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Updated: Dec 30, 2025

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody mAb by Neutralizing TNF Using an In Vitro Bioanalytical Method

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody mAb by Neutralizing TNF Using an In Vitro Bioanalytical Method

Published on: September 16, 2017

Methods for Studying TNFα-Induced Autophagy.

Sheyda Najafi¹, Ehab M Abo-Ali¹, Vikas V Dukhande²

¹Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.

Methods in Molecular Biology (Clifton, N.J.)

|January 16, 2020

Summary

This summary is machine-generated.

This study explores how tumor necrosis factor-alpha (TNFα) influences autophagy, a key cellular process for maintaining homeostasis. We detail methods like immunoblotting and fluorescence microscopy to measure autophagy changes induced by TNFα.

Keywords:

Apoptosis Autophagy Bafilomycin A1 Chloroquine Fluorescence microscopy Immunoblotting LC3 TNFα p62

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Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody mAb by Neutralizing TNF Using an In Vitro Bioanalytical Method

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Published on: July 21, 2017

Area of Science:

Cellular Biology
Molecular Biology
Biochemistry

Background:

Autophagy is a fundamental eukaryotic process crucial for cellular homeostasis, involving the degradation of damaged components and long-lived proteins.
Cytokines, such as tumor necrosis factor-alpha (TNFα), are signaling proteins that modulate diverse biological activities, including inflammation and cell death.
TNFα is known to induce both inflammation and autophagy, highlighting its role in cellular stress responses.

Purpose of the Study:

To describe experimental techniques for quantifying autophagy.
To investigate the impact of TNFα on cellular autophagy.
To provide a framework for studying cytokine-mediated autophagy.

Main Methods:

Immunoblotting techniques to detect autophagy-related proteins.
Fluorescence microscopy to visualize autophagic structures.
Cell treatment with TNFα to induce autophagy.

Main Results:

TNFα treatment demonstrably alters autophagy markers.
Specific experimental methods allow for the measurement of these alterations.
The study provides a basis for further research into TNFα-autophagy interactions.

Conclusions:

Autophagy is a critical cellular mechanism regulated by external stimuli like TNFα.
Established techniques like immunoblotting and fluorescence microscopy are effective for studying TNFα-induced autophagy.
Understanding these pathways is vital for cellular homeostasis and disease research.