anti-ki67 Search Results


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  • 93
    Abcam anti ki 67
    Cells treated with antioxidants at quiescent state are reversibly arrested in the late G 1 phase. ( A , B ) Cell cycle progression of the synchronized eMSCs after serum stimulation. Flow cytometry histograms ( A ) and quantification of G 0 /G 1 , S, and G 2 /M cell fractions ( B ) in the control and Q-AO-treated eMSCs reveal G 0 /G 1 -block of cell proliferation induced by AO treatment. Data are presented as mean ± SD of three independent experiments. ( C , D ) Immunofluorescence analysis of <t>Ki-67</t> (proliferation marker protein) expression in the control and Q-AO-treated eMSCs. Representative images ( C ) and dynamics of Ki-67 + cell fraction accumulation ( D ) confirm not G 0 , but G 1 -blocking of cell proliferation after Q-AO-treatment. At least 7 images with at least 30 cells were processed for each time point. Data are presented as mean ± SD. ( E ) Cell growth curves for Q-AO-treated eMSCs, either constantly incubated with AO (left panel) or washed of AO after 8-hour incubation (right panel), show the reversible character of AO-induced G 1 -block (n = 3). Results are the mean ± SD of three measurements. Abbreviations: eMSCs, endometrial mesenchymal stem cells; AO, antioxidant Tempol at 1 mM concentration; Q-AO-treated cells, eMSCs exposed to 1 mM of Tempol at 2 h post-serum stimulation; DAPI, 4′,6-diamidino-2-phenylindole; SD, standard deviation.
    Anti Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 1234 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam primary anti ki 67
    Cells treated with antioxidants at quiescent state are reversibly arrested in the late G 1 phase. ( A , B ) Cell cycle progression of the synchronized eMSCs after serum stimulation. Flow cytometry histograms ( A ) and quantification of G 0 /G 1 , S, and G 2 /M cell fractions ( B ) in the control and Q-AO-treated eMSCs reveal G 0 /G 1 -block of cell proliferation induced by AO treatment. Data are presented as mean ± SD of three independent experiments. ( C , D ) Immunofluorescence analysis of <t>Ki-67</t> (proliferation marker protein) expression in the control and Q-AO-treated eMSCs. Representative images ( C ) and dynamics of Ki-67 + cell fraction accumulation ( D ) confirm not G 0 , but G 1 -blocking of cell proliferation after Q-AO-treatment. At least 7 images with at least 30 cells were processed for each time point. Data are presented as mean ± SD. ( E ) Cell growth curves for Q-AO-treated eMSCs, either constantly incubated with AO (left panel) or washed of AO after 8-hour incubation (right panel), show the reversible character of AO-induced G 1 -block (n = 3). Results are the mean ± SD of three measurements. Abbreviations: eMSCs, endometrial mesenchymal stem cells; AO, antioxidant Tempol at 1 mM concentration; Q-AO-treated cells, eMSCs exposed to 1 mM of Tempol at 2 h post-serum stimulation; DAPI, 4′,6-diamidino-2-phenylindole; SD, standard deviation.
    Primary Anti Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Abcam polyclonal anti ki 67
    Immunostaining analysis of <t>Ki-67</t> and CD31. Sections from uterine tissues of all treatment groups were stained with anti-Ki-67 ( A ) and anti-CD31 ( B ) antibodies (×400). ( C ) H-score showing the intensity of Ki-67 staining in epithelium and stroma for each treatment. ( D ) Showing MVD by CD31 staining. Data are expressed as the mean ± SEM. * P
    Polyclonal Anti Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 133 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam rabbit anti ki 67
    Immunohistochemistry for <t>Ki-67</t> in the dentate gyrus of the vehicle (A), scopolamine (SCO) (B), SCO+ vanillin (C), and SCO+4-hydroxybenzyl alcohol (4-HBA) (D) groups. In the vehicle group, Ki-67–immunoreactive cells (arrows) are shown in the subgranular zone. Ki-67-immunoreactive cells are significantly decreased in the SCO group; however, they are increased in the SCO+vanillin and SCO+4-HBA groups. GCL, granule cell layer; ML, molecular layer; PL, polymorphic layer. Scale bar=100 µm. (E) The mean number of Ki-67–immunoreactive cells per group (n=14 per group; * P
    Rabbit Anti Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 719 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam primary anti ki 67 antibody
    Immunohistochemistry for <t>Ki-67</t> in the dentate gyrus of the vehicle (A), scopolamine (SCO) (B), SCO+ vanillin (C), and SCO+4-hydroxybenzyl alcohol (4-HBA) (D) groups. In the vehicle group, Ki-67–immunoreactive cells (arrows) are shown in the subgranular zone. Ki-67-immunoreactive cells are significantly decreased in the SCO group; however, they are increased in the SCO+vanillin and SCO+4-HBA groups. GCL, granule cell layer; ML, molecular layer; PL, polymorphic layer. Scale bar=100 µm. (E) The mean number of Ki-67–immunoreactive cells per group (n=14 per group; * P
    Primary Anti Ki 67 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Boster Bio anti ki67
    Coimmunolabeling of Islet1 and CHX10 in human fetal retinal and retinal organoid. (a–c) CHX10 did not colocalize with Islet1 in the early stage, indicating CHX10 is a retinal progenitor marker during this period. (d, e) Layer of double-positive bipolar cells settled in the INL in the fetal retina. (f–i) CHX10-labeled retinal progenitors in the neuroblast layer in retinal organoids. (j) Some CHX10-positive cells colabeled with Islet1. (j, k) Another neural progenitor marker, MCM2, revealed undifferentiated cells in the fetal retina. (m–o) MCM2 and cell cycle marker, <t>Ki67,</t> confirmed that CHX10 was expressed in progenitors in this period rather than in bipolar cells. (p) To Dwk 26, CHX10-positive bipolar cells were MCM2 negative (scale bar = 100 μ m).
    Anti Ki67, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam monoclonal anti ki 67
    Microscopical analysis of xenograft tumors. ( A ) IL-4Rα downregulation was without effect on tumor morphology (left panels). <t>Ki-67</t> immunohistochemistry was performed for all tumors (right panels); ( B ) Box plots of Ki-67 immunohistochemistry (N9: n = 100; 2-11: n = 114; 3-20: n = 106), revealing reduced proliferation after IL-4Rα knockdown (* p
    Monoclonal Anti Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Boster Bio anti ki67 antibody
    COX2/PGE 2 mediates the proliferation promoting function of IL-33. a , b The relative mRNA levels of <t>Ki67</t> ( a ) and PCNA ( b ) in primary CRC cells responding to rhIL-33 (100 ng/mL) incubation and/ or indicated inhibitors (SB203580, 10 μg/mL; PD98059, 20 μg/mL; SP600125, 10 μg/mL; BIX01294, 2 μM; 5Aza, 10 μM; SC560, 0.1 μg/mL; celecoxib, 20 μg/mL) for 24 h. c The relative mRNA levels of Ki67 and PCNA in HT-29 cells incubated with rhIL-33 (100 ng/mL) or/ and celecoxib (CXB) (20 μg/mL) in medium for 24 h. d The relative mRNA levels of Ki67 and PCNA in MC38 cells incubated with rmIL-33 (100 ng/mL) or/ and celecoxib (CXB) (20 μg/mL) in medium for 24 h. e , f The mRNA ( e ) and protein ( f ) expression of COX2 in primary CRC cells incubated with 0, 50 or 100 ng/mL of rhIL-33 in medium for 24 h. g PGE 2 concentrations in the supernatants of primary CRC cells incubated with rhIL-33-contained RPMI medium or blank RPMI medium for 48 h. h Cell viabilities of primary CRC cells incubated with or without PGE 2 (50 ng/mL) in medium. i The flat colony formation of primary CRC cells incubated for 15 days in medium containing different factors as indicated (IL-33, 100 ng/mL; celecoxib, 20 μg/mL; anti-PGE 2 , 2 μg/mL). The representative images of colonies and the statistical data are shown. Three parallel wells were set for each treatment. Each experiment was performed three times. Data expressed as mean ± SEM. * P
    Anti Ki67 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Abcam rabbit monoclonal anti ki 67
    Histological characterization of MCTS of different sizes Sections from HT29 MCTS at the indicated stages or from xenografts generated in immunodeficient mice were stained with H E panels A-D. or stained with anti-HIF-1α (panels E-H. ; upper panel HIF-1α and counterstaining with Hematoxylin, lower panel color deconvolution to show the HIF-1α positivity only), anti-cleaved Caspase 3 (cC3, panels I-L. , green) or <t>anti-Ki-67</t> antibodies (panels M-P. , green). Sections from panels I-P were counterstained with DAPI (blue). Panels A-D, G, H: magnification 10x; panels F, G, I-P: magnification 20x; panel E: magnification 40x. Scale bar 100μm.
    Rabbit Monoclonal Anti Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 89/100, based on 65 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Cells treated with antioxidants at quiescent state are reversibly arrested in the late G 1 phase. ( A , B ) Cell cycle progression of the synchronized eMSCs after serum stimulation. Flow cytometry histograms ( A ) and quantification of G 0 /G 1 , S, and G 2 /M cell fractions ( B ) in the control and Q-AO-treated eMSCs reveal G 0 /G 1 -block of cell proliferation induced by AO treatment. Data are presented as mean ± SD of three independent experiments. ( C , D ) Immunofluorescence analysis of Ki-67 (proliferation marker protein) expression in the control and Q-AO-treated eMSCs. Representative images ( C ) and dynamics of Ki-67 + cell fraction accumulation ( D ) confirm not G 0 , but G 1 -blocking of cell proliferation after Q-AO-treatment. At least 7 images with at least 30 cells were processed for each time point. Data are presented as mean ± SD. ( E ) Cell growth curves for Q-AO-treated eMSCs, either constantly incubated with AO (left panel) or washed of AO after 8-hour incubation (right panel), show the reversible character of AO-induced G 1 -block (n = 3). Results are the mean ± SD of three measurements. Abbreviations: eMSCs, endometrial mesenchymal stem cells; AO, antioxidant Tempol at 1 mM concentration; Q-AO-treated cells, eMSCs exposed to 1 mM of Tempol at 2 h post-serum stimulation; DAPI, 4′,6-diamidino-2-phenylindole; SD, standard deviation.

    Journal: Scientific Reports

    Article Title: High doses of synthetic antioxidants induce premature senescence in cultivated mesenchymal stem cells

    doi: 10.1038/s41598-018-37972-y

    Figure Lengend Snippet: Cells treated with antioxidants at quiescent state are reversibly arrested in the late G 1 phase. ( A , B ) Cell cycle progression of the synchronized eMSCs after serum stimulation. Flow cytometry histograms ( A ) and quantification of G 0 /G 1 , S, and G 2 /M cell fractions ( B ) in the control and Q-AO-treated eMSCs reveal G 0 /G 1 -block of cell proliferation induced by AO treatment. Data are presented as mean ± SD of three independent experiments. ( C , D ) Immunofluorescence analysis of Ki-67 (proliferation marker protein) expression in the control and Q-AO-treated eMSCs. Representative images ( C ) and dynamics of Ki-67 + cell fraction accumulation ( D ) confirm not G 0 , but G 1 -blocking of cell proliferation after Q-AO-treatment. At least 7 images with at least 30 cells were processed for each time point. Data are presented as mean ± SD. ( E ) Cell growth curves for Q-AO-treated eMSCs, either constantly incubated with AO (left panel) or washed of AO after 8-hour incubation (right panel), show the reversible character of AO-induced G 1 -block (n = 3). Results are the mean ± SD of three measurements. Abbreviations: eMSCs, endometrial mesenchymal stem cells; AO, antioxidant Tempol at 1 mM concentration; Q-AO-treated cells, eMSCs exposed to 1 mM of Tempol at 2 h post-serum stimulation; DAPI, 4′,6-diamidino-2-phenylindole; SD, standard deviation.

    Article Snippet: For the immunofluorescence staining, cells were fixed with 4% formalin in PBS, permeabilized with 0.1% Triton X-100, incubated with 1% bovine serum albumin solution in 0.1% Tween-20 in PBS for 1 hour at room temperature and then treated with following primary antibodies: anti-Ki-67 (1:500), anti-γH2AX (1:500), and anti-phospho-аtaxia telangiectasia mutated kinase (pATM, 1:200, all from Abcam) either for 1 hour at room temperature (for Ki-67) or overnight at 4 °C (for γH2AX and pATM).

    Techniques: Flow Cytometry, Cytometry, Blocking Assay, Immunofluorescence, Marker, Expressing, Incubation, Concentration Assay, Standard Deviation

    IHC analysis on healed wound skin. (a) IHC evaluation of the full-thickness skin wounds (scale bar = 1 mm). (b) The number of vessels/HPF in healed wound tissue. (c) The number of Ki-67 brown-positive proliferating cells/HPF in healed wound tissue. ** p

    Journal: Cell Transplantation

    Article Title: The Healing Effects of Conditioned Medium Derived from Mesenchymal Stem Cells on Radiation-Induced Skin Wounds in Rats

    doi: 10.1177/0963689718807410

    Figure Lengend Snippet: IHC analysis on healed wound skin. (a) IHC evaluation of the full-thickness skin wounds (scale bar = 1 mm). (b) The number of vessels/HPF in healed wound tissue. (c) The number of Ki-67 brown-positive proliferating cells/HPF in healed wound tissue. ** p

    Article Snippet: After that, cells were incubated with anti-Ki-67 antibody (Abcam, Cambridge, UK), 1:200 dilution, and goat anti-rabbit immunoglobulin (Ig)G, (Abcam), 1:1000 dilution.

    Techniques: Immunohistochemistry

    Protein and gene expressions on healed skin tissue. (a–c) Ki-67 and α-SMA protein expression. (d–f) Col1A2, Ki-67 and α-SMA gene expression. * p

    Journal: Cell Transplantation

    Article Title: The Healing Effects of Conditioned Medium Derived from Mesenchymal Stem Cells on Radiation-Induced Skin Wounds in Rats

    doi: 10.1177/0963689718807410

    Figure Lengend Snippet: Protein and gene expressions on healed skin tissue. (a–c) Ki-67 and α-SMA protein expression. (d–f) Col1A2, Ki-67 and α-SMA gene expression. * p

    Article Snippet: After that, cells were incubated with anti-Ki-67 antibody (Abcam, Cambridge, UK), 1:200 dilution, and goat anti-rabbit immunoglobulin (Ig)G, (Abcam), 1:1000 dilution.

    Techniques: Expressing

    Effects of MSC-CM on HUVEC proliferation, inflammation and angiogenesis gene expression. (a) Immunofluorescence staining of HUVECs labeled with Ki-67. (b) The percentages of Ki-67-positive cells in HUVECs. Scale bar = 100 μm, * p

    Journal: Cell Transplantation

    Article Title: The Healing Effects of Conditioned Medium Derived from Mesenchymal Stem Cells on Radiation-Induced Skin Wounds in Rats

    doi: 10.1177/0963689718807410

    Figure Lengend Snippet: Effects of MSC-CM on HUVEC proliferation, inflammation and angiogenesis gene expression. (a) Immunofluorescence staining of HUVECs labeled with Ki-67. (b) The percentages of Ki-67-positive cells in HUVECs. Scale bar = 100 μm, * p

    Article Snippet: After that, cells were incubated with anti-Ki-67 antibody (Abcam, Cambridge, UK), 1:200 dilution, and goat anti-rabbit immunoglobulin (Ig)G, (Abcam), 1:1000 dilution.

    Techniques: Expressing, Immunofluorescence, Staining, Labeling

    Immunostaining analysis of Ki-67 and CD31. Sections from uterine tissues of all treatment groups were stained with anti-Ki-67 ( A ) and anti-CD31 ( B ) antibodies (×400). ( C ) H-score showing the intensity of Ki-67 staining in epithelium and stroma for each treatment. ( D ) Showing MVD by CD31 staining. Data are expressed as the mean ± SEM. * P

    Journal: Biology of Reproduction

    Article Title: Bone marrow-derived cells or C-X-C motif chemokine 12 (CXCL12) treatment improve thin endometrium in a mouse model

    doi: 10.1093/biolre/ioy175

    Figure Lengend Snippet: Immunostaining analysis of Ki-67 and CD31. Sections from uterine tissues of all treatment groups were stained with anti-Ki-67 ( A ) and anti-CD31 ( B ) antibodies (×400). ( C ) H-score showing the intensity of Ki-67 staining in epithelium and stroma for each treatment. ( D ) Showing MVD by CD31 staining. Data are expressed as the mean ± SEM. * P

    Article Snippet: The sections were incubated overnight at 4°C with different primary antibodies anti-Ki-67, (#ab15580, 1:500), anti-CD45 (#ab25286; 1:300); anti-CD31 (#ab28364, 1:200), anti-LIF (#ab138002, 1:200), anti-GFP (#ab6556, 1:1000) purchased from Abcam, Cambridge, MA, USA.

    Techniques: Immunostaining, Staining

    Downregulation of linc00665 suppressed LUAD tumor growth and metastasis in vivo. a Representative images of tumors collected from mice. b Tumor volume curve of mice upon shRNA-NC or shRNA-Linc00665 treatment. c Tumor weights were represented. d Relative linc00665 expression in xenograft tumors was detected by qRT-PCR, normalized to GAPDH. e Histopathology of xenograft tumors. The tumor sections were under HE staining and immunohistochemical staining using antibodies against Ki-67. f Ki-67 index calculated as the percentage of Ki-67-positive cells. g Representative images of lung metastasis and HE staining of sections. The metastasis was marked with box. Scale bar = 200 μm; NC negative control, HE hematoxylin and eosin, qRT-PCR quantitative real-time PCR; ** p

    Journal: Cell Death & Disease

    Article Title: Long non-coding RNA linc00665 promotes lung adenocarcinoma progression and functions as ceRNA to regulate AKR1B10-ERK signaling by sponging miR-98

    doi: 10.1038/s41419-019-1361-3

    Figure Lengend Snippet: Downregulation of linc00665 suppressed LUAD tumor growth and metastasis in vivo. a Representative images of tumors collected from mice. b Tumor volume curve of mice upon shRNA-NC or shRNA-Linc00665 treatment. c Tumor weights were represented. d Relative linc00665 expression in xenograft tumors was detected by qRT-PCR, normalized to GAPDH. e Histopathology of xenograft tumors. The tumor sections were under HE staining and immunohistochemical staining using antibodies against Ki-67. f Ki-67 index calculated as the percentage of Ki-67-positive cells. g Representative images of lung metastasis and HE staining of sections. The metastasis was marked with box. Scale bar = 200 μm; NC negative control, HE hematoxylin and eosin, qRT-PCR quantitative real-time PCR; ** p

    Article Snippet: Primary antibody anti-Ki-67 (1:400, Abcam, ab15580, USA) was used to evaluate the proliferation, and the staining positivity was quantified in three different high-power fields of each section.

    Techniques: In Vivo, Mouse Assay, shRNA, Expressing, Quantitative RT-PCR, Histopathology, Staining, Immunohistochemistry, Negative Control, Real-time Polymerase Chain Reaction

    Effects of UCMS and 4 weeks treatment of fluoxetine (FLX 15 mg/kg/day ip) on cell proliferation and neurogenesis in the hippocampus . HS: High suppressers, LS: Low suppressers, VEH: vehicle, FLX: fluoxetine. (A) Densitiy of cell proliferation using ki-67 staining in the granule cell layer in the whole, dorsal, intermediate, and ventral hippocampus (whole, temporal and intermediate hippocampus: HS VEH ( n = 9), HS FLX ( n = 6), LS VEH ( n = 7), LS FLX ( n = 6); septal hippocampus: HS VEH ( n = 7), HS FLX ( n = 6), LS VEH ( n = 7), LS FLX ( n = 5)). (B) Density of immature neurons using doublecortin (DCX) labeling in the GCL (whole, temporal and intermediate parts: HS VEH ( n = 5), HS FLX ( n = 6), LS VEH ( n = 6), LS FLX ( n = 4); septal parts: HS VEH ( n = 5), HS FLX ( n = 5), LS VEH ( n = 6), LS FLX ( n = 4)). HS VEH vs. HS FLX: # p

    Journal: Frontiers in Behavioral Neuroscience

    Article Title: Dysregulation of the hypothalamus-pituitary-adrenal axis predicts some aspects of the behavioral response to chronic fluoxetine: association with hippocampal cell proliferation

    doi: 10.3389/fnbeh.2014.00340

    Figure Lengend Snippet: Effects of UCMS and 4 weeks treatment of fluoxetine (FLX 15 mg/kg/day ip) on cell proliferation and neurogenesis in the hippocampus . HS: High suppressers, LS: Low suppressers, VEH: vehicle, FLX: fluoxetine. (A) Densitiy of cell proliferation using ki-67 staining in the granule cell layer in the whole, dorsal, intermediate, and ventral hippocampus (whole, temporal and intermediate hippocampus: HS VEH ( n = 9), HS FLX ( n = 6), LS VEH ( n = 7), LS FLX ( n = 6); septal hippocampus: HS VEH ( n = 7), HS FLX ( n = 6), LS VEH ( n = 7), LS FLX ( n = 5)). (B) Density of immature neurons using doublecortin (DCX) labeling in the GCL (whole, temporal and intermediate parts: HS VEH ( n = 5), HS FLX ( n = 6), LS VEH ( n = 6), LS FLX ( n = 4); septal parts: HS VEH ( n = 5), HS FLX ( n = 5), LS VEH ( n = 6), LS FLX ( n = 4)). HS VEH vs. HS FLX: # p

    Article Snippet: Sections were incubated at room temperature in a rabbit anti ki-67 antibody (Abcam, ab15580, 1:1000) followed by three washes in 0.1 M PBS and a 2 h-incubation in secondary donkey anti-rabbit IgG biotynilated antibody (Jackson immuno Research diluted 1:500).

    Techniques: Staining, Labeling

    Immunohistochemistry for Ki-67 in the dentate gyrus of the vehicle (A), scopolamine (SCO) (B), SCO+ vanillin (C), and SCO+4-hydroxybenzyl alcohol (4-HBA) (D) groups. In the vehicle group, Ki-67–immunoreactive cells (arrows) are shown in the subgranular zone. Ki-67-immunoreactive cells are significantly decreased in the SCO group; however, they are increased in the SCO+vanillin and SCO+4-HBA groups. GCL, granule cell layer; ML, molecular layer; PL, polymorphic layer. Scale bar=100 µm. (E) The mean number of Ki-67–immunoreactive cells per group (n=14 per group; * P

    Journal: Anatomy & Cell Biology

    Article Title: Vanillin and 4-hydroxybenzyl alcohol attenuate cognitive impairment and the reduction of cell proliferation and neuroblast differentiation in the dentate gyrus in a mouse model of scopolamine-induced amnesia

    doi: 10.5115/acb.2017.50.2.143

    Figure Lengend Snippet: Immunohistochemistry for Ki-67 in the dentate gyrus of the vehicle (A), scopolamine (SCO) (B), SCO+ vanillin (C), and SCO+4-hydroxybenzyl alcohol (4-HBA) (D) groups. In the vehicle group, Ki-67–immunoreactive cells (arrows) are shown in the subgranular zone. Ki-67-immunoreactive cells are significantly decreased in the SCO group; however, they are increased in the SCO+vanillin and SCO+4-HBA groups. GCL, granule cell layer; ML, molecular layer; PL, polymorphic layer. Scale bar=100 µm. (E) The mean number of Ki-67–immunoreactive cells per group (n=14 per group; * P

    Article Snippet: Immunohistochemistry As previously described [ ], immunohistochemical staining for neuronal nuclear antigen (NeuN, a marker for neurons), Ki-67 (a marker for proliferating cell) and doublecortin (DCX, a marker for neuroblast) was performed using rabbit anti-NeuN (1:1,000, Chemicon International, Temecula, CA, USA), rabbit anti-Ki-67 (1:100, Abcam, Cambridge, UK), or goat anti-DCX (1:100, Santa Cruz Biotechnology, Santa Cruz, CA, USA) as primary antibodies, and biotinylated goat anti-rabbit or rabbit anti-goat immunoglobulin G (1:200, Vector Laboratories, Burlingame, CA, USA) and streptavidin peroxidase complex (1:200, Vector Laboratories) as secondary antibodies.

    Techniques: Immunohistochemistry

    Coimmunolabeling of Islet1 and CHX10 in human fetal retinal and retinal organoid. (a–c) CHX10 did not colocalize with Islet1 in the early stage, indicating CHX10 is a retinal progenitor marker during this period. (d, e) Layer of double-positive bipolar cells settled in the INL in the fetal retina. (f–i) CHX10-labeled retinal progenitors in the neuroblast layer in retinal organoids. (j) Some CHX10-positive cells colabeled with Islet1. (j, k) Another neural progenitor marker, MCM2, revealed undifferentiated cells in the fetal retina. (m–o) MCM2 and cell cycle marker, Ki67, confirmed that CHX10 was expressed in progenitors in this period rather than in bipolar cells. (p) To Dwk 26, CHX10-positive bipolar cells were MCM2 negative (scale bar = 100 μ m).

    Journal: Stem Cells International

    Article Title: Islet1 and Brn3 Expression Pattern Study in Human Retina and hiPSC-Derived Retinal Organoid

    doi: 10.1155/2019/8786396

    Figure Lengend Snippet: Coimmunolabeling of Islet1 and CHX10 in human fetal retinal and retinal organoid. (a–c) CHX10 did not colocalize with Islet1 in the early stage, indicating CHX10 is a retinal progenitor marker during this period. (d, e) Layer of double-positive bipolar cells settled in the INL in the fetal retina. (f–i) CHX10-labeled retinal progenitors in the neuroblast layer in retinal organoids. (j) Some CHX10-positive cells colabeled with Islet1. (j, k) Another neural progenitor marker, MCM2, revealed undifferentiated cells in the fetal retina. (m–o) MCM2 and cell cycle marker, Ki67, confirmed that CHX10 was expressed in progenitors in this period rather than in bipolar cells. (p) To Dwk 26, CHX10-positive bipolar cells were MCM2 negative (scale bar = 100 μ m).

    Article Snippet: The following primary antibodies were diluted in 2% (wt/vol) donkey serum, 0.04% (vol/vol) Triton X-100 in PBS: anti-Islet1 antibody (mouse, 1 : 200, Abcam, Cambridge, UK), anti-MCM2 antibody (rabbit, 1 : 200, Abcam), anti-VSX2 antibody (sheep, 1 : 500, Millipore, Billerica, MA, USA), anti-Brn3 antibody (goat, 1 : 200, Santa Cruz Biotechnology, Dallas, TX, USA), anti-Brn3a antibody (mouse, 1 : 20, Santa Cruz Biotechnology, Dallas, TX, USA), anti-RPBMS antibody (rabbit, 1 : 200, Abcam), anti-HuD antibody (mouse, 1 : 100, Santa Cruz Biotechnology), anti-AP2α antibody (goat, 1 : 200, Abcam), anti-Recoverin antibody (rabbit, 1 : 500, Abcam), anti-Rhodopsin antibody (mouse, 1 : 200, Abcam), anti-Ki67 (rabbit, 1 : 50, Boster, Wuhan, China), anti-S-opsin (rabbit, 1 : 5000), and anti-L/M-opsin (rabbit, 1 : 5000), which were donated by Jeremy Nathans (Department of Molecular Biology and Genetics, Neuroscience, and Ophthalmology, the Johns Hopkins University School of Medicine).

    Techniques: Marker, Labeling

    Microscopical analysis of xenograft tumors. ( A ) IL-4Rα downregulation was without effect on tumor morphology (left panels). Ki-67 immunohistochemistry was performed for all tumors (right panels); ( B ) Box plots of Ki-67 immunohistochemistry (N9: n = 100; 2-11: n = 114; 3-20: n = 106), revealing reduced proliferation after IL-4Rα knockdown (* p

    Journal: International Journal of Molecular Sciences

    Article Title: Endogenously Expressed IL-4Rα Promotes the Malignant Phenotype of Human Pancreatic Cancer In Vitro and In Vivo

    doi: 10.3390/ijms18040716

    Figure Lengend Snippet: Microscopical analysis of xenograft tumors. ( A ) IL-4Rα downregulation was without effect on tumor morphology (left panels). Ki-67 immunohistochemistry was performed for all tumors (right panels); ( B ) Box plots of Ki-67 immunohistochemistry (N9: n = 100; 2-11: n = 114; 3-20: n = 106), revealing reduced proliferation after IL-4Rα knockdown (* p

    Article Snippet: Monoclonal anti-Ki-67 (Abcam ab92742, 1:500, Cambridge, UK) was used as first antibody, followed by incubation with anti-rabbit immunoglobulins conjugated to peroxidase-labeled dextran polymers (N -histofine H; Nichirei Corporation, Tokyo, Japan).

    Techniques: Immunohistochemistry

    COX2/PGE 2 mediates the proliferation promoting function of IL-33. a , b The relative mRNA levels of Ki67 ( a ) and PCNA ( b ) in primary CRC cells responding to rhIL-33 (100 ng/mL) incubation and/ or indicated inhibitors (SB203580, 10 μg/mL; PD98059, 20 μg/mL; SP600125, 10 μg/mL; BIX01294, 2 μM; 5Aza, 10 μM; SC560, 0.1 μg/mL; celecoxib, 20 μg/mL) for 24 h. c The relative mRNA levels of Ki67 and PCNA in HT-29 cells incubated with rhIL-33 (100 ng/mL) or/ and celecoxib (CXB) (20 μg/mL) in medium for 24 h. d The relative mRNA levels of Ki67 and PCNA in MC38 cells incubated with rmIL-33 (100 ng/mL) or/ and celecoxib (CXB) (20 μg/mL) in medium for 24 h. e , f The mRNA ( e ) and protein ( f ) expression of COX2 in primary CRC cells incubated with 0, 50 or 100 ng/mL of rhIL-33 in medium for 24 h. g PGE 2 concentrations in the supernatants of primary CRC cells incubated with rhIL-33-contained RPMI medium or blank RPMI medium for 48 h. h Cell viabilities of primary CRC cells incubated with or without PGE 2 (50 ng/mL) in medium. i The flat colony formation of primary CRC cells incubated for 15 days in medium containing different factors as indicated (IL-33, 100 ng/mL; celecoxib, 20 μg/mL; anti-PGE 2 , 2 μg/mL). The representative images of colonies and the statistical data are shown. Three parallel wells were set for each treatment. Each experiment was performed three times. Data expressed as mean ± SEM. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGE2

    doi: 10.1186/s13046-018-0839-7

    Figure Lengend Snippet: COX2/PGE 2 mediates the proliferation promoting function of IL-33. a , b The relative mRNA levels of Ki67 ( a ) and PCNA ( b ) in primary CRC cells responding to rhIL-33 (100 ng/mL) incubation and/ or indicated inhibitors (SB203580, 10 μg/mL; PD98059, 20 μg/mL; SP600125, 10 μg/mL; BIX01294, 2 μM; 5Aza, 10 μM; SC560, 0.1 μg/mL; celecoxib, 20 μg/mL) for 24 h. c The relative mRNA levels of Ki67 and PCNA in HT-29 cells incubated with rhIL-33 (100 ng/mL) or/ and celecoxib (CXB) (20 μg/mL) in medium for 24 h. d The relative mRNA levels of Ki67 and PCNA in MC38 cells incubated with rmIL-33 (100 ng/mL) or/ and celecoxib (CXB) (20 μg/mL) in medium for 24 h. e , f The mRNA ( e ) and protein ( f ) expression of COX2 in primary CRC cells incubated with 0, 50 or 100 ng/mL of rhIL-33 in medium for 24 h. g PGE 2 concentrations in the supernatants of primary CRC cells incubated with rhIL-33-contained RPMI medium or blank RPMI medium for 48 h. h Cell viabilities of primary CRC cells incubated with or without PGE 2 (50 ng/mL) in medium. i The flat colony formation of primary CRC cells incubated for 15 days in medium containing different factors as indicated (IL-33, 100 ng/mL; celecoxib, 20 μg/mL; anti-PGE 2 , 2 μg/mL). The representative images of colonies and the statistical data are shown. Three parallel wells were set for each treatment. Each experiment was performed three times. Data expressed as mean ± SEM. * P

    Article Snippet: The sections were labeled with anti-Ki67 antibody (Arigo, 1:200) and anti-PCNA antibody (Boster, 1:200).

    Techniques: Incubation, Expressing

    IL-33 promotes CRC proliferation both in vivo and in vitro. a Correlation between IL-33 transcripts and the genes involved in the regulation of cell proliferation in CRC. Gene set enrichment analysis was performed using CRC TCGA database. NES = 1.03, P = 0.03. b Growth curves of MC38 tumors inoculated in IL-33 transgenic mice (IL-33 TG) or wild-type mice (WT). n = 7. c , d Immunohistochemical staining of Ki67 ( c ) and PCNA ( d ) in the MC38 tumors recovered from wild-type and IL-33 transgenic mice at Day 22 post inoculation. The representative images and the statistical proportions of positive cells are shown. Scale bar, 50 μm. n = 7. Data expressed as mean ± SEM. **, P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGE2

    doi: 10.1186/s13046-018-0839-7

    Figure Lengend Snippet: IL-33 promotes CRC proliferation both in vivo and in vitro. a Correlation between IL-33 transcripts and the genes involved in the regulation of cell proliferation in CRC. Gene set enrichment analysis was performed using CRC TCGA database. NES = 1.03, P = 0.03. b Growth curves of MC38 tumors inoculated in IL-33 transgenic mice (IL-33 TG) or wild-type mice (WT). n = 7. c , d Immunohistochemical staining of Ki67 ( c ) and PCNA ( d ) in the MC38 tumors recovered from wild-type and IL-33 transgenic mice at Day 22 post inoculation. The representative images and the statistical proportions of positive cells are shown. Scale bar, 50 μm. n = 7. Data expressed as mean ± SEM. **, P

    Article Snippet: The sections were labeled with anti-Ki67 antibody (Arigo, 1:200) and anti-PCNA antibody (Boster, 1:200).

    Techniques: In Vivo, In Vitro, Transgenic Assay, Mouse Assay, Immunohistochemistry, Staining

    Histological characterization of MCTS of different sizes Sections from HT29 MCTS at the indicated stages or from xenografts generated in immunodeficient mice were stained with H E panels A-D. or stained with anti-HIF-1α (panels E-H. ; upper panel HIF-1α and counterstaining with Hematoxylin, lower panel color deconvolution to show the HIF-1α positivity only), anti-cleaved Caspase 3 (cC3, panels I-L. , green) or anti-Ki-67 antibodies (panels M-P. , green). Sections from panels I-P were counterstained with DAPI (blue). Panels A-D, G, H: magnification 10x; panels F, G, I-P: magnification 20x; panel E: magnification 40x. Scale bar 100μm.

    Journal: Oncotarget

    Article Title: Induction of hypoxia and necrosis in multicellular tumor spheroids is associated with resistance to chemotherapy treatment

    doi: 10.18632/oncotarget.13857

    Figure Lengend Snippet: Histological characterization of MCTS of different sizes Sections from HT29 MCTS at the indicated stages or from xenografts generated in immunodeficient mice were stained with H E panels A-D. or stained with anti-HIF-1α (panels E-H. ; upper panel HIF-1α and counterstaining with Hematoxylin, lower panel color deconvolution to show the HIF-1α positivity only), anti-cleaved Caspase 3 (cC3, panels I-L. , green) or anti-Ki-67 antibodies (panels M-P. , green). Sections from panels I-P were counterstained with DAPI (blue). Panels A-D, G, H: magnification 10x; panels F, G, I-P: magnification 20x; panel E: magnification 40x. Scale bar 100μm.

    Article Snippet: Immunofluorescence For immunofluorescence staining, sections were blocked with PBS 2% goat serum 0.3% Triton X-100 for one hour at RT, and then incubated with rabbit monoclonal anti-Ki-67 (Abcam, 1:200), rabbit monoclonal anti-cleaved caspase 3 (Cell Signaling Technology, 1:200), or mouse monoclonal anti-EBP50 (BD Biosciences, 1:50) for one hour at 37°C.

    Techniques: Generated, Mouse Assay, Staining