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anti ki67  (Cell Signaling Technology Inc)


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    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 1197 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ki67/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1197 article reviews
    anti ki67 - by Bioz Stars, 2026-06
    96/100 stars

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    In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for <t>Ki67</t> (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.
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    Cell Signaling Technology Inc anti ki67
    In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for <t>Ki67</t> (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.
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    Cell Signaling Technology Inc rabbit anti mouse ki67 monoclonal antibody
    In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for <t>Ki67</t> (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.
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    Cell Signaling Technology Inc ki67
    AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. <t>Ki67</t> ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.
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    AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. <t>Ki67</t> ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.
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    Cell Signaling Technology Inc anti human ki67
    AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. <t>Ki67</t> ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.
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    Santa Cruz Biotechnology mouse anti ki67
    AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. <t>Ki67</t> ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.
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    AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. <t>Ki67</t> ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.
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    Image Search Results


    In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

    Journal: Bioactive Materials

    Article Title: Countering postoperative immune suppression with a self-assembling dendritic cell nanovaccine

    doi: 10.1016/j.bioactmat.2026.05.005

    Figure Lengend Snippet: In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

    Article Snippet: Anti-Ki67 mouse mAb (Cat# GB121141-100), anti-CD3 mouse mAb (Cat# GB15014-100), FITC-conjugated goat anti-mouse IgG (H + L) (Cat# GB22301), and Cy5-conjugated goat anti-mouse IgG (H + L) (Cat# GB27301) for immunofluorescence assays, and DAB (SA-HRP) TUNEL apoptosis detection kit were supplied by Servicebio (Wuhan, China).

    Techniques: In Vivo, Drug discovery, Staining, TUNEL Assay, Immunofluorescence

    AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. Ki67 ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.

    Journal: The Journal of Biological Chemistry

    Article Title: AKAP2 is required for assembly of cytoskeletal signaling complexes that promote growth and metastasis of triple-negative breast cancer

    doi: 10.1016/j.jbc.2026.111329

    Figure Lengend Snippet: AKAP2 is upregulated in basal-like triple-negative breast cancer. A , average AKAP2 iBAQ intensity across 20 cell lines organized by subtype. “N” indicates normal-like. Data were reported in Lawrence, et al. . Error bars indicate standard deviation. B , immunoblot analysis of AKAP2 isoform levels and a selected list of EMT markers. Actin served as a loading control. C , densitometric quantification of AKAP2 protein expression normalized to actin. Error bars indicate SEM and statistical significance was determined by ordinary one way ANOVA with Sidak’s multiple comparisons test (∗p adj < 0.05, ∗∗ p adj < 0.01). D , AKAP2 mRNA expression from the METABRIC dataset analyzed through cBioportal. Center lines indicate median and dotted lines indicate quartiles. Statistical significance was determined by Kruskal-Wallis test with Dunn’s multiple comparisons test (∗p adj < 0.05, ∗∗∗∗ p adj < 0.0001). E , immunofluorescent detection of AKAP2 ( green ) in a TNBC patient tumor. Ki67 ( magenta ) positive nuclei ( blue ) were used as a tumor marker. F , immunofluorescent detection of AKAP2 ( green ) of a field of MDA-MB-231 cells co-stained with tubulin ( magenta ) and DAPI ( blue ). G , a higher magnification view of a single MDA-MB-231 cell stained with AKAP2 ( green ), tubulin ( magenta ), and DAPI ( blue ) to visualize subcellular distribution of AKAP2. H , immunofluorescent detection of AKAP2 ( green ) in a MDA-MB-231 cell co-stained with VASP ( magenta ). I , immunoblot analysis of AKAP2 isoform levels in control and shAKAP2 MDA-MB-231 cells. Ponceau S served as a loading control. J , densitometric quantification of AKAP2 isoform expression with expression normalized to Ponceau S and subsequent normalization to shScr untreated control cells. Error bars indicate SEM and statistical significance was determined by two-way ANOVA with Dunnet’s multiple comparisons test (ns: not significant, ∗∗p adj < 0.01). N values indicate biological replicates.

    Article Snippet: Slides were incubated with primary antibodies against AKAP2 (1:100, Novus Biological, NB100-61604) and Ki67 (1:1000, Cell Signaling Technology, 9449) in blocking solution overnight at room temperature in a humidity chamber.

    Techniques: Standard Deviation, Western Blot, Control, Expressing, Marker, Staining