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biotin-labeled lineage marker flow cytometry kit  (Thermo Fisher)


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    Thermo Fisher biotin-labeled lineage marker flow cytometry kit
    Loss of Puma prevents compensatory proliferation of stem cells upon DNA damage. (A) To compare the rates of proliferation in different stem cell populations, the mice of the indicated genotpyes were exposed to IR, and, on days 3 and 7, were injected i.p. with a single dose of BrdU. Four hours later, mice were sacrificed, and the percentage of BrdU+ cells was assessed by flow <t>cytometry</t> in the individual stem cell subsets or total bone marrow. The relative increase in proliferation (BrdU+ cells) in relation to untreated controls was calculated by using the following equation: (IR-induced proliferation percent − spontaneous proliferation percent)/(100 − spontaneous proliferation percent). Bars represent fold induction of BrdU+ cycling cells as mean ± SEM of three to four animals per genotype and three independent experiments. (*) Significant differences in BrdU uptake were observed between wild-type and puma−/− or p53−/− MPP (P < 0.03) and LT-HSC (P < 0.01) subsets at days 3 or 7 post-IR. (B) Mice were fed BrdU in drinking water for 12 d, yielding between 70% and 90% of labeling efficiency in both genotypes alike. Then mice were exposed to 1.75 Gy IR at days 0 and 7. The percentage of BrdU+ stem cell subsets was assessed by flow cytometry. IR-induced loss of BrdU as an indirect measure of proliferation was calculated by subtracting the percentage of BrdU+ cells of mice pre-exposed to IR from the percentage of BrdU+ cells in control animals. Symbols represent mean ± SEM of three to four animals per genotype and time point. Spontaneous BrdU loss was not different between genotypes (P > 0.78). (*) BrdU loss was significantly different at all time points after IR in MPP (P < 0.014) and LSK (P < 0.026) cells at days 3 and 7, and in LT-HSCs (P < 0.014) at days 7 and 10. (C) Cell cycle analysis using Ki67 was performed in control mice or mice exposed to IR 7 d before. The percentage of cells in G0 is plotted. Bars represent mean ± SEM of three animals per genotype. (*) The percentage of stem/progenitor cells in G0 was significantly higher in puma+/−, puma−/−, and p53−/− when compared with wild-type mice (P < 0.04).
    Biotin Labeled Lineage Marker Flow Cytometry Kit, supplied by Thermo Fisher, 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/biotin-labeled+lineage+marker+flow+cytometry+kit/biotin+labeled+lineage+marker+flow+cytometry+kit/pmc02912557-237-7-12
    Average 90 stars, based on 1 article reviews
    biotin-labeled lineage marker flow cytometry kit - by Bioz Stars, 2026-10
    90/100 stars

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    1) Product Images from "Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation"

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation

    Journal: Genes & Development

    doi: 10.1101/gad.1940210

    Loss of Puma prevents compensatory proliferation of stem cells upon DNA damage. (A) To compare the rates of proliferation in different stem cell populations, the mice of the indicated genotpyes were exposed to IR, and, on days 3 and 7, were injected i.p. with a single dose of BrdU. Four hours later, mice were sacrificed, and the percentage of BrdU+ cells was assessed by flow cytometry in the individual stem cell subsets or total bone marrow. The relative increase in proliferation (BrdU+ cells) in relation to untreated controls was calculated by using the following equation: (IR-induced proliferation percent − spontaneous proliferation percent)/(100 − spontaneous proliferation percent). Bars represent fold induction of BrdU+ cycling cells as mean ± SEM of three to four animals per genotype and three independent experiments. (*) Significant differences in BrdU uptake were observed between wild-type and puma−/− or p53−/− MPP (P < 0.03) and LT-HSC (P < 0.01) subsets at days 3 or 7 post-IR. (B) Mice were fed BrdU in drinking water for 12 d, yielding between 70% and 90% of labeling efficiency in both genotypes alike. Then mice were exposed to 1.75 Gy IR at days 0 and 7. The percentage of BrdU+ stem cell subsets was assessed by flow cytometry. IR-induced loss of BrdU as an indirect measure of proliferation was calculated by subtracting the percentage of BrdU+ cells of mice pre-exposed to IR from the percentage of BrdU+ cells in control animals. Symbols represent mean ± SEM of three to four animals per genotype and time point. Spontaneous BrdU loss was not different between genotypes (P > 0.78). (*) BrdU loss was significantly different at all time points after IR in MPP (P < 0.014) and LSK (P < 0.026) cells at days 3 and 7, and in LT-HSCs (P < 0.014) at days 7 and 10. (C) Cell cycle analysis using Ki67 was performed in control mice or mice exposed to IR 7 d before. The percentage of cells in G0 is plotted. Bars represent mean ± SEM of three animals per genotype. (*) The percentage of stem/progenitor cells in G0 was significantly higher in puma+/−, puma−/−, and p53−/− when compared with wild-type mice (P < 0.04).
    Figure Legend Snippet: Loss of Puma prevents compensatory proliferation of stem cells upon DNA damage. (A) To compare the rates of proliferation in different stem cell populations, the mice of the indicated genotpyes were exposed to IR, and, on days 3 and 7, were injected i.p. with a single dose of BrdU. Four hours later, mice were sacrificed, and the percentage of BrdU+ cells was assessed by flow cytometry in the individual stem cell subsets or total bone marrow. The relative increase in proliferation (BrdU+ cells) in relation to untreated controls was calculated by using the following equation: (IR-induced proliferation percent − spontaneous proliferation percent)/(100 − spontaneous proliferation percent). Bars represent fold induction of BrdU+ cycling cells as mean ± SEM of three to four animals per genotype and three independent experiments. (*) Significant differences in BrdU uptake were observed between wild-type and puma−/− or p53−/− MPP (P < 0.03) and LT-HSC (P < 0.01) subsets at days 3 or 7 post-IR. (B) Mice were fed BrdU in drinking water for 12 d, yielding between 70% and 90% of labeling efficiency in both genotypes alike. Then mice were exposed to 1.75 Gy IR at days 0 and 7. The percentage of BrdU+ stem cell subsets was assessed by flow cytometry. IR-induced loss of BrdU as an indirect measure of proliferation was calculated by subtracting the percentage of BrdU+ cells of mice pre-exposed to IR from the percentage of BrdU+ cells in control animals. Symbols represent mean ± SEM of three to four animals per genotype and time point. Spontaneous BrdU loss was not different between genotypes (P > 0.78). (*) BrdU loss was significantly different at all time points after IR in MPP (P < 0.014) and LSK (P < 0.026) cells at days 3 and 7, and in LT-HSCs (P < 0.014) at days 7 and 10. (C) Cell cycle analysis using Ki67 was performed in control mice or mice exposed to IR 7 d before. The percentage of cells in G0 is plotted. Bars represent mean ± SEM of three animals per genotype. (*) The percentage of stem/progenitor cells in G0 was significantly higher in puma+/−, puma−/−, and p53−/− when compared with wild-type mice (P < 0.04).

    Techniques Used: Injection, Flow Cytometry, Labeling, Cell Cycle Assay

    Related Articles

    Marker:

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: Flow cytometry, BrdU labeling, pH3, and Ki67 staining HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Flow Cytometry:

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: Flow cytometry, BrdU labeling, pH3, and Ki67 staining HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Injection:

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: Flow cytometry, BrdU labeling, pH3, and Ki67 staining HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Labeling:

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: Flow cytometry, BrdU labeling, pH3, and Ki67 staining HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Cell Cycle Assay:

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: Flow cytometry, BrdU labeling, pH3, and Ki67 staining HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Staining:

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation
    Article Snippet: Flow cytometry, BrdU labeling, pH3, and Ki67 staining HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).



    Similar Products

    biotin-labeled lineage marker flow cytometry kit  (Thermo Fisher)
    90
    Thermo Fisher biotin-labeled lineage marker flow cytometry kit
    Loss of Puma prevents compensatory proliferation of stem cells upon DNA damage. (A) To compare the rates of proliferation in different stem cell populations, the mice of the indicated genotpyes were exposed to IR, and, on days 3 and 7, were injected i.p. with a single dose of BrdU. Four hours later, mice were sacrificed, and the percentage of BrdU+ cells was assessed by flow <t>cytometry</t> in the individual stem cell subsets or total bone marrow. The relative increase in proliferation (BrdU+ cells) in relation to untreated controls was calculated by using the following equation: (IR-induced proliferation percent − spontaneous proliferation percent)/(100 − spontaneous proliferation percent). Bars represent fold induction of BrdU+ cycling cells as mean ± SEM of three to four animals per genotype and three independent experiments. (*) Significant differences in BrdU uptake were observed between wild-type and puma−/− or p53−/− MPP (P < 0.03) and LT-HSC (P < 0.01) subsets at days 3 or 7 post-IR. (B) Mice were fed BrdU in drinking water for 12 d, yielding between 70% and 90% of labeling efficiency in both genotypes alike. Then mice were exposed to 1.75 Gy IR at days 0 and 7. The percentage of BrdU+ stem cell subsets was assessed by flow cytometry. IR-induced loss of BrdU as an indirect measure of proliferation was calculated by subtracting the percentage of BrdU+ cells of mice pre-exposed to IR from the percentage of BrdU+ cells in control animals. Symbols represent mean ± SEM of three to four animals per genotype and time point. Spontaneous BrdU loss was not different between genotypes (P > 0.78). (*) BrdU loss was significantly different at all time points after IR in MPP (P < 0.014) and LSK (P < 0.026) cells at days 3 and 7, and in LT-HSCs (P < 0.014) at days 7 and 10. (C) Cell cycle analysis using Ki67 was performed in control mice or mice exposed to IR 7 d before. The percentage of cells in G0 is plotted. Bars represent mean ± SEM of three animals per genotype. (*) The percentage of stem/progenitor cells in G0 was significantly higher in puma+/−, puma−/−, and p53−/− when compared with wild-type mice (P < 0.04).
    Biotin Labeled Lineage Marker Flow Cytometry Kit, supplied by Thermo Fisher, 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/biotin-labeled+lineage+marker+flow+cytometry+kit/biotin+labeled+lineage+marker+flow+cytometry+kit/pmc02912557-237-7-12
    Average 90 stars, based on 1 article reviews
    biotin-labeled lineage marker flow cytometry kit - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    Loss of Puma prevents compensatory proliferation of stem cells upon DNA damage. (A) To compare the rates of proliferation in different stem cell populations, the mice of the indicated genotpyes were exposed to IR, and, on days 3 and 7, were injected i.p. with a single dose of BrdU. Four hours later, mice were sacrificed, and the percentage of BrdU+ cells was assessed by flow cytometry in the individual stem cell subsets or total bone marrow. The relative increase in proliferation (BrdU+ cells) in relation to untreated controls was calculated by using the following equation: (IR-induced proliferation percent − spontaneous proliferation percent)/(100 − spontaneous proliferation percent). Bars represent fold induction of BrdU+ cycling cells as mean ± SEM of three to four animals per genotype and three independent experiments. (*) Significant differences in BrdU uptake were observed between wild-type and puma−/− or p53−/− MPP (P < 0.03) and LT-HSC (P < 0.01) subsets at days 3 or 7 post-IR. (B) Mice were fed BrdU in drinking water for 12 d, yielding between 70% and 90% of labeling efficiency in both genotypes alike. Then mice were exposed to 1.75 Gy IR at days 0 and 7. The percentage of BrdU+ stem cell subsets was assessed by flow cytometry. IR-induced loss of BrdU as an indirect measure of proliferation was calculated by subtracting the percentage of BrdU+ cells of mice pre-exposed to IR from the percentage of BrdU+ cells in control animals. Symbols represent mean ± SEM of three to four animals per genotype and time point. Spontaneous BrdU loss was not different between genotypes (P > 0.78). (*) BrdU loss was significantly different at all time points after IR in MPP (P < 0.014) and LSK (P < 0.026) cells at days 3 and 7, and in LT-HSCs (P < 0.014) at days 7 and 10. (C) Cell cycle analysis using Ki67 was performed in control mice or mice exposed to IR 7 d before. The percentage of cells in G0 is plotted. Bars represent mean ± SEM of three animals per genotype. (*) The percentage of stem/progenitor cells in G0 was significantly higher in puma+/−, puma−/−, and p53−/− when compared with wild-type mice (P < 0.04).

    Journal: Genes & Development

    Article Title: Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation

    doi: 10.1101/gad.1940210

    Figure Lengend Snippet: Loss of Puma prevents compensatory proliferation of stem cells upon DNA damage. (A) To compare the rates of proliferation in different stem cell populations, the mice of the indicated genotpyes were exposed to IR, and, on days 3 and 7, were injected i.p. with a single dose of BrdU. Four hours later, mice were sacrificed, and the percentage of BrdU+ cells was assessed by flow cytometry in the individual stem cell subsets or total bone marrow. The relative increase in proliferation (BrdU+ cells) in relation to untreated controls was calculated by using the following equation: (IR-induced proliferation percent − spontaneous proliferation percent)/(100 − spontaneous proliferation percent). Bars represent fold induction of BrdU+ cycling cells as mean ± SEM of three to four animals per genotype and three independent experiments. (*) Significant differences in BrdU uptake were observed between wild-type and puma−/− or p53−/− MPP (P < 0.03) and LT-HSC (P < 0.01) subsets at days 3 or 7 post-IR. (B) Mice were fed BrdU in drinking water for 12 d, yielding between 70% and 90% of labeling efficiency in both genotypes alike. Then mice were exposed to 1.75 Gy IR at days 0 and 7. The percentage of BrdU+ stem cell subsets was assessed by flow cytometry. IR-induced loss of BrdU as an indirect measure of proliferation was calculated by subtracting the percentage of BrdU+ cells of mice pre-exposed to IR from the percentage of BrdU+ cells in control animals. Symbols represent mean ± SEM of three to four animals per genotype and time point. Spontaneous BrdU loss was not different between genotypes (P > 0.78). (*) BrdU loss was significantly different at all time points after IR in MPP (P < 0.014) and LSK (P < 0.026) cells at days 3 and 7, and in LT-HSCs (P < 0.014) at days 7 and 10. (C) Cell cycle analysis using Ki67 was performed in control mice or mice exposed to IR 7 d before. The percentage of cells in G0 is plotted. Bars represent mean ± SEM of three animals per genotype. (*) The percentage of stem/progenitor cells in G0 was significantly higher in puma+/−, puma−/−, and p53−/− when compared with wild-type mice (P < 0.04).

    Article Snippet: HSC populations were defined using a biotin-labeled lineage marker flow cytometry kit (e-Bioscience).

    Techniques: Injection, Flow Cytometry, Labeling, Cell Cycle Assay