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triacsin c (MedChemExpress)

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MedChemExpress triacsin c

PTEN KO HepG2 cells generate more TG and less PC than do control cells upon treatment with OA:PA. Shown are lipidomic analyses of ( A ) phosphatidylcholine that contains OA or PA; ( B ) phosphatidylethanolamine that contains OA or PA; and ( C ) triglycerides that contain OA or PA. ( D ) Cells were treated with or without <t>Triacsin</t> <t>C</t> (2.5 µM) for 8 h alone or together with OA:PA for the indicated times. Tg treatment (2.5 µg/mL, 8 h) was used as a positive control. Shown is a representative immunoblot of three repetitions. p97 and β-actin were used as a loading control.

Triacsin C, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hy-n6707/Triacsin+C/pmc13027169-236-0-3
Average 94 stars, based on 20 article reviews

triacsin c - by Bioz Stars, 2026-10

94/100 stars

Images

1) Product Images from "Deficiency of PTEN Confers Hypersensitivity to Fatty Acid-Mediated ER Stress in Transformed Hepatocytes"

Article Title: Deficiency of PTEN Confers Hypersensitivity to Fatty Acid-Mediated ER Stress in Transformed Hepatocytes

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms27062778

Figure Legend Snippet: PTEN KO HepG2 cells generate more TG and less PC than do control cells upon treatment with OA:PA. Shown are lipidomic analyses of ( A ) phosphatidylcholine that contains OA or PA; ( B ) phosphatidylethanolamine that contains OA or PA; and ( C ) triglycerides that contain OA or PA. ( D ) Cells were treated with or without Triacsin C (2.5 µM) for 8 h alone or together with OA:PA for the indicated times. Tg treatment (2.5 µg/mL, 8 h) was used as a positive control. Shown is a representative immunoblot of three repetitions. p97 and β-actin were used as a loading control.

Techniques Used: Control, Positive Control, Western Blot

Solvent:

Article Title: ACSL5 programs fatty acid metabolism and mitochondrial fitness to sustain pathogenic T cells and exacerbate Sjögren's syndrome
Article Snippet: To activate the Jurkat T cells, the cells were plated in 6-well plates precoated with anti-CD3 (1 μg/mL; Thermo Fisher, Cat# 16-0037-81) and anti-CD28 (2 μg/mL; Thermo Fisher, Cat# 16-0281-82) antibodies. .. Female NOD/Ltj mice (8 weeks old; GemPharmatech, Nanjing, China) under specific pathogen-free (SPF) conditions received intraperitoneal injections of etomoxir (15 mg/kg; Selleck, Houston, TX, USA; Cat# S8244), Triacsin C (15 mg/kg; MedChemExpress, Monmouth Junction, NJ, USA; Cat# HY-N6707), or the solvent control twice weekly for one month. ..

Control:

other:

Article Title: A Polarity-Sensitive Lipid Droplet Probe Reveals Aβ Species-Dependent Lipid Droplet Remodeling in Microglia.
Article Snippet: ABSTRACT: Microglial lipid metabolic alterations are increasingly implicated in Alzheimer’s disease (AD), yet the specific β-amyloid (Aβ) species involved in lipid droplet (LD) remodeling remain unclear.. Precise visualization of LD morphology in complex biological systems is limited by the availability of selective and photostable probes.. Herein, we report a polarity-sensitive LD probe, BODIPY-LD, constructed with a donor−π−acceptor−π−donor (D−π−A−π−D) framework that enables hydrophobic targeting and intramolecular charge transfer (ICT)-based fluorescence activation in low-polarity environments.

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LD reduction induces lipid peroxidation and mitochondrial dysfunction in DGAT1-deficient cells. A–C, Representative immunofluorescence images ( A ) and relative integrated intensities of LD staining ( B and C ) in control and DGAT1- KO or pradigastat-treated B16F10 cells. Scale bars, 25 µm. D and E, Quantification of MDA levels in control and DGAT1-KO ( D ) or pradigastat-treated ( E ) B16F10 cells. F–J, Levels of TG ( F ), DHA-cholesteryl ester (DHA-CE) 22:6 ( G ), HexCer d18:2/20:0 ( H ), HexCer d18:2/22:0 ( I ), and HexCer d18:2/23:0 ( J ) in control and DGAT1-KO B16F10 cells. K–M, JC-1 dye staining showing representative immunofluorescence images of MMP ( K ) and monomer/aggregate ratios in control ( L ), DGAT1- KO ( M ), or pradigastat-treated B16F10 cells. Scale bars, 25 µm. N and O, Flow cytometry analysis of ROS levels ( N ) and mean fluorescence intensity (MFI; O ) in control and DGAT1- KO B16F10 cells. P and Q, Flow cytometry analysis of ROS levels ( P ) and MFI ( Q ) in control and pradigastat-treated B16F10 cells. R and S, Representative immunofluorescence images ( R ) and relative integrated intensities of LD staining ( S ) in control and triacsin C–treated B16F10 cells. Scale bars, 25 µm. T, Quantification of MDA levels in control and triacsin C–treated B16F10 cells. U and V, Flow cytometry analysis of ROS levels ( U ) and mean fluorescence intensity ( V ) in control and triacsin C–treated B16F10 cells. Error bars represent ±SEM throughout the figure. P values were calculated using an unpaired t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. VC, vector control.

Journal: Cancer Research

Article Title: DGAT1 Inhibition Induces Ferroptosis and Enhances Cancer Immunotherapy Efficacy

doi: 10.1158/0008-5472.CAN-25-0840

Figure Lengend Snippet: LD reduction induces lipid peroxidation and mitochondrial dysfunction in DGAT1-deficient cells. A–C, Representative immunofluorescence images ( A ) and relative integrated intensities of LD staining ( B and C ) in control and DGAT1- KO or pradigastat-treated B16F10 cells. Scale bars, 25 µm. D and E, Quantification of MDA levels in control and DGAT1-KO ( D ) or pradigastat-treated ( E ) B16F10 cells. F–J, Levels of TG ( F ), DHA-cholesteryl ester (DHA-CE) 22:6 ( G ), HexCer d18:2/20:0 ( H ), HexCer d18:2/22:0 ( I ), and HexCer d18:2/23:0 ( J ) in control and DGAT1-KO B16F10 cells. K–M, JC-1 dye staining showing representative immunofluorescence images of MMP ( K ) and monomer/aggregate ratios in control ( L ), DGAT1- KO ( M ), or pradigastat-treated B16F10 cells. Scale bars, 25 µm. N and O, Flow cytometry analysis of ROS levels ( N ) and mean fluorescence intensity (MFI; O ) in control and DGAT1- KO B16F10 cells. P and Q, Flow cytometry analysis of ROS levels ( P ) and MFI ( Q ) in control and pradigastat-treated B16F10 cells. R and S, Representative immunofluorescence images ( R ) and relative integrated intensities of LD staining ( S ) in control and triacsin C–treated B16F10 cells. Scale bars, 25 µm. T, Quantification of MDA levels in control and triacsin C–treated B16F10 cells. U and V, Flow cytometry analysis of ROS levels ( U ) and mean fluorescence intensity ( V ) in control and triacsin C–treated B16F10 cells. Error bars represent ±SEM throughout the figure. P values were calculated using an unpaired t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. VC, vector control.

Article Snippet: Triacsin C (2 μmol/L; MCE, cat. #HY-N6707) was administered to cells for 48 hours to induce the LDs.

Techniques: Immunofluorescence, Staining, Control, Flow Cytometry, Fluorescence, Plasmid Preparation

DGAT1 deficiency induces GPX4 depletion and a ferroptosis phenotype. A–D, Quantification of GSH levels in control and DGAT1- KO or pradigastat-treated B16F10 ( A and B ) and A375 ( C and D ) cells. E, Quantification of GSH levels in control and triacsin C–treated B16F10 cells. F, Representative TEM images of mitochondria in control and DGAT1-KO or pradigastat-treated B16F10 cells. Scale bars, 0.5 µm. G and H, Western blot analysis of GPX4 expression in control and DGAT1- KO or pradigastat-treated B16F10 ( G ) and A375 ( H ) cells. I and J, Representative TEM images of mitochondria in control and DGAT1-KO ( I ) or pradigastat-treated ( J ) B16F10 cells combined with Fer-1 treatment. Scale bars, 0.5 µm. K and L, Western blot analysis of GPX4 levels in control and DGAT1- KO ( K ) or pradigastat-treated ( L ) B16F10 cells combined with Fer-1 treatment. M and N, Tumor growth delay ( M ) and Kaplan–Meier survival curves ( N ) in C57BL/6 mice inoculated subcutaneously with 1 × 10 5 DGAT1- KO B16F10 cells and treated with Fer-1 and anti–PD-1 antibody or isotype control. O, Quantification of MDA levels in control, DGAT1- KO, RSL3, and DGAT1-KO combined RSL3-treated B16F10 cells. P and Q, Tumor growth delay ( P ) and Kaplan–Meier survival curves ( Q ) in C57BL/6 mice inoculated subcutaneously with 1 × 10 5 DGAT1- KO B16F10 cells and treated with RSL3 and anti–PD-1 antibody or isotype control. Error bars represent ±SEM throughout the figure. P values were determined by unpaired t test ( A–E and O ), two-way ANOVA ( M and P ), and log-rank test ( N and Q ), respectively. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant. VC, vector control.

Journal: Cancer Research

Article Title: DGAT1 Inhibition Induces Ferroptosis and Enhances Cancer Immunotherapy Efficacy

doi: 10.1158/0008-5472.CAN-25-0840

Figure Lengend Snippet: DGAT1 deficiency induces GPX4 depletion and a ferroptosis phenotype. A–D, Quantification of GSH levels in control and DGAT1- KO or pradigastat-treated B16F10 ( A and B ) and A375 ( C and D ) cells. E, Quantification of GSH levels in control and triacsin C–treated B16F10 cells. F, Representative TEM images of mitochondria in control and DGAT1-KO or pradigastat-treated B16F10 cells. Scale bars, 0.5 µm. G and H, Western blot analysis of GPX4 expression in control and DGAT1- KO or pradigastat-treated B16F10 ( G ) and A375 ( H ) cells. I and J, Representative TEM images of mitochondria in control and DGAT1-KO ( I ) or pradigastat-treated ( J ) B16F10 cells combined with Fer-1 treatment. Scale bars, 0.5 µm. K and L, Western blot analysis of GPX4 levels in control and DGAT1- KO ( K ) or pradigastat-treated ( L ) B16F10 cells combined with Fer-1 treatment. M and N, Tumor growth delay ( M ) and Kaplan–Meier survival curves ( N ) in C57BL/6 mice inoculated subcutaneously with 1 × 10 5 DGAT1- KO B16F10 cells and treated with Fer-1 and anti–PD-1 antibody or isotype control. O, Quantification of MDA levels in control, DGAT1- KO, RSL3, and DGAT1-KO combined RSL3-treated B16F10 cells. P and Q, Tumor growth delay ( P ) and Kaplan–Meier survival curves ( Q ) in C57BL/6 mice inoculated subcutaneously with 1 × 10 5 DGAT1- KO B16F10 cells and treated with RSL3 and anti–PD-1 antibody or isotype control. Error bars represent ±SEM throughout the figure. P values were determined by unpaired t test ( A–E and O ), two-way ANOVA ( M and P ), and log-rank test ( N and Q ), respectively. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant. VC, vector control.

Article Snippet: Triacsin C (2 μmol/L; MCE, cat. #HY-N6707) was administered to cells for 48 hours to induce the LDs.

Techniques: Control, Western Blot, Expressing, Plasmid Preparation

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triacsin c (MedChemExpress)

Structured Review

Images

1) Product Images from "Deficiency of PTEN Confers Hypersensitivity to Fatty Acid-Mediated ER Stress in Transformed Hepatocytes"

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