forkhead box m1 (foxm1) antibody  (Cell Signaling Technology Inc)

Journal: Breast Cancer Research : BCR

Article Title: Short-term consumption of the modified standard American diet perturbed the metabolic balance and altered DNA damage in MMTV-PyMT transgenic mice

doi: 10.1186/s13058-025-02075-w

Figure Lengend Snippet: SAD2 diet promotes changes in DNA damage and response markers. Immunofluorescence was used to measure various types of DNA damage and response markers in MMTV tumors from individual mice ( n = 7 normal chow and n = 8 SAD2). ( A ) Forkhead box M1 (Foxm1), ( B ) poly-ADP ribose (PAR), ( C ) DNA polymerase beta (Polβ), and ( D ) apurinic/apyrimidinic endonuclease 1 (Ape1). The intensity levels were evaluated using a binary threshold to detect the fluorescence intensity. The graphs are displayed as the means ± SEMs via GraphPad Prism, and the significance levels are as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. The images are representative, and the scale bar is 100 μm

Article Snippet: The following dilutions were used for each antibody: forkhead box M1 (Foxm1) (1:500, 13147-1-AP, ProteinTech, Rosemont, IL, USA), poly(ADP-ribose) (PAR) (1:200, ab14460, Abcam), DNA polymerase beta (Polβ) (1:200, ab26343, Abcam), apurinic/apyrimidinic endonuclease 1 (Ape1) (1:200, ab189474, Abcam), advanced glycation end products (AGE) (1:500, ab23722, Abcam), methylglyoxal (MG) (1:200, MABN1838, Millipore Sigma, Burlington, MA, USA), tumor suppressor p53 binding protein 1 (53BP1), (1:500, NB100-304, Novus Biologicals, Centennial, CO, USA) and glucose transporter 1 (Glut1) (1:100, ab115730, Abcam).

Techniques: Immunofluorescence, Fluorescence

Journal: International Journal of Nanomedicine

Article Title: Copper-Based Metal-Organic Framework Nanoplatform for miRNA Delivery: Synergistic Antitumor Therapy

doi: 10.2147/IJN.S523766

Figure Lengend Snippet: Research on the antitumor mechanism of miR-4521@MOF-199. ( A ) The amount of intracellular GSH in HGC-27 cells subjected to treatments with varying concentrations of miR-4521@MOF-199 (n = 3). ( B ) Fluorescence images of ROS production in HGC-27 cells after various treatments. ( C ) Flow cytometric quantitative analyses of ROS levels in HGC-27 cells after various treatments. ( D ) Analysis of the expression level of FOXM1 mRNA in HGC-27 cells by RT-qPCR after various treatments (n = 3). ( E ) Analysis of the protein expression levels of FOXM1 and FDX1 in HGC-27 cells by WB after different treatments. ( F ) Statistical analysis of the FOXM1 protein (n = 3). ( G ) Immunofluorescence images of DLAT in HGC-27 cells after different treatments. ( H and I ) Analysis and statistics of the MMP in HGC-27 cells after different treatments (n = 3). (***p < 0.001).

Article Snippet: Forkhead box M1 (FOXM1), ferredoxin-1 (FDX1) and beta-actin antibody were purchased from Proteintech (Wuhan China). miR-4521, FAM-labeled miR-4521 and Cy5-labeled miR-4521 were procured from GenePharma (Shanghai China).

Techniques: Fluorescence, Expressing, Quantitative RT-PCR, Immunofluorescence

Journal: International Journal of Nanomedicine

Article Title: Copper-Based Metal-Organic Framework Nanoplatform for miRNA Delivery: Synergistic Antitumor Therapy

doi: 10.2147/IJN.S523766

Figure Lengend Snippet: In vivo tumor suppression of miR-4521@MOF-199. ( A ) In vivo fluorescence images of HGC-27 tumor-bearing mice treated with Cy5-miR-4521@MOF-199 at various time points. ( B ) Fluorescent images of tumors and primary organs in mice after 24 h. ( C ) General flowchart of the miR-4521@MOF-199 in vivo experiment. ( D ) Overview of tumor volume in HGC-27 tumor-bearing mice after different treatments (n = 4). ( E ) Tumor volume in each group of HGC-27 tumor-bearing mice after the treatment (n = 4). ( F ) Tumor images and ( G ) tumor weight statistics after different treatments (n = 4). ( H ) RT-qPCR analysis of FOXM1 mRNA in solid tumors after different treatments (n = 4). ( I ) H&E staining analysis of tumor tissues after different treatments. (***p < 0.001).

Article Snippet: Forkhead box M1 (FOXM1), ferredoxin-1 (FDX1) and beta-actin antibody were purchased from Proteintech (Wuhan China). miR-4521, FAM-labeled miR-4521 and Cy5-labeled miR-4521 were procured from GenePharma (Shanghai China).

Techniques: In Vivo, Fluorescence, Quantitative RT-PCR, Staining

Journal: Aging and Disease

Article Title: SIRT6 in Vascular Diseases, from Bench to Bedside

doi: 10.14336/AD.2021.1204

Figure Lengend Snippet: SIRT6 function in regulating vascular disease (Central Illustration) . ( A ) SIRT6 represses the initiation, development, and plaque instability of atherosclerosis. In endothelial cells, SIRT6 epigenetically represses the production of pro-inflammatory angiocrine factors and senescence-associated secretory phenotype, thus inhibiting endothelial dysfunction and senescence to reduce initiation and development of atherosclerosis. In macrophages, SIRT6 deacetylates H3K9ac and H3K56ac to reduce the expression of natural-killer group 2, member D (NKG2D) ligands, inhibiting the activation of immune cells and atherosclerosis development. SIRT6 also maintains the telomere integrity by deacetylating H3K9ac at the telomere and inhibiting 53BP1 binding, thus suppressing vascular smooth muscle cells (VSMCs) senescence. SIRT6 deficiency leads to VSMC senescence and plaque instability of atherosclerosis. PAI1, plasminogen activator inhibitor-1; TNFSF4, TNF superfamily member 4; FoxM1, Forkhead box protein M1; ICAM1, intercellular adhesion molecule-1. ( B ) SIRT6 suppresses hypertension. By deacetylating H3K9ac, endothelial SIRT6 inhibits NKX3.2 (NK3 homeobox 2) expression to reduce the transcription of GATA5 (GATA-binding protein 5), a transcriptional factor controlling blood pressure. Endothelial loss of SIRT6 facilitates hypertension and associated cardiorenal injury. SIRT6-mediated suppression of VSMC may also contribute to its role in preventing hypertension. ( C ) SIRT6 inhibits ischemic stroke. Endothelial loss of SIRT6 induces AKT inhibition via an unknown mechanism, which activates Caspase 3 to cause endothelial apoptosis and subsequent blood-brain barrier (BBB) injury and ischemic stroke. It remains unknown whether SIRT6 regulates endothelial senescence and angiocrine phenotype to participate in ischemic stroke. Chemical drug MDL-811 can activate macrophage SIRT6 and repress ischemic stroke via targeting histone acetylation and EZH2 activation to promote the expression of FOXC1.

Article Snippet: In human endothelial cells, SIRT6 represses the expression of senescence-associated angiocrine factors, such as plasminogen activator inhibitor-1 and TNF superfamily member 4, and that of forkhead box M1 [ - ].

Techniques: Expressing, Activation Assay, Binding Assay, Inhibition