Membrane interaction of TNF is not sufficient to trigger increase in membrane conductance in mammalian cells

FEBS Letters

Dunant, Yves²  Hribar, Marusa⁵  De Baetselier, Patrick¹  Lucas, Rudolf⁵  Fransen, Lucie⁴  Pugin, Jérôme⁵  van der Goot, F.Gisou³  Bloc, Alain² 

[1] Cellular Immunology, VIB, University of Brussels, Brussels, Belgium;Department of Pharmacology, University of Geneva, Geneva, Switzerland;Department of Biochemistry, Sciences II, University of Geneva, Quai Ernest-Ansermet, 1211 Geneva, Switzerland;Innogenetics, Ghent, Belgium;Division of Medical Intensive Care, University of Geneva, Geneva, Switzerland

关键词: Tumor necrosis factor;    Channel;    Membrane;    Unfolding;   

DOI  :  10.1016/S0014-5793(99)01294-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Tumor necrosis factor (TNF) can trigger increases in membrane conductance of mammalian cells in a receptor-independent manner via its lectin-like domain. A lectin-deficient TNF mutant, lacking this activity, was able to bind to artificial liposomes in a pH-dependent manner, but not to insert into the bilayer, just like wild type TNF. A peptide mimicking the lectin-like domain, which can still trigger increases in membrane currents in cells, failed to interact with liposomes. Thus, the capacity of TNF to trigger increases in membrane conductance in mammalian cells does not correlate with its ability to interact with membranes, suggesting that the cytokine does not form channels itself, but rather interacts with endogenous ion channels or with plasma membrane proteins that are coupled to ion channels.

【 授权许可】

Unknown