mouse anti brdu  (Millipore)

 
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    Name:
    Anti BrdU antibody
    Description:
    5 Bromo 2 deoxyuridine BrdU is a carcinogen that may be absorbed by skin or inhalation BrdU solutions are sensitive to light Bromodeoxyuridine 5 Bromo 2 Deoxyuridine BrdU is an analogue of thymidine that is selectively incorporated into cell DNA at the S phase of the cell cycle Anti BrdU antibody Mouse monoclonal mouse IgG1 is derived from the BU 33 hybridoma produced by the fusion of murine myeloma cells and splenocytes from BALB c mouse immunized with bromodeoxyuridine BrdU conjugated to KLH 5 Bromo 2 deoxyuridine BrdU staining is predominantly used to observe the multiplication of tumor cells and other tissues in vivo
    Catalog Number:
    B8434
    Price:
    None
    Applications:
    Anti-BrdU antibody has been used in:. BrdU labeling. immunohistochemistry. immunostaining . BrdU assay
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    Structured Review

    Millipore mouse anti brdu
    Anti BrdU antibody
    5 Bromo 2 deoxyuridine BrdU is a carcinogen that may be absorbed by skin or inhalation BrdU solutions are sensitive to light Bromodeoxyuridine 5 Bromo 2 Deoxyuridine BrdU is an analogue of thymidine that is selectively incorporated into cell DNA at the S phase of the cell cycle Anti BrdU antibody Mouse monoclonal mouse IgG1 is derived from the BU 33 hybridoma produced by the fusion of murine myeloma cells and splenocytes from BALB c mouse immunized with bromodeoxyuridine BrdU conjugated to KLH 5 Bromo 2 deoxyuridine BrdU staining is predominantly used to observe the multiplication of tumor cells and other tissues in vivo
    https://www.bioz.com/result/mouse anti brdu/product/Millipore
    Average 97 stars, based on 1 article reviews
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    mouse anti brdu - by Bioz Stars, 2021-04
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    Images

    1) Product Images from "Postischemic IGF-1 gene transfer promotes neurovascular regeneration after experimental stroke"

    Article Title: Postischemic IGF-1 gene transfer promotes neurovascular regeneration after experimental stroke

    Journal: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

    doi: 10.1038/jcbfm.2009.75

    Co-localization of DCX and BrdU positive cells
    Figure Legend Snippet: Co-localization of DCX and BrdU positive cells

    Techniques Used:

    2) Product Images from "Perturbed Neurogenesis in the Adult Hippocampus Associated with Presenilin-1 A246E Mutation"

    Article Title: Perturbed Neurogenesis in the Adult Hippocampus Associated with Presenilin-1 A246E Mutation

    Journal:

    doi:

    Neuronal differentiation of progenitor cells is unchanged by PS1 mutation. Double immunofluorescent labeling of BrdU and NeuN was performed on brain sections 4 weeks after BrdU injections to confirm neuronal differentiation. A: NeuN-positive cells (red)
    Figure Legend Snippet: Neuronal differentiation of progenitor cells is unchanged by PS1 mutation. Double immunofluorescent labeling of BrdU and NeuN was performed on brain sections 4 weeks after BrdU injections to confirm neuronal differentiation. A: NeuN-positive cells (red)

    Techniques Used: Mutagenesis, Labeling

    3) Product Images from "Mitochondrial Dysfunction in Astrocytes Impairs the Generation of Reactive Astrocytes and Enhances Neuronal Cell Death in the Cortex Upon Photothrombotic Lesion"

    Article Title: Mitochondrial Dysfunction in Astrocytes Impairs the Generation of Reactive Astrocytes and Enhances Neuronal Cell Death in the Cortex Upon Photothrombotic Lesion

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2019.00040

    Mitochondrial dysfunction led to reduced generation of reactive astrocytes and increased neuronal death in the perilesional area. (A) Lesion volumetry revealed no difference between Tfam ctrl and Tfam cko mice. (B–D) Confocal picture of Tfam ctrl (B) and Tfam cko (C) animal stained against BrdU (red), GFP (green), and GFAP (white). (D) Percentage of GFAP + /GFP + cells amongst all BrdU + cells was sigificantly reduced in Tfam cko mice in comparison to Tfam ctrl . (E–G) Confocal images and quantification of Casp3 immunostaining (red) in Tfam ctrl and Tfam cko mice; GFP + shows recombined cells (green); NeuN labels neurons (white); DAPI indicates cell nuclei. Tfam deletion in astrocytes significant increased neuronal cell death in the perilesional area (G) . (A–D) n ctrl = 6 animals, n cko = 8 animals; (E–G) n ctrl = 4 animals, n cko = 4 animals. Data represented as mean ± SEM; t -test was performed to determine significance; all scale bars = 20 μm.
    Figure Legend Snippet: Mitochondrial dysfunction led to reduced generation of reactive astrocytes and increased neuronal death in the perilesional area. (A) Lesion volumetry revealed no difference between Tfam ctrl and Tfam cko mice. (B–D) Confocal picture of Tfam ctrl (B) and Tfam cko (C) animal stained against BrdU (red), GFP (green), and GFAP (white). (D) Percentage of GFAP + /GFP + cells amongst all BrdU + cells was sigificantly reduced in Tfam cko mice in comparison to Tfam ctrl . (E–G) Confocal images and quantification of Casp3 immunostaining (red) in Tfam ctrl and Tfam cko mice; GFP + shows recombined cells (green); NeuN labels neurons (white); DAPI indicates cell nuclei. Tfam deletion in astrocytes significant increased neuronal cell death in the perilesional area (G) . (A–D) n ctrl = 6 animals, n cko = 8 animals; (E–G) n ctrl = 4 animals, n cko = 4 animals. Data represented as mean ± SEM; t -test was performed to determine significance; all scale bars = 20 μm.

    Techniques Used: Mouse Assay, Staining, Immunostaining

    4) Product Images from "Negative regulation of G2-M by ATR (mei-41)/Chk1(Grapes) facilitates tracheoblast growth and tracheal hypertrophy in Drosophila"

    Article Title: Negative regulation of G2-M by ATR (mei-41)/Chk1(Grapes) facilitates tracheoblast growth and tracheal hypertrophy in Drosophila

    Journal: eLife

    doi: 10.7554/eLife.29988

    Role for Chk1 in the regulation of tracheoblast proliferation post mitotic entry. ( A ). Graph shows cell numbers in Tr2 DT at WL3 in tub-Gal80 ts /UAS-Chk1 RNAi ; Btl-Gal4/+ larvae grown at 18°C (uninduced (wild type), black) or grown at 29°C from the embryonic period (constitutively induced, grey) (mean ± standard deviation, n = 10 tracheae per condition). ( B ) Graph shows cell numbers in Tr2 DT at WL3 in tub-Gal80 ts /UAS-Chk1 RNAi ; Btl-Gal4/+ larvae grown at 18°C (uninduced (wild type), black, same as ( A )) or grown at 29°C from the embryonic period till 24 h L3 then shifted to 18°C till WL3 (conditionally induced, grey) (mean ± standard deviation, n = 10 tracheae per condition). ( C ) Graph showing relative frequencies of BrdU + or pH3 + cells in Tr2 DT in wild type ( UAS-nuGFP; Btl-Gal4/TM3,Ser )and Btl-Chk1 RNAi at 48–56 h (mean ± standard deviation, n = 10 tracheae per timepoint). ( D ) Graph showing frequency of cleaved-Caspase 3 + cells in Tr2 DT in wild type ( UAS-nuGFP; Btl-Gal4/TM3,Ser ) and Btl-Chk1 RNAi WL3 larvae (mean ± standard deviation, n = 13 tracheae each). Student's paired t-test: *p
    Figure Legend Snippet: Role for Chk1 in the regulation of tracheoblast proliferation post mitotic entry. ( A ). Graph shows cell numbers in Tr2 DT at WL3 in tub-Gal80 ts /UAS-Chk1 RNAi ; Btl-Gal4/+ larvae grown at 18°C (uninduced (wild type), black) or grown at 29°C from the embryonic period (constitutively induced, grey) (mean ± standard deviation, n = 10 tracheae per condition). ( B ) Graph shows cell numbers in Tr2 DT at WL3 in tub-Gal80 ts /UAS-Chk1 RNAi ; Btl-Gal4/+ larvae grown at 18°C (uninduced (wild type), black, same as ( A )) or grown at 29°C from the embryonic period till 24 h L3 then shifted to 18°C till WL3 (conditionally induced, grey) (mean ± standard deviation, n = 10 tracheae per condition). ( C ) Graph showing relative frequencies of BrdU + or pH3 + cells in Tr2 DT in wild type ( UAS-nuGFP; Btl-Gal4/TM3,Ser )and Btl-Chk1 RNAi at 48–56 h (mean ± standard deviation, n = 10 tracheae per timepoint). ( D ) Graph showing frequency of cleaved-Caspase 3 + cells in Tr2 DT in wild type ( UAS-nuGFP; Btl-Gal4/TM3,Ser ) and Btl-Chk1 RNAi WL3 larvae (mean ± standard deviation, n = 13 tracheae each). Student's paired t-test: *p

    Techniques Used: Standard Deviation

    5) Product Images from "Early Seizure Activity Accelerates Depletion of Hippocampal Neural Stem Cells and Impairs Spatial Discrimination in an Alzheimer’s Disease Model"

    Article Title: Early Seizure Activity Accelerates Depletion of Hippocampal Neural Stem Cells and Impairs Spatial Discrimination in an Alzheimer’s Disease Model

    Journal: Cell reports

    doi: 10.1016/j.celrep.2019.05.101

    APP Mice Have Higher Fraction of NSCs Engaged in Consecutive Divisions Early in Life than NTG Mice Do (A) Administration of BrdU and EdU 22 h apart captures NSCs that were dividing only on day 1 (BrdU+ NSCs), only on day 2 (EdU+ NSCs), or on both days 1 and 2 (BrdU+ EdU+ NSCs; “consecutively dividing NSCs”). Scale bar, 20 μm. (B and C) Number of consecutively dividing NSCs at 3 weeks (n = 6 mice per genotype) and at 2 (n = 6–8 mice per genotype), 6 (n = 6–8 mice per genotype), and 12 (n = 5–8 mice per genotype) months of age, normalized to the average of the NTG mice at each time point (B) or 3-week-old NTG mice (C). *p
    Figure Legend Snippet: APP Mice Have Higher Fraction of NSCs Engaged in Consecutive Divisions Early in Life than NTG Mice Do (A) Administration of BrdU and EdU 22 h apart captures NSCs that were dividing only on day 1 (BrdU+ NSCs), only on day 2 (EdU+ NSCs), or on both days 1 and 2 (BrdU+ EdU+ NSCs; “consecutively dividing NSCs”). Scale bar, 20 μm. (B and C) Number of consecutively dividing NSCs at 3 weeks (n = 6 mice per genotype) and at 2 (n = 6–8 mice per genotype), 6 (n = 6–8 mice per genotype), and 12 (n = 5–8 mice per genotype) months of age, normalized to the average of the NTG mice at each time point (B) or 3-week-old NTG mice (C). *p

    Techniques Used: Mouse Assay

    6) Product Images from "Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure"

    Article Title: Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure

    Journal: Frontiers in Behavioral Neuroscience

    doi: 10.3389/fnbeh.2017.00151

    Neurogenesis stages in the DG of the adult hippocampus and SVZ of lateral ventricle. (A) Schematic diagram representing the progression of neuronal development (Bonaguidi et al., 2012 ), and specific markers in the different developmental stages of the adult DG, such SOX2, Tbr2, Prox1, DCX and PV. Ki67 protein is present during all active phases of the cell cycle (G 1 , S, G 2 , and mitosis), but is absent from resting cells (G 0 ). Bromodeoxyuridine (BrdU), used in the detection of proliferating cells in living tissues as exogenous marker, is incorporated into the newly synthesized DNA of replicating cells (during the S phase of the cell cycle). For the proliferation study, animals were sacrificed 2 h after injecting BrdU with 300 mg/kg (i.p.). For the survival study, animals were sacrificed 4 weeks after injecting BrdU with 150 mg/kg (i.p.) for 14 days. (B) Schematic diagram representing the progression of neuronal development, and specific markers in the different developmental stages of the adult SVZ, such as SOX2, nestin, Mash1, DCX and Dlx2. ↓ at P57, decreased at postnatal day 57; ↓ at P95, decreased at postnatal day 95; ↑ at P57, increased at postnatal days 57; ↑ at P95, increased at postnatal days 95.
    Figure Legend Snippet: Neurogenesis stages in the DG of the adult hippocampus and SVZ of lateral ventricle. (A) Schematic diagram representing the progression of neuronal development (Bonaguidi et al., 2012 ), and specific markers in the different developmental stages of the adult DG, such SOX2, Tbr2, Prox1, DCX and PV. Ki67 protein is present during all active phases of the cell cycle (G 1 , S, G 2 , and mitosis), but is absent from resting cells (G 0 ). Bromodeoxyuridine (BrdU), used in the detection of proliferating cells in living tissues as exogenous marker, is incorporated into the newly synthesized DNA of replicating cells (during the S phase of the cell cycle). For the proliferation study, animals were sacrificed 2 h after injecting BrdU with 300 mg/kg (i.p.). For the survival study, animals were sacrificed 4 weeks after injecting BrdU with 150 mg/kg (i.p.) for 14 days. (B) Schematic diagram representing the progression of neuronal development, and specific markers in the different developmental stages of the adult SVZ, such as SOX2, nestin, Mash1, DCX and Dlx2. ↓ at P57, decreased at postnatal day 57; ↓ at P95, decreased at postnatal day 95; ↑ at P57, increased at postnatal days 57; ↑ at P95, increased at postnatal days 95.

    Techniques Used: Marker, Synthesized

    7) Product Images from "The ROS-generating oxidase Nox1 is required for epithelial restitution following colitis"

    Article Title: The ROS-generating oxidase Nox1 is required for epithelial restitution following colitis

    Journal: Experimental Animals

    doi: 10.1538/expanim.15-0127

    Inhibition of Nox1 suppresses recovery from DSS-induced colitis, which is accompanied by decreased growth and migration of colonic cells. (A) Representative pictures of colon tissues on day 9 in WT mice with and without administration of DSS, followed by recovery from colitis. Colon sections were stained with H E. The lengths of the analyzed colons were 6 cm and 4.5 cm for DSS-treated and DSS-untreated mice, respectively. (B and C) WT control and Nox1 -/Y mice were given DSS (B). Alternatively, WT mice were given DSS together with DPI or DMSO (C). Then, the animals were allowed to recover from colitis. Histological damage was quantified by estimating the percentage of intact crypts found within an entire section of the colon (4.5 to 6 cm length). Histograms represent mean ± SD values [n=12 for WT and Nox1 -/Y mice (B) and n=5 for DMSO and DPI-treated mice (C)]. (D) Immunohistochemical analysis of Cox-2 expression on day 9 in WT and Nox1 -/Y mice treated with DSS, followed by recovery from colitis in the colon. Histograms represent the percentages of Cox-2-positive cells found within 0.1 mm 2 sections of colons (mean ± SD, n=5 for WT and Nox1 -/Y mice). (E) Immunoblotting analysis of Cox-2, HSP70, and IκB expression in the colon. Colonic extracts were prepared from WT and Nox1 KO mice at 5 days after termination of DSS administration. β-actin was used as a loading control. (F) WT and Nox1 -/Y mice were treated with 2% DSS and allowed to recover from colitis. Colon sections were stained with anti-Ki-67 antibodies. Histograms represent the number of Ki-67-positive cells per crypt (mean ± SD, n=5 for WT and Nox1 -/Y mice). (G) WT and Nox1 -/Y mice were treated with DSS and allowed to recover from colitis. Colon sections were prepared following administration of BrdU 2 h prior to sacrifice and stained with anti-BrdU antibodies. Histograms represent the number of BrdU-positive cells per crypt (mean ± SD, n=5 for WT and Nox1 -/Y mice). (H) WT and Nox1 -/Y mice were treated with DSS and allowed to recover as in Fig. 1A. Colon sections were stained with anti-phospho-MAPK (Erk) Thr-202/Tyr-204 antibodies. (Insert): magnification x3.5. Histograms represent the percentage of crypts with nuclear phospho-MAPK-positive cells (arrowheads) per 30 crypts (mean ± SD, n=5 for WT and Nox1 -/Y mice). (I) WT and Nox1 -/Y mice were treated with DSS, allowed to recover from colitis, administered BrdU, 2 h before sacrifice, and stained with anti-BrdU antibodies. Histograms represent the percentage of crypts with BrdU-positive cells in their upper 2/3 regions per 20 crypts (mean ± SD, n=5 for WT and Nox1 -/Y mice. Scale bar=50 µ m.
    Figure Legend Snippet: Inhibition of Nox1 suppresses recovery from DSS-induced colitis, which is accompanied by decreased growth and migration of colonic cells. (A) Representative pictures of colon tissues on day 9 in WT mice with and without administration of DSS, followed by recovery from colitis. Colon sections were stained with H E. The lengths of the analyzed colons were 6 cm and 4.5 cm for DSS-treated and DSS-untreated mice, respectively. (B and C) WT control and Nox1 -/Y mice were given DSS (B). Alternatively, WT mice were given DSS together with DPI or DMSO (C). Then, the animals were allowed to recover from colitis. Histological damage was quantified by estimating the percentage of intact crypts found within an entire section of the colon (4.5 to 6 cm length). Histograms represent mean ± SD values [n=12 for WT and Nox1 -/Y mice (B) and n=5 for DMSO and DPI-treated mice (C)]. (D) Immunohistochemical analysis of Cox-2 expression on day 9 in WT and Nox1 -/Y mice treated with DSS, followed by recovery from colitis in the colon. Histograms represent the percentages of Cox-2-positive cells found within 0.1 mm 2 sections of colons (mean ± SD, n=5 for WT and Nox1 -/Y mice). (E) Immunoblotting analysis of Cox-2, HSP70, and IκB expression in the colon. Colonic extracts were prepared from WT and Nox1 KO mice at 5 days after termination of DSS administration. β-actin was used as a loading control. (F) WT and Nox1 -/Y mice were treated with 2% DSS and allowed to recover from colitis. Colon sections were stained with anti-Ki-67 antibodies. Histograms represent the number of Ki-67-positive cells per crypt (mean ± SD, n=5 for WT and Nox1 -/Y mice). (G) WT and Nox1 -/Y mice were treated with DSS and allowed to recover from colitis. Colon sections were prepared following administration of BrdU 2 h prior to sacrifice and stained with anti-BrdU antibodies. Histograms represent the number of BrdU-positive cells per crypt (mean ± SD, n=5 for WT and Nox1 -/Y mice). (H) WT and Nox1 -/Y mice were treated with DSS and allowed to recover as in Fig. 1A. Colon sections were stained with anti-phospho-MAPK (Erk) Thr-202/Tyr-204 antibodies. (Insert): magnification x3.5. Histograms represent the percentage of crypts with nuclear phospho-MAPK-positive cells (arrowheads) per 30 crypts (mean ± SD, n=5 for WT and Nox1 -/Y mice). (I) WT and Nox1 -/Y mice were treated with DSS, allowed to recover from colitis, administered BrdU, 2 h before sacrifice, and stained with anti-BrdU antibodies. Histograms represent the percentage of crypts with BrdU-positive cells in their upper 2/3 regions per 20 crypts (mean ± SD, n=5 for WT and Nox1 -/Y mice. Scale bar=50 µ m.

    Techniques Used: Inhibition, Migration, Mouse Assay, Staining, Immunohistochemistry, Expressing

    8) Product Images from "Regulation of Brn3b by DLX1 and DLX2 is required for retinal ganglion cell differentiation in the vertebrate retina"

    Article Title: Regulation of Brn3b by DLX1 and DLX2 is required for retinal ganglion cell differentiation in the vertebrate retina

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.142042

    More retinal progenitors adopt an amacrine cell fate in the Dlx1 / Dlx2 −/− Brn3b −/− mutant GCL. (A,B,E,F) BrdU pulse labeling at E12.5 and co-expression with BRN3A or syntaxin reveal few RGCs in the TKO (A,B, arrows); more cells differentiate as amacrine cells and migrate to the GCL (E,F, arrows). Most E12.5 BrdU pulse-labeled cells are located in the GCL (B″,F″). (C,D,G,H) BrdU pulses at E16.5 identify more displaced amacrine cells in the TKO, although most BrdU+ cells remain in the NBL. Arrows in C and H mark BrdU+ cells that neither express BRN3A (C) nor syntaxin (H) in the GCL. (I-K) E12.5, E13.5 and E16.5 birth-dated cells identified similar quantities of BrdU+ cells in the GCL of wild-type and TKO retinas (I). At all stages tested, RPCs of the TKO adopt an amacrine rather than a RGC fate in the GCL (J,K). Data are mean±s.d., n =4, * P
    Figure Legend Snippet: More retinal progenitors adopt an amacrine cell fate in the Dlx1 / Dlx2 −/− Brn3b −/− mutant GCL. (A,B,E,F) BrdU pulse labeling at E12.5 and co-expression with BRN3A or syntaxin reveal few RGCs in the TKO (A,B, arrows); more cells differentiate as amacrine cells and migrate to the GCL (E,F, arrows). Most E12.5 BrdU pulse-labeled cells are located in the GCL (B″,F″). (C,D,G,H) BrdU pulses at E16.5 identify more displaced amacrine cells in the TKO, although most BrdU+ cells remain in the NBL. Arrows in C and H mark BrdU+ cells that neither express BRN3A (C) nor syntaxin (H) in the GCL. (I-K) E12.5, E13.5 and E16.5 birth-dated cells identified similar quantities of BrdU+ cells in the GCL of wild-type and TKO retinas (I). At all stages tested, RPCs of the TKO adopt an amacrine rather than a RGC fate in the GCL (J,K). Data are mean±s.d., n =4, * P

    Techniques Used: Mutagenesis, Labeling, Expressing

    9) Product Images from "Early expressions of hypoxia-inducible factor 1alpha and vascular endothelial growth factor increase the neuronal plasticity of activated endogenous neural stem cells after focal cerebral ischemia"

    Article Title: Early expressions of hypoxia-inducible factor 1alpha and vascular endothelial growth factor increase the neuronal plasticity of activated endogenous neural stem cells after focal cerebral ischemia

    Journal: Neural Regeneration Research

    doi: 10.4103/1673-5374.133136

    Immunohistochemistry for BrdU and nestin co-labeling after focal cerebral ischemia. Many ependymal lining cells were co-localized with nestin in the sub-ventricular zone among the BrdU-labeled cells in the subventricular zone 7 days after focal cerebral ischemia. Red: BrdU; green: nestin. Scale bar: 50 μm. BrdU: 5-Bromo-2′-deoxyuridine.
    Figure Legend Snippet: Immunohistochemistry for BrdU and nestin co-labeling after focal cerebral ischemia. Many ependymal lining cells were co-localized with nestin in the sub-ventricular zone among the BrdU-labeled cells in the subventricular zone 7 days after focal cerebral ischemia. Red: BrdU; green: nestin. Scale bar: 50 μm. BrdU: 5-Bromo-2′-deoxyuridine.

    Techniques Used: Immunohistochemistry, Labeling

    10) Product Images from "Training on an Appetitive Trace-Conditioning Task Increases Adult Hippocampal Neurogenesis and the Expression of Arc, Erk and CREB Proteins in the Dorsal Hippocampus"

    Article Title: Training on an Appetitive Trace-Conditioning Task Increases Adult Hippocampal Neurogenesis and the Expression of Arc, Erk and CREB Proteins in the Dorsal Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2020.00089

    The number of newly proliferated cells progressed towards the neuronal lineage in the DG of the hippocampus after 7 days of appetitive conditioning in the delay- and trace-conditioned animals. (A) Photomicrographs (20X magnification) showing BrdU +ve , DCX +ve , and BrdU +ve and DCX +ve double-labeled cells in the DG of the hippocampus in the un-conditioned, delay-conditioned, and trace-conditioned animals. Green dots show the BrdU +ve , red dots show DCX +ve , and yellow and orange dots show BrdU +ve DCX +ve double-labeled cells. Magnified views of BrdU +ve , DCX +ve , and BrdU +ve DCX +ve cells are shown in the inset. An average number of (B) BrdU +ve cells/mm 3 of DG (C) double-labeled BrdU +ve and DCX +ve cells/mm 3 of DG in the un-conditioned ( n = 6), delay-conditioned ( n = 6) and trace-conditioned ( n = 6) animals. The BrdU +ve cells significantly increased in the trace-conditioned animals (*** p
    Figure Legend Snippet: The number of newly proliferated cells progressed towards the neuronal lineage in the DG of the hippocampus after 7 days of appetitive conditioning in the delay- and trace-conditioned animals. (A) Photomicrographs (20X magnification) showing BrdU +ve , DCX +ve , and BrdU +ve and DCX +ve double-labeled cells in the DG of the hippocampus in the un-conditioned, delay-conditioned, and trace-conditioned animals. Green dots show the BrdU +ve , red dots show DCX +ve , and yellow and orange dots show BrdU +ve DCX +ve double-labeled cells. Magnified views of BrdU +ve , DCX +ve , and BrdU +ve DCX +ve cells are shown in the inset. An average number of (B) BrdU +ve cells/mm 3 of DG (C) double-labeled BrdU +ve and DCX +ve cells/mm 3 of DG in the un-conditioned ( n = 6), delay-conditioned ( n = 6) and trace-conditioned ( n = 6) animals. The BrdU +ve cells significantly increased in the trace-conditioned animals (*** p

    Techniques Used: Labeling

    Experimental protocols: (A) time and days of BrdU (100 mg/kg) injection in (a) un-conditioned, (b) delay-conditioned and (c) trace-conditioned groups. BrdU was injected three times a day at an interval of 3 h, for three consecutive days (from day 3 to day 5) in all groups. In the conditioned groups: the first injection was given 2 h before the exposure/training, the second injection was given immediately after the completion of exposure/training, and the third injection was given 3 h after the exposure/training. In un-conditioned controls, no training was performed, but BrdU injection was given at the time-matched hours. Conditioned animals were tested for their learned tasks the next day at the same time and sacrificed 3 h after the testing. un-conditioned animals were sacrificed at the time matchedhours of trace/delay conditioned animals. For quantification of DCX +ve cells, the animals were sacrificed on Day 13 (7 days after appetitive-conditioned training) at time-matched hour. (B) Trace- and delay-conditioning protocols: training for trace-conditioning was performed in five sessions. During training, after 5 min of habituation, house light was presented for 20 s as the conditioned stimulus (CS) followed by a trace interval (TI) of 5 s. After trace interval (TI), fruit juice was presented for 15 s as the unconditioned stimulus (US), which is then followed by an inter presentation interval (IPI) of 20 s. Thus, the entire presentation period was of 60-sec duration. Fifteen such presentations were repeated during one session. Complete training comprised of a total of 75 CS and US presentations. The next day, testing was performed at the time matched hour. The testing protocol was similar to that of training. Delay-conditioning: training was performed in five sessions. After 5 min of habituation, house light was presented as CS for 40 s. After 20 s of CS onset, fruit juice was presented as the US for 20 s. Both the CS and US were co-terminated at the end of 40 s, followed by 20-s IPI. The entire presentation was of 60-s duration. Ten such CS-US pairs were presented in one session. Complete training comprised of a total of 60 CS-US presentations. The animal was tested the next day for the learned task using a similar protocol, as was presented during the training. (C) Learning curve of the trace- and (D) delay-conditioned animals. Animals showed an increased number of head entries across all sessions on the testing day during the US presentation phase in the trace-conditioning and during the CS-US paired presentation phase in the delay-conditioning. * p
    Figure Legend Snippet: Experimental protocols: (A) time and days of BrdU (100 mg/kg) injection in (a) un-conditioned, (b) delay-conditioned and (c) trace-conditioned groups. BrdU was injected three times a day at an interval of 3 h, for three consecutive days (from day 3 to day 5) in all groups. In the conditioned groups: the first injection was given 2 h before the exposure/training, the second injection was given immediately after the completion of exposure/training, and the third injection was given 3 h after the exposure/training. In un-conditioned controls, no training was performed, but BrdU injection was given at the time-matched hours. Conditioned animals were tested for their learned tasks the next day at the same time and sacrificed 3 h after the testing. un-conditioned animals were sacrificed at the time matchedhours of trace/delay conditioned animals. For quantification of DCX +ve cells, the animals were sacrificed on Day 13 (7 days after appetitive-conditioned training) at time-matched hour. (B) Trace- and delay-conditioning protocols: training for trace-conditioning was performed in five sessions. During training, after 5 min of habituation, house light was presented for 20 s as the conditioned stimulus (CS) followed by a trace interval (TI) of 5 s. After trace interval (TI), fruit juice was presented for 15 s as the unconditioned stimulus (US), which is then followed by an inter presentation interval (IPI) of 20 s. Thus, the entire presentation period was of 60-sec duration. Fifteen such presentations were repeated during one session. Complete training comprised of a total of 75 CS and US presentations. The next day, testing was performed at the time matched hour. The testing protocol was similar to that of training. Delay-conditioning: training was performed in five sessions. After 5 min of habituation, house light was presented as CS for 40 s. After 20 s of CS onset, fruit juice was presented as the US for 20 s. Both the CS and US were co-terminated at the end of 40 s, followed by 20-s IPI. The entire presentation was of 60-s duration. Ten such CS-US pairs were presented in one session. Complete training comprised of a total of 60 CS-US presentations. The animal was tested the next day for the learned task using a similar protocol, as was presented during the training. (C) Learning curve of the trace- and (D) delay-conditioned animals. Animals showed an increased number of head entries across all sessions on the testing day during the US presentation phase in the trace-conditioning and during the CS-US paired presentation phase in the delay-conditioning. * p

    Techniques Used: Injection

    11) Product Images from "Sustained Axon–Glial Signaling Induces Schwann Cell Hyperproliferation, Remak Bundle Myelination, and Tumorigenesis"

    Article Title: Sustained Axon–Glial Signaling Induces Schwann Cell Hyperproliferation, Remak Bundle Myelination, and Tumorigenesis

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1753-09.2009

    Increased Schwann proliferation rate but not axon size or density drives to nerve enlargement. a , Axonal density is lower in the mutant mice, suggesting that an increase in the number of axons does not contribute to nerve enlargement. b , The distribution of axon perimeter is shifted to the left in the P20 mutant mice, ruling out that axon swelling could contribute to nerve enlargement. Axon density and size were estimated in optical and EM images obtained from sections of two or more sciatic nerves from mice of the indicated age. c , d , BrdU experiments show increased proliferation of Schwann cells in mutant mice. Number of BrdU-labeled cells in sciatic nerves of P5 and P14 NSE–hSMDF # 1 +/− mice and wild-type littermates were counted and normalized to S100 + Schwann cells (see Materials and Methods). A notable increase in the Schwann cell proliferation in the mutants could be observed at P5 but not at P14. e , f , Similar results were obtained when the mitotic index (phospho-Histone H3 + ) was estimated. Two to three animals per genotype and age were used. Data are given as mean ± SE (*** p
    Figure Legend Snippet: Increased Schwann proliferation rate but not axon size or density drives to nerve enlargement. a , Axonal density is lower in the mutant mice, suggesting that an increase in the number of axons does not contribute to nerve enlargement. b , The distribution of axon perimeter is shifted to the left in the P20 mutant mice, ruling out that axon swelling could contribute to nerve enlargement. Axon density and size were estimated in optical and EM images obtained from sections of two or more sciatic nerves from mice of the indicated age. c , d , BrdU experiments show increased proliferation of Schwann cells in mutant mice. Number of BrdU-labeled cells in sciatic nerves of P5 and P14 NSE–hSMDF # 1 +/− mice and wild-type littermates were counted and normalized to S100 + Schwann cells (see Materials and Methods). A notable increase in the Schwann cell proliferation in the mutants could be observed at P5 but not at P14. e , f , Similar results were obtained when the mitotic index (phospho-Histone H3 + ) was estimated. Two to three animals per genotype and age were used. Data are given as mean ± SE (*** p

    Techniques Used: Mutagenesis, Mouse Assay, Labeling

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    Article Snippet: .. The following primary antibodies were used: rabbit anti-SOX9, 1:2,000 ( ); guinea pig anti-PDX1, 1:10,000 (provided by C. Wright, Vanderbilt University, Nashville, TN); guinea pig anti-insulin, 1:5,000 (Linco Research, St. Charles, MO); mouse anti-glucagon, 1:5,000 (Sigma, St. Louis, MO); rabbit anti-amylase, 1:500 (Sigma); mouse anti-BrdU, 1:200 (Chemicon, Temecula, CA); rabbit anti-HES1, 1:5,000 (provided by T. Sudo, Toray Industries, Inc., Tokyo, Japan); guinea pig anti-NGN3, 1:1,000 and guinea pig anti-NKX6.1, 1:1,000 (both ref. ); mouse anti-ISL1, 1:20 [kindly provided by T. Jessell (Columbia University, New York, NY)/Developmental Studies Hybridoma Bank (DSHB), Iowa City, IA]; Armenian hamster anti-MUC-1, 1:500 (Lab Vision Corporation, Fremont, CA); mouse anti-NKX2.2, 1:50 (T. Jessell/DSHB); goat anti-MAFB, 1:10,000 , and rat anti-E-cadherin, 1:2,000 (Sigma). ..

    BrdU Incorporation Assay:

    Article Title: Origins of Cortical Interneuron Subtypes
    Article Snippet: .. BrdU incorporation was detected by pretreatment with nuclease (Amersham Biosciences, Arlington Heights, IL) at 37°C for 30 min followed by double-labeling [rabbit anti-GFP, 1:2000 (Molecular Probes), and mouse anti-BrdU (Chemicon), 1:400; visualized with 488 or 594 Alexa-Fluor secondary antibodies] or triple-labeling immunofluorescence [chick anti-GFP, 1:2000 (Molecular Probes); rabbit anti-calretinin and mouse anti-BrdU]. .. For triple labeling the mouse anti-BrdU was detected using Cy5 anti-mouse secondary antibodies (Molecular Probes) imaged with a cooled digital camera (Coolsnap HQ, Roper) and Metamorph software.

    Immunofluorescence:

    Article Title: Origins of Cortical Interneuron Subtypes
    Article Snippet: .. BrdU incorporation was detected by pretreatment with nuclease (Amersham Biosciences, Arlington Heights, IL) at 37°C for 30 min followed by double-labeling [rabbit anti-GFP, 1:2000 (Molecular Probes), and mouse anti-BrdU (Chemicon), 1:400; visualized with 488 or 594 Alexa-Fluor secondary antibodies] or triple-labeling immunofluorescence [chick anti-GFP, 1:2000 (Molecular Probes); rabbit anti-calretinin and mouse anti-BrdU]. .. For triple labeling the mouse anti-BrdU was detected using Cy5 anti-mouse secondary antibodies (Molecular Probes) imaged with a cooled digital camera (Coolsnap HQ, Roper) and Metamorph software.

    Article Title: Chromatin-remodelling factor Brg1 regulates myocardial proliferation and regeneration in zebrafish
    Article Snippet: After washing in water and PBS, the sections were blocked in 10% FBS in PBT (1% tween 20 in PBS), and then incubated with primary antibodies (1:50 diluted in PBT containing 10% FBS) overnight at 4 °C. .. The primary antibodies used for immunofluorescence were anti-BrdU (B8434; Sigma), anti-Mef2c (sc-313; Santa Cruz), anti-GFP (A-11122; Invitrogen), anti-PCNA (18-0110; Invitrogen), anti-GFP (BE2001; EASYBIO), anti-RFP (BE2023; EASYBIO), anti-myosin heavy-chain monoclonal antibody (hybridoma product MF20; Developmental Studies Hybridoma Bank, Iowa City, IA) and The Brg1 JI antibody, which was raised against a glutathione S-transferase–BRG1 fusion protein (human BRG1 amino acids 1,086–1,307) . .. Secondary antibodies (1:100 diluted in PBT) were Alexa Fluor 488 goat anti-mouse IgG (A21121; Invitrogen), Alexa Fluor 488 goat anti-rabbit IgG (A11034; Invitrogen), Alexa Fluor 555 goat anti-mouse IgG (A21424; Invitrogen) and Alexa Fluor 555 goat anti-rabbit IgG (A21428; Invitrogen).

    Incubation:

    Article Title: Possible Mechanism of Therapeutic Effect of 3-Methyl-1-phenyl-2-pyrazolin-5-one and Bone Marrow Stromal Cells Combination Treatment in Rat Ischemic Stroke Model
    Article Snippet: Double-immunofluorescence staining was employed to visualize the cellular colocalization of BrdU and Nestin for engrafted BMSCs and neuronal stem cells. .. Sections were incubated in 2 mol/L HCl at 37°C for 30 min to denature DNA and exposed BrdU, rinsed thoroughly in PBS and incubated in a mixture of mouse anti-BrdU (1:100, Sigma, USA) and rabbit anti-Nestin (1:100, Sigma, USA) at room temperature for 2 h. After incubation, sections were washed in PBS and placed for 2 h in tetramethyl rhodamine isothiocyanate-conjugated goat anti-mouse IgG (1:100, Sigma, USA) for BrdU and FITC-conjugated goat anti-rabbit IgG (1:100, Sigma, USA) for Nestin. ..

    Article Title: Tamalin is a critical mediator of electroconvulsive shock-induced adult neuroplasticity
    Article Snippet: Double-labeled immunofluorescence staining was used to determine the co-localization of the BrdU signal with the mature neuronal marker NeuN ( ). .. Sections subjected to antigen retrieval were incubated with both rat anti-BrdU (1:500, Accurate Biochemicals) and mouse anti-NeuN (1:500 Millipore) antibodies overnight at RT. .. The secondary antibodies Alexa Fluor Goat anti-mouse 488 (1:500, Invitrogen) and Alexa Fluor goat anti-rat 568 (1:500 Invitrogen) were also used in combination for 2h.

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    Millipore anti mcm2 antibody produced in rabbit
    MCM distribution and replication in yeasts and human. (A) Left 3 panels show budding yeast (chr. XI), middle three panels show fission yeast (chr. II) and right 3 panels show HeLa cells (chr. 18). For <t>Mcm2-ChEC</t> experiments (top 2 rows), budding yeast were arrested for 2 hours with alpha factor, log phase fission yeast were transferred to medium containing 15 mM HU for 3 hours, and HeLa cells were arrested with contact inhibition. Top row: Mcm2 binding visualized by plotting chromosomal location on the x axis, fragment size on the y axis, and read depth indicated by color intensity. The budding yeast image corresponds to ARS1103 and the fission yeast to II-448. Middle row: Mcm2-ChEC read depths plotted across 240 kb (both yeasts) or 80 Mb (HeLa). Green line in the middle plot ( S. pombe ) shows Mcm2-ChEC read depths divided into 1 kb bins and smoothed with a 15 bin sliding window. Red triangles in both yeasts indicate known origins of replication, as listed in oridb.org. Red arrows indicate regions of correspondence between the top and middle rows. Bottom row: Replication as determined by S to G1 ratio of flow sorted cells for budding and fission yeast, and by BrdU incorporation for HeLa. (B) Replication, as determined by BrdU incorporation ( Davis et al., 2018 ), (upper left panel) and MCM binding (lower left panel) is shown for HeLa cells. Right panel shows blow-up of indicated area with fraction of forks involved in synthesizing the Watson strand that are moving to the right (red and blue dots are used to emphasize direction of majority of synthesis; data from Petryk et al. ( Petryk et al., 2016 )) and MCM binding (black). Blue to red transitions denote the initiation zones, which coincide with local MCM maxima. (C) MCM distribution expressed as log 10 fraction of median value for 5 kb-binned Mcm2-ChEC signal. S. cerevisiae, S. pombe , and HeLa are shown in black, green and purple, respectively. (D) Cumulative distribution of 5 kb-binned Mcm2-ChEC signal in S. cerevisiae (black), S. pombe (green), and HeLa (purple).
    Anti Mcm2 Antibody Produced In Rabbit, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore rat monoclonal anti brdu antibody
    Enhanced post-ischemic neurogenesis in ephrin-B3 −/− mice does not exclusively correlate to the extent of brain injury. All data a – f refer to day 28 post-stroke. a – c Animals were exposed to 20 min (ephrin-B3 −/− ) or 30 min (ephrin-B3 +/+ ) of cerebral ischemia followed by <t>NeuN</t> staining for assessment of “neuronal density” ( a ). Post-ischemic neurogenesis was assessed analyzing total absolute amounts of Dcx + ( b ) and NeuN + <t>/BrdU</t> + ( c ) cells in both animal strains. d – f Analysis of “neuronal density” ( d ) and numbers of Dcx + ( e ) as well as NeuN + /BrdU + ( f ) cells in ephrin-B3 −/− mice that received intraventricular infusion for 28 days of either ephrin-B3-Fc or Fc-fragments as control. *Significantly different from ephrin-B3 +/+ or ephrin-B3 −/− control mice, p
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    Millipore anti cre recombinase
    Heterochromatin excludes intertwines. ( A ) Loop out topology was analyzed over a time course of HMR locus excision following R <t>recombinase</t> induction in G2/M (Noc)-arrested cells. A sample of exponentially cycling (Cyc) cells before recombinase induction is included for comparison. ( B ) Comparison of topoisomer distributions of the HMR loop out in wild-type and sir2 Δ cells treated as indicated with α factor (α) or nocodazole (Noc). Cell cycle stages were confirmed by FACS analysis of DNA content. We note that loop outs from the sir2 Δ strain migrate distinctly faster, which could be caused by a different supercoiling status, although we do not know the reason.
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    Combination therapy improved the transplantation and differentiation of BMSCs in ischemic brain. (a) Immunofluorescence staining for <t>BrdU</t> and <t>Nestin</t> positive cells at day 7 after MCAO. BrdU (red, 1) and Nestin (green, 2) in BMSCs monotherapy group, BrdU (red, 4) and Nestin (green, 5) in the combination group. Panels 3 and 6 are the merged images, respectively. Arrows represent the double-immunofluorescence cells. Scale bar indicates 200 μm in BMSC and combination group. (b) The number of engrafted-BMSCs (i) and Nestin positive cells (ii) in BMSCs monotherapy group and combination group. * P
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    MCM distribution and replication in yeasts and human. (A) Left 3 panels show budding yeast (chr. XI), middle three panels show fission yeast (chr. II) and right 3 panels show HeLa cells (chr. 18). For Mcm2-ChEC experiments (top 2 rows), budding yeast were arrested for 2 hours with alpha factor, log phase fission yeast were transferred to medium containing 15 mM HU for 3 hours, and HeLa cells were arrested with contact inhibition. Top row: Mcm2 binding visualized by plotting chromosomal location on the x axis, fragment size on the y axis, and read depth indicated by color intensity. The budding yeast image corresponds to ARS1103 and the fission yeast to II-448. Middle row: Mcm2-ChEC read depths plotted across 240 kb (both yeasts) or 80 Mb (HeLa). Green line in the middle plot ( S. pombe ) shows Mcm2-ChEC read depths divided into 1 kb bins and smoothed with a 15 bin sliding window. Red triangles in both yeasts indicate known origins of replication, as listed in oridb.org. Red arrows indicate regions of correspondence between the top and middle rows. Bottom row: Replication as determined by S to G1 ratio of flow sorted cells for budding and fission yeast, and by BrdU incorporation for HeLa. (B) Replication, as determined by BrdU incorporation ( Davis et al., 2018 ), (upper left panel) and MCM binding (lower left panel) is shown for HeLa cells. Right panel shows blow-up of indicated area with fraction of forks involved in synthesizing the Watson strand that are moving to the right (red and blue dots are used to emphasize direction of majority of synthesis; data from Petryk et al. ( Petryk et al., 2016 )) and MCM binding (black). Blue to red transitions denote the initiation zones, which coincide with local MCM maxima. (C) MCM distribution expressed as log 10 fraction of median value for 5 kb-binned Mcm2-ChEC signal. S. cerevisiae, S. pombe , and HeLa are shown in black, green and purple, respectively. (D) Cumulative distribution of 5 kb-binned Mcm2-ChEC signal in S. cerevisiae (black), S. pombe (green), and HeLa (purple).

    Journal: bioRxiv

    Article Title: Chromosomal Mcm2-7 distribution is the primary driver of the genome replication program in species from yeast to humans

    doi: 10.1101/737742

    Figure Lengend Snippet: MCM distribution and replication in yeasts and human. (A) Left 3 panels show budding yeast (chr. XI), middle three panels show fission yeast (chr. II) and right 3 panels show HeLa cells (chr. 18). For Mcm2-ChEC experiments (top 2 rows), budding yeast were arrested for 2 hours with alpha factor, log phase fission yeast were transferred to medium containing 15 mM HU for 3 hours, and HeLa cells were arrested with contact inhibition. Top row: Mcm2 binding visualized by plotting chromosomal location on the x axis, fragment size on the y axis, and read depth indicated by color intensity. The budding yeast image corresponds to ARS1103 and the fission yeast to II-448. Middle row: Mcm2-ChEC read depths plotted across 240 kb (both yeasts) or 80 Mb (HeLa). Green line in the middle plot ( S. pombe ) shows Mcm2-ChEC read depths divided into 1 kb bins and smoothed with a 15 bin sliding window. Red triangles in both yeasts indicate known origins of replication, as listed in oridb.org. Red arrows indicate regions of correspondence between the top and middle rows. Bottom row: Replication as determined by S to G1 ratio of flow sorted cells for budding and fission yeast, and by BrdU incorporation for HeLa. (B) Replication, as determined by BrdU incorporation ( Davis et al., 2018 ), (upper left panel) and MCM binding (lower left panel) is shown for HeLa cells. Right panel shows blow-up of indicated area with fraction of forks involved in synthesizing the Watson strand that are moving to the right (red and blue dots are used to emphasize direction of majority of synthesis; data from Petryk et al. ( Petryk et al., 2016 )) and MCM binding (black). Blue to red transitions denote the initiation zones, which coincide with local MCM maxima. (C) MCM distribution expressed as log 10 fraction of median value for 5 kb-binned Mcm2-ChEC signal. S. cerevisiae, S. pombe , and HeLa are shown in black, green and purple, respectively. (D) Cumulative distribution of 5 kb-binned Mcm2-ChEC signal in S. cerevisiae (black), S. pombe (green), and HeLa (purple).

    Article Snippet: The expression of tagged MCM2 in HeLa and Patski cells was confirmed by Western blot using anti-MCM2 rabbit polyclonal antibody (HPA031495 Sigma) at 1:1,000 dilution.

    Techniques: Inhibition, Binding Assay, BrdU Incorporation Assay

    MCM distribution and replication on the X chromosome. (A) Replication (upper panel) and MCM binding (lower panel) in the mouse hybrid Patski cells for chr16 (left) and chrX (right). M. musculus and M. spretus parental chromosomes are shown in black and red, respectively. Replication is plotted as fraction of median read depth, with larger fluctuations from the median reflecting more active replication. Scale for MCM2 binding is arbitrary. (B) Fluctuation in BrdU incorporation across two copies of chr. X in human female cell line GM12878. Relative levels are normalized for the two chromosomes (data from ENCODE consortium ( Davis et al., 2018 )).

    Journal: bioRxiv

    Article Title: Chromosomal Mcm2-7 distribution is the primary driver of the genome replication program in species from yeast to humans

    doi: 10.1101/737742

    Figure Lengend Snippet: MCM distribution and replication on the X chromosome. (A) Replication (upper panel) and MCM binding (lower panel) in the mouse hybrid Patski cells for chr16 (left) and chrX (right). M. musculus and M. spretus parental chromosomes are shown in black and red, respectively. Replication is plotted as fraction of median read depth, with larger fluctuations from the median reflecting more active replication. Scale for MCM2 binding is arbitrary. (B) Fluctuation in BrdU incorporation across two copies of chr. X in human female cell line GM12878. Relative levels are normalized for the two chromosomes (data from ENCODE consortium ( Davis et al., 2018 )).

    Article Snippet: The expression of tagged MCM2 in HeLa and Patski cells was confirmed by Western blot using anti-MCM2 rabbit polyclonal antibody (HPA031495 Sigma) at 1:1,000 dilution.

    Techniques: Binding Assay, BrdU Incorporation Assay

    Streaking out strains on rich medium (YEPD) indicates that tagging MCM2, MCM4 and MCM6 with MNase did not affect growth rates.

    Journal: bioRxiv

    Article Title: Chromosomal Mcm2-7 distribution is the primary driver of the genome replication program in species from yeast to humans

    doi: 10.1101/737742

    Figure Lengend Snippet: Streaking out strains on rich medium (YEPD) indicates that tagging MCM2, MCM4 and MCM6 with MNase did not affect growth rates.

    Article Snippet: The expression of tagged MCM2 in HeLa and Patski cells was confirmed by Western blot using anti-MCM2 rabbit polyclonal antibody (HPA031495 Sigma) at 1:1,000 dilution.

    Techniques:

    Fragment size distributions for Mcm2-MNase libraries prepared from fission yeast.

    Journal: bioRxiv

    Article Title: Chromosomal Mcm2-7 distribution is the primary driver of the genome replication program in species from yeast to humans

    doi: 10.1101/737742

    Figure Lengend Snippet: Fragment size distributions for Mcm2-MNase libraries prepared from fission yeast.

    Article Snippet: The expression of tagged MCM2 in HeLa and Patski cells was confirmed by Western blot using anti-MCM2 rabbit polyclonal antibody (HPA031495 Sigma) at 1:1,000 dilution.

    Techniques:

    Enhanced post-ischemic neurogenesis in ephrin-B3 −/− mice does not exclusively correlate to the extent of brain injury. All data a – f refer to day 28 post-stroke. a – c Animals were exposed to 20 min (ephrin-B3 −/− ) or 30 min (ephrin-B3 +/+ ) of cerebral ischemia followed by NeuN staining for assessment of “neuronal density” ( a ). Post-ischemic neurogenesis was assessed analyzing total absolute amounts of Dcx + ( b ) and NeuN + /BrdU + ( c ) cells in both animal strains. d – f Analysis of “neuronal density” ( d ) and numbers of Dcx + ( e ) as well as NeuN + /BrdU + ( f ) cells in ephrin-B3 −/− mice that received intraventricular infusion for 28 days of either ephrin-B3-Fc or Fc-fragments as control. *Significantly different from ephrin-B3 +/+ or ephrin-B3 −/− control mice, p

    Journal: Acta Neuropathologica

    Article Title: Enhancement of endogenous neurogenesis in ephrin-B3 deficient mice after transient focal cerebral ischemia

    doi: 10.1007/s00401-011-0856-5

    Figure Lengend Snippet: Enhanced post-ischemic neurogenesis in ephrin-B3 −/− mice does not exclusively correlate to the extent of brain injury. All data a – f refer to day 28 post-stroke. a – c Animals were exposed to 20 min (ephrin-B3 −/− ) or 30 min (ephrin-B3 +/+ ) of cerebral ischemia followed by NeuN staining for assessment of “neuronal density” ( a ). Post-ischemic neurogenesis was assessed analyzing total absolute amounts of Dcx + ( b ) and NeuN + /BrdU + ( c ) cells in both animal strains. d – f Analysis of “neuronal density” ( d ) and numbers of Dcx + ( e ) as well as NeuN + /BrdU + ( f ) cells in ephrin-B3 −/− mice that received intraventricular infusion for 28 days of either ephrin-B3-Fc or Fc-fragments as control. *Significantly different from ephrin-B3 +/+ or ephrin-B3 −/− control mice, p

    Article Snippet: For double staining against BrdU and NeuN or CNPase, a rat monoclonal anti-BrdU antibody (see above) and a mouse monoclonal anti-NeuN antibody (1:200, 18 h, 4°C; Chemicon, UK) or a mouse monoclonal anti-CNPase antibody (1:400; Chemicon, Germany) were used.

    Techniques: Mouse Assay, Staining

    Analysis of post-ischemic cell proliferation and differentiation. Cell proliferation in ephrin-B3 +/+ and ephrin-B3 −/− mice was analyzed using Ki-67 ( a ) and BrdU ( b ) staining. BrdU + cells were scattered within the ischemic striatum as exemplarily depicted on day 28 for ephrin-B3 +/+ ( c ) and ephrin-B3 −/− mice ( d ). Differentiation analysis of BrdU + cells performed at the time points given referred to induction of stroke ( e ). Stainings were performed against GFAP ( f – g ), Dcx ( h , i ) and NeuN ( j ). Quantitative analyses were performed in both the subventricular zone (SVZ) and the ischemic striatum followed by calculation of total cell numbers. Data are given as percentages of co-localizations of BrdU and the specific marker referred to total numbers of BrdU + cells. Arrows indicate co-localization. Scale bar 40 μm. *Significantly different from ephrin-B3 +/+ mice, p

    Journal: Acta Neuropathologica

    Article Title: Enhancement of endogenous neurogenesis in ephrin-B3 deficient mice after transient focal cerebral ischemia

    doi: 10.1007/s00401-011-0856-5

    Figure Lengend Snippet: Analysis of post-ischemic cell proliferation and differentiation. Cell proliferation in ephrin-B3 +/+ and ephrin-B3 −/− mice was analyzed using Ki-67 ( a ) and BrdU ( b ) staining. BrdU + cells were scattered within the ischemic striatum as exemplarily depicted on day 28 for ephrin-B3 +/+ ( c ) and ephrin-B3 −/− mice ( d ). Differentiation analysis of BrdU + cells performed at the time points given referred to induction of stroke ( e ). Stainings were performed against GFAP ( f – g ), Dcx ( h , i ) and NeuN ( j ). Quantitative analyses were performed in both the subventricular zone (SVZ) and the ischemic striatum followed by calculation of total cell numbers. Data are given as percentages of co-localizations of BrdU and the specific marker referred to total numbers of BrdU + cells. Arrows indicate co-localization. Scale bar 40 μm. *Significantly different from ephrin-B3 +/+ mice, p

    Article Snippet: For double staining against BrdU and NeuN or CNPase, a rat monoclonal anti-BrdU antibody (see above) and a mouse monoclonal anti-NeuN antibody (1:200, 18 h, 4°C; Chemicon, UK) or a mouse monoclonal anti-CNPase antibody (1:400; Chemicon, Germany) were used.

    Techniques: Mouse Assay, Staining, Marker

    Post-ischemic neurogenesis is increased in ephrin-B3 −/− mice. Absolute amounts of Dcx + ( a – e ) and NeuN + /BrdU + ( f ) cells were determined in ephrin-B3 +/+ and ephrin-B3 −/− mice. In ephrin-B3 −/− mice, Dcx + cells were significantly increased ( a ) in both the subventricular zone (SVZ, c ) of the lateral ventricle (LV) and in the ischemic striatum ( e ). On the contrary, Dcx + cells in ephrin-B3 +/+ mice were reduced in both the SVZ ( b ) and the striatum ( d ). Images ( b – e ) represent data from day 28 post-stroke, whereas arrows indicate the location of the SVZ. Likewise, the number of NeuN + /BrdU + cells was significantly increased in the ischemic striatum of ephrin-B3 −/− mice 4 weeks after stroke ( f ). Scale bar 40 μm. *Significantly different from ephrin-B3 +/+ mice; p

    Journal: Acta Neuropathologica

    Article Title: Enhancement of endogenous neurogenesis in ephrin-B3 deficient mice after transient focal cerebral ischemia

    doi: 10.1007/s00401-011-0856-5

    Figure Lengend Snippet: Post-ischemic neurogenesis is increased in ephrin-B3 −/− mice. Absolute amounts of Dcx + ( a – e ) and NeuN + /BrdU + ( f ) cells were determined in ephrin-B3 +/+ and ephrin-B3 −/− mice. In ephrin-B3 −/− mice, Dcx + cells were significantly increased ( a ) in both the subventricular zone (SVZ, c ) of the lateral ventricle (LV) and in the ischemic striatum ( e ). On the contrary, Dcx + cells in ephrin-B3 +/+ mice were reduced in both the SVZ ( b ) and the striatum ( d ). Images ( b – e ) represent data from day 28 post-stroke, whereas arrows indicate the location of the SVZ. Likewise, the number of NeuN + /BrdU + cells was significantly increased in the ischemic striatum of ephrin-B3 −/− mice 4 weeks after stroke ( f ). Scale bar 40 μm. *Significantly different from ephrin-B3 +/+ mice; p

    Article Snippet: For double staining against BrdU and NeuN or CNPase, a rat monoclonal anti-BrdU antibody (see above) and a mouse monoclonal anti-NeuN antibody (1:200, 18 h, 4°C; Chemicon, UK) or a mouse monoclonal anti-CNPase antibody (1:400; Chemicon, Germany) were used.

    Techniques: Mouse Assay

    Heterochromatin excludes intertwines. ( A ) Loop out topology was analyzed over a time course of HMR locus excision following R recombinase induction in G2/M (Noc)-arrested cells. A sample of exponentially cycling (Cyc) cells before recombinase induction is included for comparison. ( B ) Comparison of topoisomer distributions of the HMR loop out in wild-type and sir2 Δ cells treated as indicated with α factor (α) or nocodazole (Noc). Cell cycle stages were confirmed by FACS analysis of DNA content. We note that loop outs from the sir2 Δ strain migrate distinctly faster, which could be caused by a different supercoiling status, although we do not know the reason.

    Journal: Genes & Development

    Article Title: Observation of DNA intertwining along authentic budding yeast chromosomes

    doi: 10.1101/gad.305557.117

    Figure Lengend Snippet: Heterochromatin excludes intertwines. ( A ) Loop out topology was analyzed over a time course of HMR locus excision following R recombinase induction in G2/M (Noc)-arrested cells. A sample of exponentially cycling (Cyc) cells before recombinase induction is included for comparison. ( B ) Comparison of topoisomer distributions of the HMR loop out in wild-type and sir2 Δ cells treated as indicated with α factor (α) or nocodazole (Noc). Cell cycle stages were confirmed by FACS analysis of DNA content. We note that loop outs from the sir2 Δ strain migrate distinctly faster, which could be caused by a different supercoiling status, although we do not know the reason.

    Article Snippet: Following Western transfer, antibodies used for detection were anti-Cre recombinase (clone 2D8; Millipore), anti-Pk (clone SV5-Pk1; Serotec), and anti-α-tubulin (clone TAT-1; Crick Cell Services).

    Techniques: FACS

    Excision of a chromosomal region in G2/M results in catenated loop outs. ( A ) Schematic to illustrate the possible outcomes of excising a chromosomal region as circular loop outs. Intertwines between sister chromatids might result in catenated loop outs. ( B ) Time course of Cre recombinase induction in G2/M-arrested cells. The Western blot shows Cre levels; tubulin served as a loading control. A Southern blot following BamHI digestion confirms Cre-mediated excision of the TER501 region flanked by the two loxP for a genomic map). Electrophoresis of the untreated DNA samples reveals a number of topoisomers. ( C ) Topological analysis of loop outs (LOs) from G1-arrested and G2/M (Noc)-arrested cells together with enzyme treatments to assign band identities. The fraction of nicked catenanes as a percentage of all loop out species is indicated. Note that non-loop out DNA (non-LO) migrates at the exclusion limit for linear DNAs, and the relative position of circular species changes depending on the length of the gel run. (Nick) Nicking enzyme Nt.Bpu10I. ( D ) Quantification of the indicated topoisomers as a percentage of all loop out species from the four last time points following Cre induction in B . The means ± standard error are shown.

    Journal: Genes & Development

    Article Title: Observation of DNA intertwining along authentic budding yeast chromosomes

    doi: 10.1101/gad.305557.117

    Figure Lengend Snippet: Excision of a chromosomal region in G2/M results in catenated loop outs. ( A ) Schematic to illustrate the possible outcomes of excising a chromosomal region as circular loop outs. Intertwines between sister chromatids might result in catenated loop outs. ( B ) Time course of Cre recombinase induction in G2/M-arrested cells. The Western blot shows Cre levels; tubulin served as a loading control. A Southern blot following BamHI digestion confirms Cre-mediated excision of the TER501 region flanked by the two loxP for a genomic map). Electrophoresis of the untreated DNA samples reveals a number of topoisomers. ( C ) Topological analysis of loop outs (LOs) from G1-arrested and G2/M (Noc)-arrested cells together with enzyme treatments to assign band identities. The fraction of nicked catenanes as a percentage of all loop out species is indicated. Note that non-loop out DNA (non-LO) migrates at the exclusion limit for linear DNAs, and the relative position of circular species changes depending on the length of the gel run. (Nick) Nicking enzyme Nt.Bpu10I. ( D ) Quantification of the indicated topoisomers as a percentage of all loop out species from the four last time points following Cre induction in B . The means ± standard error are shown.

    Article Snippet: Following Western transfer, antibodies used for detection were anti-Cre recombinase (clone 2D8; Millipore), anti-Pk (clone SV5-Pk1; Serotec), and anti-α-tubulin (clone TAT-1; Crick Cell Services).

    Techniques: Western Blot, Southern Blot, Electrophoresis

    Intertwines arise during DNA replication elongation. Cells were released from an α-factor-induced G1 block into medium containing 0.1 M HU, and galactose was added 30 min later to induce Cre recombinase expression. ( A ) BrdU incorporation at 60 and 90 min was analyzed by BrdU immunoprecipitation as a marker for replication fork progression. ( B ) The loop out topology of a region containing ARS508 was analyzed in samples taken from the G1 arrest, 90 min in HU, and cells released from G1 to progress into a nocodazole-imposed G2/M arrest (Noc). The fraction of catenated loop outs was quantified in four independent repeats of the experiment and were normalized to the fraction in G2/M. The means ± standard error are shown. An unpaired t -test revealed no significant difference between the two conditions. ( C ) A model for catenane formation and distribution along eukaryotic chromosomes. Proximity between sister chromatids, maintained by the cohesin complex, allows retention of sister chromatid intertwining but does not restrict intertwine distribution along chromosomes.

    Journal: Genes & Development

    Article Title: Observation of DNA intertwining along authentic budding yeast chromosomes

    doi: 10.1101/gad.305557.117

    Figure Lengend Snippet: Intertwines arise during DNA replication elongation. Cells were released from an α-factor-induced G1 block into medium containing 0.1 M HU, and galactose was added 30 min later to induce Cre recombinase expression. ( A ) BrdU incorporation at 60 and 90 min was analyzed by BrdU immunoprecipitation as a marker for replication fork progression. ( B ) The loop out topology of a region containing ARS508 was analyzed in samples taken from the G1 arrest, 90 min in HU, and cells released from G1 to progress into a nocodazole-imposed G2/M arrest (Noc). The fraction of catenated loop outs was quantified in four independent repeats of the experiment and were normalized to the fraction in G2/M. The means ± standard error are shown. An unpaired t -test revealed no significant difference between the two conditions. ( C ) A model for catenane formation and distribution along eukaryotic chromosomes. Proximity between sister chromatids, maintained by the cohesin complex, allows retention of sister chromatid intertwining but does not restrict intertwine distribution along chromosomes.

    Article Snippet: Following Western transfer, antibodies used for detection were anti-Cre recombinase (clone 2D8; Millipore), anti-Pk (clone SV5-Pk1; Serotec), and anti-α-tubulin (clone TAT-1; Crick Cell Services).

    Techniques: Blocking Assay, Expressing, BrdU Incorporation Assay, Immunoprecipitation, Marker

    Combination therapy improved the transplantation and differentiation of BMSCs in ischemic brain. (a) Immunofluorescence staining for BrdU and Nestin positive cells at day 7 after MCAO. BrdU (red, 1) and Nestin (green, 2) in BMSCs monotherapy group, BrdU (red, 4) and Nestin (green, 5) in the combination group. Panels 3 and 6 are the merged images, respectively. Arrows represent the double-immunofluorescence cells. Scale bar indicates 200 μm in BMSC and combination group. (b) The number of engrafted-BMSCs (i) and Nestin positive cells (ii) in BMSCs monotherapy group and combination group. * P

    Journal: Chinese Medical Journal

    Article Title: Possible Mechanism of Therapeutic Effect of 3-Methyl-1-phenyl-2-pyrazolin-5-one and Bone Marrow Stromal Cells Combination Treatment in Rat Ischemic Stroke Model

    doi: 10.4103/0366-6999.183418

    Figure Lengend Snippet: Combination therapy improved the transplantation and differentiation of BMSCs in ischemic brain. (a) Immunofluorescence staining for BrdU and Nestin positive cells at day 7 after MCAO. BrdU (red, 1) and Nestin (green, 2) in BMSCs monotherapy group, BrdU (red, 4) and Nestin (green, 5) in the combination group. Panels 3 and 6 are the merged images, respectively. Arrows represent the double-immunofluorescence cells. Scale bar indicates 200 μm in BMSC and combination group. (b) The number of engrafted-BMSCs (i) and Nestin positive cells (ii) in BMSCs monotherapy group and combination group. * P

    Article Snippet: Sections were incubated in 2 mol/L HCl at 37°C for 30 min to denature DNA and exposed BrdU, rinsed thoroughly in PBS and incubated in a mixture of mouse anti-BrdU (1:100, Sigma, USA) and rabbit anti-Nestin (1:100, Sigma, USA) at room temperature for 2 h. After incubation, sections were washed in PBS and placed for 2 h in tetramethyl rhodamine isothiocyanate-conjugated goat anti-mouse IgG (1:100, Sigma, USA) for BrdU and FITC-conjugated goat anti-rabbit IgG (1:100, Sigma, USA) for Nestin.

    Techniques: Transplantation Assay, Immunofluorescence, Staining