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anti cdk4  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti cdk4
    Anti Cdk4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 968 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+cdk4/CDK4+Rabbit+mAb/pm41874002-195-26-27
    Average 96 stars, based on 968 article reviews
    anti cdk4 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    other:

    Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle
    Article Snippet: The following primary antibodies were used in the present study: Anti-HAT1 (1:1,000; cat no. 11432-1-AP; Proteintech Group, Inc.), anti-CDK2 (1:1,000; cat no. 10122-1-AP; Proteintech Group, Inc.), anti-FOXA1 (1:1,000; cat no. 20411-1-AP; Proteintech Group, Inc.), anti-CDK4 (1:1,000; cat no. 12790; Cell Signaling Technology, Inc.), anti-cyclin E (1:1,000; cat no. 20808; Cell Signaling Technology, Inc.) and anti-GAPDH (1:5,000; cat no. 60004-1-Ig; Proteintech Group, Inc.).

    Article Title: Repurposing T-type calcium channel blocker Lomerizine as a therapeutic strategy for glioblastoma.
    Article Snippet: The following primary antibodies were 464 used in this study: anti-Akt (Cell Signaling; #9272), anti-pAkt (Cell Signaling; #4058), anti-β-465 actin (FUJIFILM Wako Pure Chemical Corporation; 010-27841), anti-CDK4 (Cell Signaling; 466 #12790), anti-CDK6 (Cell Signaling; #13331), anti-ERK (Cell Signaling; #4695), anti-pERK 467 (Cell Signaling; #4370), anti-SOX2 (Gene Tex; GTX101507), anti-STAT3 (Cell Signaling; 468 #12640), anti-pSTAT3 S727 (Cell Signaling; #9134), anti-pSTAT3 Y705 (Cell Signaling; #9145), 469 and anti-PARP (Cell Signaling; #9542) , anti-Cleaved PARP (Cell Signaling; #5625).

    Article Title: Integrative Mechanistic Investigation of the Anticancer Effects of Panax notoginseng in Colorectal Cancer.
    Article Snippet: Antibodies against CDK4, Cyclin D1, CDK6, p27, p21, CDK2, p-ERK1/2, ERK1/2, p-JNK, JNK, p-p38, p38, p-STAT3 (Tyr705), p-STAT3 (Ser727), STAT3, p-AKT, AKT, p-PI3K, PI3K, p-AMPKα, AMPKα, Cleaved PARP, Caspase9, Survivin, Caspase-8, Bcl-2, Mcl-1, HO-1, LC3A/B, and β-actin, as well as secondary antibodies, were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Article Title: Integrative Mechanistic Investigation of the Anticancer Effects of Panax notoginseng in Colorectal Cancer
    Article Snippet: Antibodies against CDK4, Cyclin D1, CDK6, p27, p21, CDK2, p-ERK1/2, ERK1/2, p-JNK, JNK, p-p38, p38, p-STAT3 (Tyr705), p-STAT3 (Ser727), STAT3, p-AKT, AKT, p-PI3K, PI3K, p-AMPKα, AMPKα, Cleaved PARP, Caspase-9, Survivin, Caspase-8, Bcl-2, Mcl-1, HO-1, LC3A/B, and β-actin, as well as secondary antibodies, were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Article Title: Ring Finger Protein 1, a Novel Ubiquitin E3 Ligase Targeting Cancerous Inhibitor of Protein Phosphatase 2A to Suppress Smoking‐Induced Lung Tumorigenesis
    Article Snippet: The primary antibodies were purchased as follows: anti‐CIP2A (#SC‐80659, Santa Cruz Biotechnology), anti‐RING1 (#13069, Cell Signaling Technologies), anti‐β‐Actin (#SC‐47778, Santa Cruz Biotechnology), anti‐CDK4 (#12790, Cell Signaling Technologies), anti‐CyclinD (#2978, Cell Signaling Technologies), anti‐CyclinE (#4129, Cell Signaling Technologies), anti‐CyclinB1 (#SC‐752, Santa Cruz Biotechnology), anti‐c‐MYC (#SC‐42, Santa Cruz Biotechnology), anti‐PP2Ac (#2038, Cell Signaling Technologies), anti‐MYC tag (#SC‐40, Santa Cruz Biotechnology), anti‐HA tag (#MMS‐101P, Covance), anti‐FLAG tag (#2368, Cell Signaling Technologies), anti‐E2F1 (#SC‐56661, Santa Cruz Biotechnology), anti‐DNMT1 (#5032, Cell Signaling Technologies).

    Article Title: VPS35 Deficiency Markedly Reduces the Proliferation of HEK293 Cells
    Article Snippet: The following primary antibodies were used: anticaspase-3 (9662S; 1:3000), anti-poly(ADP-ribose) polymerase (PARP; 9542S; 1:3000), anticytochrome C (11940S; 1:1000), anti-CDK4 (12790S; 1:2000), anti-cyclinD1 (2978S; 1:3000), anti-Drp1 (8570S; 1:3000), and anti-pDrp1 (S616) (3455S; 1:1000) (all from Cell Signaling Technology, Danvers, MA, USA); anti-Ki-67 (ab15580; 1:1000; Abcam, Boston, MA, USA); anti-Mfn2 (sc-515647; 1:1000; Santa Cruz Biotechnology, Dallas, TX, USA); and anti-GAPDH (LF-PA0018; 1:3000; AbFrontier, Seoul, Republic of Korea).

    Article Title: VPS35 Deficiency Markedly Reduces the Proliferation of HEK293 Cells
    Article Snippet: The following primary antibodies were used: anti-caspase-3 (9662S; 1:3000), anti-poly(ADP-ribose) polymerase (PARP; 9542S; 1:3000), anticytochrome C (11940S; 1:1000), anti-CDK4 (12790S; 1:2000), anti-cyclinD1 (2978S; 1:3000), anti-Drp1 (8570S; 1:3000), and anti-pDrp1 (S616) (3455S; 1:1000) (all from Cell Signaling Technology, Danvers, MA, USA); anti-Ki-67 (ab15580; 1:1000; Abcam, Boston, MA, USA); anti-Mfn2 (sc-515647; 1:1000; Santa Cruz Biotechnology, Dallas, TX, USA); and anti-GAPDH (LF-PA0018; 1:3000; AbFrontier, Seoul, Republic of Korea).

    Control:

    Article Title: Targeting PCK1 to overcome CDK4/6 inhibitor resistance for breast cancer therapy.
    Article Snippet: Phosphoenolpyruvate carboxykinase 1 (PCK1) is known for its role in gluconeogenesis and the regulation of PCK1 expression was shown to associate with oncogenic activity in pancreatic and colorectal cancers.. However, in different cancer types such as liver cancer, PCK1 could function as a tumor suppressor, rendering complication for targeted therapy.. In this study, we used breast cancer model to delineate its involvement in malignancy, we found PCK1 associated with oncogenic function to promotes cell proliferation, enhances colony formation, and stimulates DNA synthesis in breast cancer.



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    Metabolomic Analysis Reveals Mg and Al-Mg Induce Metabolic Reprogramming in Hepatocellular and Pancreatic Cancer Cells. (A) Metabolomic profiling of PANC-1, PANC-1-Mg, PANC-1-Al-Mg, Huh7, Huh7-Mg, and Huh7-Al-Mg groups using LC-MS identified 1824 metabolites. (B) PCA illustrating clustering among different cell groups. (C) Heatmap showing differential abundances of characteristic metabolites across cell groups. (D) K-means clustering analysis highlighting metabolic differences among the cell groups. (E) Venn diagram displaying common differential metabolites among treatment groups. (F) Volcano plots of differential metabolites following Mg or Al-Mg treatment. (G) KEGG pathway enrichment analysis of differential metabolites. (H) Enrichment distribution of differential metabolites in Huh7 or PANC-1 cells treated with Mg or Al-Mg. (I) Quantitative analysis of intracellular metabolites including L-glutamine, adenine, uridine, cytidine, and guanine by ELISA with Mg or Al-Mg exposure. (J) Western blot analysis of p21, <t>CDK4,</t> and PCNA expression in PANC-1 cells after Mg or Al-Mg exposure. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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    Image Search Results


    EEDJF induces G1/S cell cycle arrest in HCT116 cells. (A) Western blot analysis of cell cycle–related proteins (p21, Cyclin D1, and CDK4) following EEDJF treatment. (B) Densitometric quantification of protein expression shown in (A) . Band intensities were quantified using ImageJ software and normalized to β-actin. (C) Flow cytometric analysis of cell cycle distribution after EEDJF treatment. (D,E) Quantitative distribution of cells in G1, S, and G2/M phases. Data are presented as mean ± SD from three independent biological experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

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    doi: 10.3389/fphar.2026.1833123

    Figure Lengend Snippet: EEDJF induces G1/S cell cycle arrest in HCT116 cells. (A) Western blot analysis of cell cycle–related proteins (p21, Cyclin D1, and CDK4) following EEDJF treatment. (B) Densitometric quantification of protein expression shown in (A) . Band intensities were quantified using ImageJ software and normalized to β-actin. (C) Flow cytometric analysis of cell cycle distribution after EEDJF treatment. (D,E) Quantitative distribution of cells in G1, S, and G2/M phases. Data are presented as mean ± SD from three independent biological experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: Antibodies were purchased as follows: p-PI3K from Bioss (Beijing, China); PI3K and p21 from Proteintech (Wuhan, China); p-Akt, Cyclin D1, and CDK4 from Wanleibio (Shenyang, China); and total AKT from Cell Signaling Technology (MA, USA).

    Techniques: Western Blot, Expressing, Software

    Metabolomic Analysis Reveals Mg and Al-Mg Induce Metabolic Reprogramming in Hepatocellular and Pancreatic Cancer Cells. (A) Metabolomic profiling of PANC-1, PANC-1-Mg, PANC-1-Al-Mg, Huh7, Huh7-Mg, and Huh7-Al-Mg groups using LC-MS identified 1824 metabolites. (B) PCA illustrating clustering among different cell groups. (C) Heatmap showing differential abundances of characteristic metabolites across cell groups. (D) K-means clustering analysis highlighting metabolic differences among the cell groups. (E) Venn diagram displaying common differential metabolites among treatment groups. (F) Volcano plots of differential metabolites following Mg or Al-Mg treatment. (G) KEGG pathway enrichment analysis of differential metabolites. (H) Enrichment distribution of differential metabolites in Huh7 or PANC-1 cells treated with Mg or Al-Mg. (I) Quantitative analysis of intracellular metabolites including L-glutamine, adenine, uridine, cytidine, and guanine by ELISA with Mg or Al-Mg exposure. (J) Western blot analysis of p21, CDK4, and PCNA expression in PANC-1 cells after Mg or Al-Mg exposure. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

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    Article Title: A promising magnesium-related alloy with metabolic reprogramming and antitumor effects in hepatocellular and pancreatic cancer

    doi: 10.1016/j.bioactmat.2025.12.039

    Figure Lengend Snippet: Metabolomic Analysis Reveals Mg and Al-Mg Induce Metabolic Reprogramming in Hepatocellular and Pancreatic Cancer Cells. (A) Metabolomic profiling of PANC-1, PANC-1-Mg, PANC-1-Al-Mg, Huh7, Huh7-Mg, and Huh7-Al-Mg groups using LC-MS identified 1824 metabolites. (B) PCA illustrating clustering among different cell groups. (C) Heatmap showing differential abundances of characteristic metabolites across cell groups. (D) K-means clustering analysis highlighting metabolic differences among the cell groups. (E) Venn diagram displaying common differential metabolites among treatment groups. (F) Volcano plots of differential metabolites following Mg or Al-Mg treatment. (G) KEGG pathway enrichment analysis of differential metabolites. (H) Enrichment distribution of differential metabolites in Huh7 or PANC-1 cells treated with Mg or Al-Mg. (I) Quantitative analysis of intracellular metabolites including L-glutamine, adenine, uridine, cytidine, and guanine by ELISA with Mg or Al-Mg exposure. (J) Western blot analysis of p21, CDK4, and PCNA expression in PANC-1 cells after Mg or Al-Mg exposure. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After blocking with 5 % nonfat milk for 1 h at room temperature, membranes were incubated overnight at 4 °C with primary antibodies, including AMPK (1:1000, CST, 2532), p-AMPK (1:1000, CST, 2535), CPT1B (1:1000, Proteintech, 22170-1-AP), CDK4 (1:1000, Proteintech, 11026-1-AP), PCNA (1:1000, Proteintech, 10205-2-AP), p21 (1:1000, Proteintech, 10355-1-AP), GAPDH (1:1000, Proteintech, 60004-1-Ig) followed by HRP-conjugated secondary antibody (1:5000, Proteintech, RGAR001) for 1 h at room temperature.

    Techniques: Liquid Chromatography with Mass Spectroscopy, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing