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anti ki67  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti ki67
    Anti Ki67, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1274 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+ki+67/Ki-67+Mouse+mAb/pm42822681-81-22-23
    Average 96 stars, based on 1274 article reviews
    anti ki67 - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    other:

    Article Title: SMAD4 Palmitoylation Drives a Metabolic-Transcriptional Circuit to Promote Tumorigenesis and Confers Radiosensitivity in Pancreatic Cancer.
    Article Snippet: qPCRs were processed using 2 × Universal SYBR Green Fast qPCR Mix (Cat# RM21203, ABclonal, China).

    Article Title: Sustainability of functional hair follicle activity: Impact of spatially anchored multifunctional tetrahedral framework nucleic acids
    Article Snippet: Apply the diluted primary antibody anti-Cytokeratin 14 (ab119695, Abcam, UK) and anti-Ki-67(9129, CST, USA) and incubate at 4 °C overnight.

    Article Title: Smaller Oxygen Nanobubbles More Effectively Suppress Colitis and Colon Carcinogenesis than Larger Oxygen Nanobubbles.
    Article Snippet: The following primary antibodies were used: anti-HIF-1α (rabbit polyclonal, Novus Biologicals, Centennial, CO, USA, NB100-479SS, https://doi.org/10.3390/ijms27041975 dilution 1:200), anti-Ki-67 (rabbit monoclonal, Cell Signaling Technology, Danvers, MA, USA, 12202, 1:200), anti-CD8 (rabbit monoclonal, Abcam, Cambridge, United Kingdom, ab209775, 1:1000), anti-FOXP3 (rabbit monoclonal, Cell Signaling Technology, 12653, 1:200), anti-CD163 (rabbit monoclonal, Abcam, ab182422, 1:500), and anti-CD68 (rabbit polyclonal, Abcam, ab125212, 1:500).

    Article Title: [ 18 F]FLT-PET as predictive non-invasive biomarker for neoadjuvant therapy with Wee1 and ATR inhibitors
    Article Snippet: anti-Ki-67 (D3B5; #12202) was purchased from Cell Signalling Technologies.

    Article Title: NRF2-TERT-ACSL4 pathway inhibits ferroptosis and regulates cytoskeletal dynamics to mitigate ovarian aging.
    Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.

    Incubation:

    Article Title: ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression.
    Article Snippet: The sections were then blocked with 5% goat serum (Beyotime, #C0265) for 1 hour to minimize nonspecific binding. .. The following day, the slides were incubated overnight at 4°C with primary antibodies: anti-MXRA8 (Abcam, #ab185444, diluted 1:200) or anti-Ki-67 (Cell Signaling Technology, #9027, diluted 1:400). .. On the next day, sections were incubated with HRP-conjugated secondary antibodies (Abcam, #ab6721), and the signals were visualized using the DAB Substrate Kit (Abcam, #ab64238).

    Article Title: Enzalutamide effectively inhibits the growth of meningiomas via p21-dependent senescence induction.
    Article Snippet: Meningiomas are the most common primary intracranial tumors, arising from the arachnoid cap cells of the meninges.. It accounts for approximately 38.3% of all central nervous system (CNS) tumors [1].. The majority are classified as World Health Organization (WHO) Grade 1, which is considered benign.

    Article Title: Mitochondria-derived peptide MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice by activating Nrf2 pathway.
    Article Snippet: Oxidative stress play key roles in the pathogenesis of bronchopulmonary dysplasia (BPD).. MOTS-c is a mitochondria-derived peptide containing 16 amino acids that is reported to be involved in the treatment of oxidative stress-related diseases.. However, whether MOTS-c functions on hyperoxia-induced BPD remains unknown.



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    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.
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    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.
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    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.
    Anti Ki67, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.
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    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.
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    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.
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    PTX/Pt@RGD inhibited tumor angiogenesis and proliferation in A549 xenografts. (A) Representative IHC images of CD31, <t>Ki-67,</t> and PCNA (magnification: ×20). (B-D) Quantitative analysis of positive area percentages. Data are the mean ± SD (n=3). ***P<0.001, ****P<0.0001 vs. control; ns, not significant (one-way ANOVA with the Tukey post hoc test). ANOVA, analysis of variance; IHC, immunohistochemistry; Pt, cisplatin; PTX, paclitaxel; RGD, arginine-glycine-aspartic acid; SD, standard deviation.
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    PTX/Pt@RGD inhibited tumor angiogenesis and proliferation in A549 xenografts. (A) Representative IHC images of CD31, <t>Ki-67,</t> and PCNA (magnification: ×20). (B-D) Quantitative analysis of positive area percentages. Data are the mean ± SD (n=3). ***P<0.001, ****P<0.0001 vs. control; ns, not significant (one-way ANOVA with the Tukey post hoc test). ANOVA, analysis of variance; IHC, immunohistochemistry; Pt, cisplatin; PTX, paclitaxel; RGD, arginine-glycine-aspartic acid; SD, standard deviation.
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    Image Search Results


    Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.

    Journal: Developmental Neurobiology

    Article Title: Molecular and Proteomic Profiling of Human Cerebral Organoid‑Derived Small Extracellular Vesicles

    doi: 10.1002/dneu.70062

    Figure Lengend Snippet: Effects sEVs obtained from static, orbital shaker and Organoid‐on‐a‐Chip conditions on U87 glioblastoma cells. (A) MTT assay for viability of U87 Glioblastoma for static, orbital shaker, and Organoid‐on‐a‐Chip sEVs. (B, C) Representative Ki67/DAPI immunofluorescence images of U87 glioblastoma cells following sEV treatment and quantification of Ki67–DAPI signal overlap using the Manders coefficient. (D, E) Migration of U87 Glioblastoma cells upon sEV treatment was observed by scratch assay up to 48 h. Scale bar 400 µm. (F, G) Diameter of spheres formed on day 2 and day 4 of sEVs treated U87 Glioblastoma by hanging drop sphere formation assay were quantified. Scale bar 200 µm. Data are presented as mean ± SEM, * p < 0.05, ** p < 0.01 compared to the control group.

    Article Snippet: The primary antibody, Ki‐67 (Bioss, bs‐2130R), was added to the samples and incubated overnight at 4°C.

    Techniques: MTT Assay, Immunofluorescence, Migration, Scratch Assay, Tube Formation Assay, Control

    PTX/Pt@RGD inhibited tumor angiogenesis and proliferation in A549 xenografts. (A) Representative IHC images of CD31, Ki-67, and PCNA (magnification: ×20). (B-D) Quantitative analysis of positive area percentages. Data are the mean ± SD (n=3). ***P<0.001, ****P<0.0001 vs. control; ns, not significant (one-way ANOVA with the Tukey post hoc test). ANOVA, analysis of variance; IHC, immunohistochemistry; Pt, cisplatin; PTX, paclitaxel; RGD, arginine-glycine-aspartic acid; SD, standard deviation.

    Journal: Translational Lung Cancer Research

    Article Title: Targeted dual-responsive nanocapsules for synergistic cisplatin and paclitaxel prodrug delivery in the treatment of lung cancer

    doi: 10.21037/tlcr-2026-0967

    Figure Lengend Snippet: PTX/Pt@RGD inhibited tumor angiogenesis and proliferation in A549 xenografts. (A) Representative IHC images of CD31, Ki-67, and PCNA (magnification: ×20). (B-D) Quantitative analysis of positive area percentages. Data are the mean ± SD (n=3). ***P<0.001, ****P<0.0001 vs. control; ns, not significant (one-way ANOVA with the Tukey post hoc test). ANOVA, analysis of variance; IHC, immunohistochemistry; Pt, cisplatin; PTX, paclitaxel; RGD, arginine-glycine-aspartic acid; SD, standard deviation.

    Article Snippet: Antibodies included primary antibodies against CD31 [cat. no. 11265-1-P; rabbit polyclonal antibody; Western blotting (WB) 1:500; immunohistochemistry (IHC) 1:100; Proteintech, Rosemont, IL, USA], Ki-67 (cat. no. 27309-1-AP; rabbit polyclonal antibody; IHC 1:200; Proteintech), PCNA (cat. no. 10205-2-AP; rabbit polyclonal antibody; IHC 1:500; Proteintech), Bcl-2 (cat. no. 12789-1-AP; WB 1:1,000; Proteintech), Caspase-9 (cat. no. 10380-1-AP; WB 1:1,000; Proteintech), Bax (cat. no. 50599-2-Ig; WB 1:2,000; Proteintech), COX-2 (cat. no. 12375-1-AP, WB 1:1000; Proteintech), and β-actin (cat. no. 66009-1-Ig; WB 1:5,000; internal control), as well as horseradish peroxidase (HRP)-conjugated goat anti-rabbit secondary antibody (cat. no. SA00001-2; WB 1:5,000; Proteintech).

    Techniques: Analysis, Control, Immunohistochemistry, Standard Deviation