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krab cas9 fusion protein  (Addgene inc)


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    Structured Review

    Addgene inc krab cas9 fusion protein
    Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). <t>CRISPR-Cas9-mediated</t> knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation
    Krab Cas9 Fusion Protein, supplied by Addgene inc, used in various techniques. Bioz Stars score: 95/100, based on 128 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cas9+mcherry+fusion+plasmid/pHR-SFFV-KRAB-dCas9-P2A-mCherry+(Plasmid+%2360954)/pmc06646342-231-15-18
    Average 95 stars, based on 128 article reviews
    krab cas9 fusion protein - by Bioz Stars, 2026-09
    95/100 stars

    Images

    1) Product Images from "Integrated analyses of murine breast cancer models reveal critical parallels with human disease"

    Article Title: Integrated analyses of murine breast cancer models reveal critical parallels with human disease

    Journal: Nature Communications

    doi: 10.1038/s41467-019-11236-3

    Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). CRISPR-Cas9-mediated knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation
    Figure Legend Snippet: Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). CRISPR-Cas9-mediated knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation

    Techniques Used: Amplification, Staining, CRISPR, Knock-Out, Two Tailed Test, Injection, Standard Deviation

    Related Articles

    Plasmid Preparation:

    Article Title: Cancer modeling by Transgene Electroporation in Adult Zebrafish (TEAZ)
    Article Snippet: .. The ubb promoter was as described previously , and the Cas9-mCherry fusion plasmid was subcloned from Addgene plasmid number 78313 ( ). ..

    Article Title: Cancer modeling by Transgene Electroporation in Adult Zebrafish (TEAZ)
    Article Snippet: .. The ubb promoter was as described previously , and the Cas9-mCherry fusion plasmid was subcloned from Addgene number 78313( ) . ..



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    Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). <t>CRISPR-Cas9-mediated</t> knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation
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    https://www.bioz.com/product/cas9+mcherry+fusion+plasmid/pHR-SFFV-KRAB-dCas9-P2A-mCherry+(Plasmid+%2360954)/pmc06646342-231-15-18
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    Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). <t>CRISPR-Cas9-mediated</t> knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation
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    Image Search Results


    Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). CRISPR-Cas9-mediated knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation

    Journal: Nature Communications

    Article Title: Integrated analyses of murine breast cancer models reveal critical parallels with human disease

    doi: 10.1038/s41467-019-11236-3

    Figure Lengend Snippet: Copy number alterations alter metastatic potential. Schematic representation of filtering of copy number variants ( a ) where copy number variants were detected from NGS and filtered to the top 11 variants by selecting those genes that encompassed both mouse models and were conserved in human breast cancer. These genes were then assayed using qPCR analysis across a larger panel of MMTV-Neu ( n = 10, green triangles) and MMTV-PyMT ( n = 15, red circles) tumors and depicted using a circos plot for genes in chromosomes 2, 6, 11, and 17 ( b ). Heterozygous deletion on the interior of the plot to a threefold amplification on the exterior of the plot is shown. A key copy number alteration in the 11D region encompassing the Col1a1 gene (boxed) was observed to correlate with reduction and lack of collagen alignment in Masson’s trichrome staining ( c ) and an increase in metastases in the lungs of mice with Col1a1 amplification in the primary tumors ( d ). CRISPR-Cas9-mediated knockout of two key genes within this region, Col1a1 and Chad , show defects in wound healing ( e , f ) (scale bar = 100 µm) ( n = 9) (Colors denote significance by students two-tailed, unpaired t -test, P < 0.01, vs. the same colored control). Knockout also impaired the ability to colonize the lung through a tail vein injection ( g , h ) (NDL2–5 n = 12, NDL2–5 Clonal n = 4, Chad KO n = 9, Col1a1 KO n = 6). (** = P < 0.01, students two-tailed, unpaired t -test, for h ). Scale bar of 20 µm displayed on histological image for reference. All error bars denote standard deviation

    Article Snippet: Lenti virus was created for stable expression of this plasmid and the stable expression of KRAB-Cas9 fusion protein (Addgene plasmid #60954) .

    Techniques: Amplification, Staining, CRISPR, Knock-Out, Two Tailed Test, Injection, Standard Deviation