotyping strategies. ( A ) PCR genotyping strategies for excision of hTFAM (ΔhTFAM). ( B ) Genotyping of excision of modified chTFAM (chTFAMvar, F + R1 panel). ( C ) Genotyping of PhiC31 and chTFAM (PhiC31 and chTFAM panels, respectively). mtDNA, nDNA, duplex PCR with two pairs of primers for the detection of hmtDNA; ( D ) Both Ch13 and Ch22 TFAM variants support the replication of hmtDNA. ( E ) Ch22-3 variant supports hmtDNA replication, whereas Ch3 and Ch13-3 variants do not. ( F ) Neither Ch13/WT nor ChWT/13 support the replication of hmtDNA. ( G ) hTFAM with “chicken” DNA contact residues does not support the replication of the hmtDNA.

    Journal: Cells

    Article Title: TFAM’s Contributions to mtDNA Replication and OXPHOS Biogenesis Are Genetically Separable

    doi: 10.3390/cells11233754

    Figure Lengend Snippet: TFAM residues making DNA contacts are critical for mtDNA replication. ( A–C ) PCR genotyping strategies. ( A ) PCR genotyping strategies for excision of hTFAM (ΔhTFAM). ( B ) Genotyping of excision of modified chTFAM (chTFAMvar, F + R1 panel). ( C ) Genotyping of PhiC31 and chTFAM (PhiC31 and chTFAM panels, respectively). mtDNA, nDNA, duplex PCR with two pairs of primers for the detection of hmtDNA; ( D ) Both Ch13 and Ch22 TFAM variants support the replication of hmtDNA. ( E ) Ch22-3 variant supports hmtDNA replication, whereas Ch3 and Ch13-3 variants do not. ( F ) Neither Ch13/WT nor ChWT/13 support the replication of hmtDNA. ( G ) hTFAM with “chicken” DNA contact residues does not support the replication of the hmtDNA.

    Article Snippet: PhiC31 recombinase for excision of chTFAM variants was delivered with rv.5136, which also encodes hygromycin resistance ( , Addgene no. 184853).

    Techniques: Modification, Variant Assay

    Journal: eLife

    Article Title: A Drosophila model of neuronal ceroid lipofuscinosis CLN4 reveals a hypermorphic gain of function mechanism

    doi: 10.7554/eLife.46607

    Figure Lengend Snippet:

    Article Snippet: Recombinant DNA reagent , pBID-UASC , , RRID: Addgene_35200 , PhiC31 attB 10xUAS vector for site specific recombinase insertions.

    Techniques: Sequencing, Construct, Recombinant, Plasmid Preparation, Clone Assay, Mutagenesis, Transformation Assay, Generated, Immunostaining, Western Blot, Software