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mouse monoclonal anti human cyclin d1  (Proteintech)


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    Structured Review

    Proteintech mouse monoclonal anti human cyclin d1
    Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, <t>Cyclin</t> <t>D1,</t> and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).
    Mouse Monoclonal Anti Human Cyclin D1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1466 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 1466 article reviews
    mouse monoclonal anti human cyclin d1 - by Bioz Stars, 2026-03
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    Images

    1) Product Images from "Prognostic value of BTG1 for predicting decitabine sensitivity in de novo acute myeloid leukemia"

    Article Title: Prognostic value of BTG1 for predicting decitabine sensitivity in de novo acute myeloid leukemia

    Journal: iScience

    doi: 10.1016/j.isci.2025.114327

    Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, Cyclin D1, and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).
    Figure Legend Snippet: Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, Cyclin D1, and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

    Techniques Used: Protein-Protein interactions, Infection, Expressing, Standard Deviation



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    Proteintech mouse monoclonal anti human cyclin d1
    Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, <t>Cyclin</t> <t>D1,</t> and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).
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    Proteintech anti ccnd1 mouse monoclonal antibody
    CXCL12 overexpression and knockdown in GCs. (A,B) Changes in the expression of CXCL12 after its overexpression and knockdown in GCs. (C,D) The mRNA expression level of PCNA , <t>CCND1</t> , CDK2 , Bcl-2 and Bax was detected after overexpressing or knocking down CXCL12 in GCs. (E) The protein expression levels of CCND1, PCNA, Bcl-2 and Bax were detected after overexpressing and knocking down CXCL12 in GCs. H, high-litter size group; L, low-itter size group; GAPDH was selected as the internal reference gene (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001; ns, not significant). GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GC, granulosa cells.
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    Proteintech mouse anti cyclin d1
    CXCL12 overexpression and knockdown in GCs. (A,B) Changes in the expression of CXCL12 after its overexpression and knockdown in GCs. (C,D) The mRNA expression level of PCNA , <t>CCND1</t> , CDK2 , Bcl-2 and Bax was detected after overexpressing or knocking down CXCL12 in GCs. (E) The protein expression levels of CCND1, PCNA, Bcl-2 and Bax were detected after overexpressing and knocking down CXCL12 in GCs. H, high-litter size group; L, low-itter size group; GAPDH was selected as the internal reference gene (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001; ns, not significant). GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GC, granulosa cells.
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    Proteintech mouse anti human ccnd1 antibody
    a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with <t>anti-CCND1</t> antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.
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    Proteintech anti mouse cyclin d1 antibody
    LU NPs Inhibit GBM Cell Proliferation via the <t>β-catenin/Cyclin</t> <t>D1</t> Pathway. ( A) Cell viability measured by CCK8 assay after LU NPs treatment with various concentrations (0, 2,4,8,16,32, 64 μg/mL). (B, C) EdU assay shown that LU NPs inhibited DNA synthesis in GL261 cells. Scale bar: 20 μm. (n = 3) ∗∗P < 0.01. (D, E) Cell cycle analysis by flow cytometry of GL261 cells after been treated with various concentrations (0, 5, 10, 20 μg/mL) LU NPs. (n = 3) ∗∗P < 0.01, ∗∗∗P < 0.001. (F–J) Cell cycle related protein expression quantified with western blot. (n = 3) ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
    Anti Mouse Cyclin D1 Antibody, supplied by Proteintech, 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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    LU NPs Inhibit GBM Cell Proliferation via the <t>β-catenin/Cyclin</t> <t>D1</t> Pathway. ( A) Cell viability measured by CCK8 assay after LU NPs treatment with various concentrations (0, 2,4,8,16,32, 64 μg/mL). (B, C) EdU assay shown that LU NPs inhibited DNA synthesis in GL261 cells. Scale bar: 20 μm. (n = 3) ∗∗P < 0.01. (D, E) Cell cycle analysis by flow cytometry of GL261 cells after been treated with various concentrations (0, 5, 10, 20 μg/mL) LU NPs. (n = 3) ∗∗P < 0.01, ∗∗∗P < 0.001. (F–J) Cell cycle related protein expression quantified with western blot. (n = 3) ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
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    Proteintech mouse α cyclin d1
    LU NPs Inhibit GBM Cell Proliferation via the <t>β-catenin/Cyclin</t> <t>D1</t> Pathway. ( A) Cell viability measured by CCK8 assay after LU NPs treatment with various concentrations (0, 2,4,8,16,32, 64 μg/mL). (B, C) EdU assay shown that LU NPs inhibited DNA synthesis in GL261 cells. Scale bar: 20 μm. (n = 3) ∗∗P < 0.01. (D, E) Cell cycle analysis by flow cytometry of GL261 cells after been treated with various concentrations (0, 5, 10, 20 μg/mL) LU NPs. (n = 3) ∗∗P < 0.01, ∗∗∗P < 0.001. (F–J) Cell cycle related protein expression quantified with western blot. (n = 3) ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
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    Image Search Results


    Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, Cyclin D1, and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

    Journal: iScience

    Article Title: Prognostic value of BTG1 for predicting decitabine sensitivity in de novo acute myeloid leukemia

    doi: 10.1016/j.isci.2025.114327

    Figure Lengend Snippet: Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, Cyclin D1, and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

    Article Snippet: Mouse monoclonal anti-human Cyclin D1 , Proteintech , Cat# 60186-1-Ig RRID: AB_10793718.

    Techniques: Protein-Protein interactions, Infection, Expressing, Standard Deviation

    CXCL12 overexpression and knockdown in GCs. (A,B) Changes in the expression of CXCL12 after its overexpression and knockdown in GCs. (C,D) The mRNA expression level of PCNA , CCND1 , CDK2 , Bcl-2 and Bax was detected after overexpressing or knocking down CXCL12 in GCs. (E) The protein expression levels of CCND1, PCNA, Bcl-2 and Bax were detected after overexpressing and knocking down CXCL12 in GCs. H, high-litter size group; L, low-itter size group; GAPDH was selected as the internal reference gene (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001; ns, not significant). GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GC, granulosa cells.

    Journal: Animal Bioscience

    Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

    doi: 10.5713/ab.24.0640

    Figure Lengend Snippet: CXCL12 overexpression and knockdown in GCs. (A,B) Changes in the expression of CXCL12 after its overexpression and knockdown in GCs. (C,D) The mRNA expression level of PCNA , CCND1 , CDK2 , Bcl-2 and Bax was detected after overexpressing or knocking down CXCL12 in GCs. (E) The protein expression levels of CCND1, PCNA, Bcl-2 and Bax were detected after overexpressing and knocking down CXCL12 in GCs. H, high-litter size group; L, low-itter size group; GAPDH was selected as the internal reference gene (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001; ns, not significant). GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GC, granulosa cells.

    Article Snippet: Protein detection was achieved using the following antibodies: anti-CCND1 mouse monoclonal antibody (1:250, Proteintech), anti-PCNA rabbit polyclonal antibody (1:250, Proteintech), anti-Bcl2 rabbit polyclonal antibody (1:250, Proteintech), anti-Bax rabbit polyclonal antibody (1:250, Proteintech), anti-CITED1 rabbit polyclonal antibody (1:50, Proteintech), anti-WNT10B mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-CXCR4 mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-phospho-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam, Cambridge, UK), anti-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam), anti-phospho-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-GAPDH mouse monoclonal antibody (1:2,500, Proteintech), 1:1,000 goat anti-rabbit secondary antibody IgG (Proteintech) and 1:1,000 goat anti-mouse secondary antibody IgG (Proteintech).

    Techniques: Over Expression, Knockdown, Expressing

    a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with anti-CCND1 antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.

    Journal: PLOS One

    Article Title: STAG2 mutations in the normal colon induce upregulation of oncogenic pathways in neighbouring wildtype cells

    doi: 10.1371/journal.pone.0332499

    Figure Lengend Snippet: a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with anti-CCND1 antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.

    Article Snippet: Primary antibodies used included rabbit anti-human STAG2 antibody (1:100, 19837–1-AP, Proteintech, USA), mouse anti-human KI67 antibody (1:500, 66555–6-Ig, Proteintech, USA), mouse anti-human P53 antibody (1:400, 60283–2-Ig, Proteintech, USA), mouse anti-human CCND1 antibody (1:100, 60186–1-Ig, Proteintech, USA), mouse anti-human TERT antibody (1: 100, MA5−16033, Invitrogen, USA), mouse anti-human KRAS antibody (1:250, 415700, Invitrogen, USA), and mouse anti-human TNFα antibody (1:50, MA5−23720, Invitrogen, USA).

    Techniques: Mutagenesis, Immunofluorescence, Staining, Cell Culture

    LU NPs Inhibit GBM Cell Proliferation via the β-catenin/Cyclin D1 Pathway. ( A) Cell viability measured by CCK8 assay after LU NPs treatment with various concentrations (0, 2,4,8,16,32, 64 μg/mL). (B, C) EdU assay shown that LU NPs inhibited DNA synthesis in GL261 cells. Scale bar: 20 μm. (n = 3) ∗∗P < 0.01. (D, E) Cell cycle analysis by flow cytometry of GL261 cells after been treated with various concentrations (0, 5, 10, 20 μg/mL) LU NPs. (n = 3) ∗∗P < 0.01, ∗∗∗P < 0.001. (F–J) Cell cycle related protein expression quantified with western blot. (n = 3) ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

    Journal: Materials Today Bio

    Article Title: Application of PVA hydrogel loaded with luteolin nanoparticles in anti EMT treatment after GBM

    doi: 10.1016/j.mtbio.2025.101956

    Figure Lengend Snippet: LU NPs Inhibit GBM Cell Proliferation via the β-catenin/Cyclin D1 Pathway. ( A) Cell viability measured by CCK8 assay after LU NPs treatment with various concentrations (0, 2,4,8,16,32, 64 μg/mL). (B, C) EdU assay shown that LU NPs inhibited DNA synthesis in GL261 cells. Scale bar: 20 μm. (n = 3) ∗∗P < 0.01. (D, E) Cell cycle analysis by flow cytometry of GL261 cells after been treated with various concentrations (0, 5, 10, 20 μg/mL) LU NPs. (n = 3) ∗∗P < 0.01, ∗∗∗P < 0.001. (F–J) Cell cycle related protein expression quantified with western blot. (n = 3) ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

    Article Snippet: The antibodies used for immunostaining were anti-mouse-Cyclin D1 antibody (60186-1-Ig, Proteintech); anti-rabbit-E-cadherin antibody (20874-1-AP; Proteintech); anti-rabbit-N-cadherin antibody (22018-1-AP; Proteintech); anti-mouse-Bcl-2 (68103-1-Ig, Proteintech), anti-rabbit-Vimentin antibody (5741; CST); anti-rabbit-β-catenin antibody (8480; CST); anti-rabbit-GAPDH antibody (GB11002-100; Servicebio) and anti-rabbit-Tubulin antibody (GB11017-100; Servicebio).

    Techniques: CCK-8 Assay, EdU Assay, DNA Synthesis, Cell Cycle Assay, Flow Cytometry, Expressing, Western Blot