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cd34 ncg  (Charles River Laboratories)

 
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    Charles River Laboratories cd34 ncg
    Cd34 Ncg, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cd34+ncg/female+mice+ncg/bio_rxiv__64898__2026__05__15__725395-72-0-8
    Average 86 stars, based on 1 article reviews
    cd34 ncg - by Bioz Stars, 2026-09
    86/100 stars

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    Article Title: Transgene Expression Kinetics and Replication Potential of Recombinant Adenovirus Serotype 4 in a Mouse Model and its Use as a Herpes Simplex Virus Vaccine
    Article Snippet: CD34+ NCG or NOG humanized mice (HuCD34+ NCG, Charles River Laboratories and HuCD34+ NOG, Taconic) were obtained at an average of 24 weeks (range 18 to 26 weeks) after human CD34+ cord blood cell infusion.



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    ALDH1A3 is necessary for tumor growth in humanized mice but not immune-deficient mice (A) SUM159-M1a cells were transiently transfected with a plasmid encoding GFP, Cas9, and ALDH1A3-targeting or scrambled guide RNAs followed by sorting for GFP+ cells. The populations were profiled by Aldefluor at passage 5 post sort. (B) Single-cell colonies isolated from (A) were profiled by Sanger sequencing of the ALDH1A3 locus in the genomic DNA. An ALDH1A3 knockout clone along with the parental population was stably transduced with ALDH1A3 or control expression plasmids. Cell populations were profiled for ALDH1A3 expression and β-actin by western blot. (C) Cells from (B) were tested by the Aldefluor assay. (D) Cells from (B) and (C) were implanted into the mammary fat pad of female NSG and <t>CD34</t> + humanized <t>NCG</t> mice validated for >80% CD45 + humanization by Charles River. Tumor growth was measured by weekly caliper measurement. N = 6 mice per arm in NSG mice and n = 3 or 4 mice per arm in CD34 + humanized NCG arms. Statistics by two-way ANOVA. No tumors initiated in the ALDH1A3 knockout arm in the humanized mice. Data are represented as mean ± SEM. (E and F) Bioluminescent quantification at the final measurement day graphed (F) and displayed as representative images (E). Data from (F) are represented as mean ± SEM.
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    ALDH1A3 is necessary for tumor growth in humanized mice but not immune-deficient mice (A) SUM159-M1a cells were transiently transfected with a plasmid encoding GFP, Cas9, and ALDH1A3-targeting or scrambled guide RNAs followed by sorting for GFP+ cells. The populations were profiled by Aldefluor at passage 5 post sort. (B) Single-cell colonies isolated from (A) were profiled by Sanger sequencing of the ALDH1A3 locus in the genomic DNA. An ALDH1A3 knockout clone along with the parental population was stably transduced with ALDH1A3 or control expression plasmids. Cell populations were profiled for ALDH1A3 expression and β-actin by western blot. (C) Cells from (B) were tested by the Aldefluor assay. (D) Cells from (B) and (C) were implanted into the mammary fat pad of female NSG and <t>CD34</t> + humanized <t>NCG</t> mice validated for >80% CD45 + humanization by Charles River. Tumor growth was measured by weekly caliper measurement. N = 6 mice per arm in NSG mice and n = 3 or 4 mice per arm in CD34 + humanized NCG arms. Statistics by two-way ANOVA. No tumors initiated in the ALDH1A3 knockout arm in the humanized mice. Data are represented as mean ± SEM. (E and F) Bioluminescent quantification at the final measurement day graphed (F) and displayed as representative images (E). Data from (F) are represented as mean ± SEM.
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    ALDH1A3 is necessary for tumor growth in humanized mice but not immune-deficient mice (A) SUM159-M1a cells were transiently transfected with a plasmid encoding GFP, Cas9, and ALDH1A3-targeting or scrambled guide RNAs followed by sorting for GFP+ cells. The populations were profiled by Aldefluor at passage 5 post sort. (B) Single-cell colonies isolated from (A) were profiled by Sanger sequencing of the ALDH1A3 locus in the genomic DNA. An ALDH1A3 knockout clone along with the parental population was stably transduced with ALDH1A3 or control expression plasmids. Cell populations were profiled for ALDH1A3 expression and β-actin by western blot. (C) Cells from (B) were tested by the Aldefluor assay. (D) Cells from (B) and (C) were implanted into the mammary fat pad of female NSG and <t>CD34</t> + humanized <t>NCG</t> mice validated for >80% CD45 + humanization by Charles River. Tumor growth was measured by weekly caliper measurement. N = 6 mice per arm in NSG mice and n = 3 or 4 mice per arm in CD34 + humanized NCG arms. Statistics by two-way ANOVA. No tumors initiated in the ALDH1A3 knockout arm in the humanized mice. Data are represented as mean ± SEM. (E and F) Bioluminescent quantification at the final measurement day graphed (F) and displayed as representative images (E). Data from (F) are represented as mean ± SEM.
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    ALDH1A3 is necessary for tumor growth in humanized mice but not immune-deficient mice (A) SUM159-M1a cells were transiently transfected with a plasmid encoding GFP, Cas9, and ALDH1A3-targeting or scrambled guide RNAs followed by sorting for GFP+ cells. The populations were profiled by Aldefluor at passage 5 post sort. (B) Single-cell colonies isolated from (A) were profiled by Sanger sequencing of the ALDH1A3 locus in the genomic DNA. An ALDH1A3 knockout clone along with the parental population was stably transduced with ALDH1A3 or control expression plasmids. Cell populations were profiled for ALDH1A3 expression and β-actin by western blot. (C) Cells from (B) were tested by the Aldefluor assay. (D) Cells from (B) and (C) were implanted into the mammary fat pad of female NSG and CD34 + humanized NCG mice validated for >80% CD45 + humanization by Charles River. Tumor growth was measured by weekly caliper measurement. N = 6 mice per arm in NSG mice and n = 3 or 4 mice per arm in CD34 + humanized NCG arms. Statistics by two-way ANOVA. No tumors initiated in the ALDH1A3 knockout arm in the humanized mice. Data are represented as mean ± SEM. (E and F) Bioluminescent quantification at the final measurement day graphed (F) and displayed as representative images (E). Data from (F) are represented as mean ± SEM.

    Journal: iScience

    Article Title: Development of retinoid nuclear receptor pathway antagonists through targeting aldehyde dehydrogenase 1A3

    doi: 10.1016/j.isci.2025.113675

    Figure Lengend Snippet: ALDH1A3 is necessary for tumor growth in humanized mice but not immune-deficient mice (A) SUM159-M1a cells were transiently transfected with a plasmid encoding GFP, Cas9, and ALDH1A3-targeting or scrambled guide RNAs followed by sorting for GFP+ cells. The populations were profiled by Aldefluor at passage 5 post sort. (B) Single-cell colonies isolated from (A) were profiled by Sanger sequencing of the ALDH1A3 locus in the genomic DNA. An ALDH1A3 knockout clone along with the parental population was stably transduced with ALDH1A3 or control expression plasmids. Cell populations were profiled for ALDH1A3 expression and β-actin by western blot. (C) Cells from (B) were tested by the Aldefluor assay. (D) Cells from (B) and (C) were implanted into the mammary fat pad of female NSG and CD34 + humanized NCG mice validated for >80% CD45 + humanization by Charles River. Tumor growth was measured by weekly caliper measurement. N = 6 mice per arm in NSG mice and n = 3 or 4 mice per arm in CD34 + humanized NCG arms. Statistics by two-way ANOVA. No tumors initiated in the ALDH1A3 knockout arm in the humanized mice. Data are represented as mean ± SEM. (E and F) Bioluminescent quantification at the final measurement day graphed (F) and displayed as representative images (E). Data from (F) are represented as mean ± SEM.

    Article Snippet: Cell populations were profiled for ALDH1A3 expression and β-actin by western blot. (C) Cells from (B) were tested by the Aldefluor assay. (D) Cells from (B) and (C) were implanted into the mammary fat pad of female NSG and CD34 + humanized NCG mice validated for >80% CD45 + humanization by Charles River.

    Techniques: Transfection, Plasmid Preparation, Isolation, Sequencing, Knock-Out, Stable Transfection, Transduction, Control, Expressing, Western Blot