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Related Concept Videos

Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
Regioselective Formation of Enolates01:33

Regioselective Formation of Enolates

As depicted in the figure below, the unsymmetrical ketones can form two possible enolates: less substituted or more substituted enolates. Usually, the thermodynamic enolates are formed from the more substituted α-carbon atom, while the kinetic enolates are formed faster by deprotonation from the less substituted position. The thermodynamic enolates have lower energy, so they are more stable. But the energy required to form kinetic enolates is less.
Regulation of Metabolism01:19

Regulation of Metabolism

Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
Enzyme Inhibition01:30

Enzyme Inhibition

Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.

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Related Experiment Video

Updated: May 28, 2026

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
07:45

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis

Published on: November 28, 2015

Selective MIF Enolase Inhibitor TE-91 Regulates M1 Polarization and Associated Metabolic Reprogramming.

Péter Deák1, Nikoletta Kálmán1, Csenge Antus1

  • 1Department of Biochemistry and Medical Chemistry, University of Pécs, Medical School, H-7624 Pécs, Hungary.

Antioxidants (Basel, Switzerland)
|May 27, 2026
PubMed
Summary
This summary is machine-generated.

The study shows that TE-91, a macrophage migration inhibitory factor (MIF) enolase inhibitor, reduces M1 macrophage polarization by altering cellular metabolism and decreasing inflammatory markers. This highlights the role of MIF

Keywords:
M1 polarizationMIFOXPHOSglycolysismetabolic reprogrammingoxidative bursttautomerase

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Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
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Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Published on: September 13, 2024

Related Experiment Videos

Last Updated: May 28, 2026

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
07:45

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis

Published on: November 28, 2015

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
11:12

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Published on: September 13, 2024

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Macrophage migration inhibitory factor (MIF) drives M1 macrophage polarization, oxidative stress, and metabolic reprogramming.
  • Selective inhibitors targeting MIF's ketonase or enolase sub-activities offer potential therapeutic strategies.

Purpose of the Study:

  • To investigate the role of MIF's enolase sub-activity in M1 macrophage polarization.
  • To evaluate the effects of the selective enolase inhibitor TE-91 on M1 polarization and associated cellular processes.

Main Methods:

  • In silico molecular docking and physicochemical characterization of TE-91.
  • Utilized LPS + IFN-γ-induced RAW264.7 cells as an M1 macrophage activation model.
  • Assessed oxidative stress (ROS), nitrite production, cytokine/chemokine levels (ELISA, qPCR, immunoblot), and cellular metabolic rates (oxygen consumption, extracellular acidification).

Main Results:

  • TE-91 demonstrated potential binding to the MIF tautomerase active site.
  • TE-91 inhibited M1 activation by enhancing oxidative phosphorylation and reducing glycolysis.
  • TE-91 decreased mRNA transcription of TNF-α, IL-6, CCL2, and iNOS, and reduced ROS, nitrite, and IL-6 production, while impacting IL-1β cleavage.

Conclusions:

  • MIF's enolase sub-activity plays a significant role in M1 macrophage polarization.
  • TE-91 effectively modulates M1 polarization and associated inflammatory responses, suggesting therapeutic potential.