c myc polyclonal antibody (Proteintech)
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C Myc Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1291 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c+myc+polyclonal+antibody/c-Myc+Antibody/pmc13018894-6-0-4
Average 96 stars, based on 1291 article reviews
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1) Product Images from "CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression"
Article Title: CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression
Journal: iScience
doi: 10.1016/j.isci.2026.115273
Figure Legend Snippet: The effect of CGF-induced ROS on the MAPK/ERK 1/2/c-MYC signaling pathway (A) Western blotting was used to analyze the expression of MEK, P-MEK, ERK 1/2, P-ERK 1/2, and c-MYC proteins in HCT116 and HT29 cells after treatment with specified CGF concentrations. (B) Immunofluorescence staining of HCT116 and HT29 cells after CGF treatment, showing changes in p-ERK (green). PMA was used to promote nuclear entry of p-ERK (200 nM, 4 h), and DAPI was used to stain the nucleus (blue), with merged images shown (scale bars, 10 μM). (C) Western blot was used to analyze the levels of MEK, P-MEK, ERK 1/2, P-ERK 1/2, and c-MYC proteins in HCT116 and HT29 cells following treatment with CGF (40 μM, 24 h) and NAC (500 μM, 24 h). (D) Untargeted metabolomics analysis of glycolytic metabolites after CGF treatment in HCT116 cells. Metabolites marked in blue represent those inhibited by CGF. (E and F) ELISA analysis of lactate secretion in the cell supernatant of HCT116 (E) and HT29 (F) cells after CGF treatment. (G and H) Analysis of mRNA expression levels of genes related to glycolysis in HCT116 and HT29 cells exposed to certain concentrations of CGF using RT-qPCR. (I) Western blot was used to analyze the expression levels of apoptosis-associated proteins (BCL2, PUMA, NOXA, C-caspase 9, and C-caspase 3) and EMT markers (N-cadherin and vimentin) in HCT116 and HT29 cells after they were treated with CGF. (J) Western blot analysis of the reversal of EMT markers N-cadherin, vimentin, SLUG, and SNAIL proteins in HCT116 and HT29 cells overexpressing c-MYC. (E–J) Data presentation is in the form of mean ± SEM. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
Techniques Used: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR
Figure Legend Snippet: Schematic diagram of the mechanism by which CGF inhibits the progression of CRC CGF treatment downregulates the expression of multiple ABC transporters (ABCA1, ABCB5, ABCC2, and CFTR). This downregulation results in an aberrant accumulation of intracellular ATP and induces severe mitochondrial dysfunction, characterized by the collapse of mitochondrial membrane potential and excessive generation of ROS. Elevated ROS levels subsequently inhibit the MEK/ERK signaling pathway and decrease c-MYC expression, thereby suppressing tumor progression (by figdraw.com , authorization ID: UYOIR77017).
Techniques Used: Expressing, Membrane
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