c myc polyclonal antibody  (Proteintech)

Journal: iScience

Article Title: CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression

doi: 10.1016/j.isci.2026.115273

Figure Lengend 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.

Article Snippet: c-MYC Polyclonal antibody , Proteintech , Cat # 10828-1-AP; RRID: AB_3740742.

Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

Journal: iScience

Article Title: CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression

doi: 10.1016/j.isci.2026.115273

Figure Lengend 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).

Article Snippet: c-MYC Polyclonal antibody , Proteintech , Cat # 10828-1-AP; RRID: AB_3740742.

Techniques: Expressing, Membrane

Journal: bioRxiv

Article Title: c-MYC is an aggregation-prone, amyloidogenic protein

doi: 10.64898/2026.03.12.711438

Figure Lengend Snippet: (A) Detection of detergent-soluble and - insoluble c-MYC proteins by immunoblotting in HeLa cells pre-treated with 30 μM CR, followed by HS at 43°C for 30 min (representative images of three independent experiments). (B) and (C) Immunoprecipitation of either exogenously expressed HA-c-MYC or endogenous c-MYC proteins in HeLa cells by A11 antibodies (representative images of three independent experiments). (D) Detection of endogenous c-MYC proteins in HeLa cells by PLA using both the goat anti-c-MYC Ab and the rabbit anti-AO (A11) Ab. Nuclei are counterstained with Hoechst 33342. Scale bar: 10 μm. (E)-(G) Detection of endogenous c-MYC proteins in human prostate adenocarcinoma, hepatocellular carcinoma, and Alzheimer’s disease brain tissues by brightfield PLA using both the goat anti-c-MYC Ab and the rabbit anti-AO (A11) Ab. Scale bar: 100 μm for low magnification and 10 μm for high magnification. (H): Quantitation of endogenous c-MYC recognized by both the goat anti-c-MYC Ab and the rabbit anti-AO (A11) Ab through In-Cell PLA ELISA in HeLa cells treated with CR (mean ± SD, n=3 independent experiments, One-way ANOVA).

Article Snippet: All antibodies were purchased commercially, including rabbit polyclonal anti-amyloid oligomer (A11) Ab (cat#SPC-506, StressMarq Biosciences Inc.), rabbit monoclonal anti-c-MYC/N-MYC (D3N8F) Ab (cat#13987, Cell Signaling Technology), rabbit monoclonal ani-MAX (E6F6Y) Ab (cat#17471, Cell Signaling Technology), mouse monoclonal anti-HSC/HSP70 (W27) Ab (cat#sc-24, Santa Cruz Biotechnology Inc.), mouse monoclonal anti-HSP90α/β (F-8) Ab (cat#sc-13119, Santa Cruz Biotechnology Inc.), rabbit monoclonal anti-cleaved caspase 3 (Asp175) (D3E9) Ab (cat#9579, Cell Signaling Technology), goat polyclonal anti-c-MYC Ab (cat#AF3696, R&D Systems Inc.), mouse monoclonal anti-HA Ab (cat#901513, BioLegend Inc.), mouse monoclonal anti-βActin (GT5512) Ab (cat#GTX629630, GeneTex Inc.), normal rabbit IgG (cat#02-6102,ThermoFisher Scientific Inc.), Peroxidase AffiniPure Goat Anti-Rabbit IgG (H+L) (cat#111-035-144, Jackson ImmunoResearch Inc.), Peroxidase AffiniPure Goat Anti-Mouse IgG (H+L) (cat#115-035-003, Jackson ImmunoResearch Inc.), and Peroxidase IgG Fraction Monoclonal Mouse Anti-Goat IgG, light chain specific (cat#205-032-176, Jackson ImmunoResearch Inc.).

Techniques: Western Blot, Immunoprecipitation, Quantitation Assay, Enzyme-linked Immunosorbent Assay