TY - JOUR
T1 - Membrane interaction of TNF is not sufficient to trigger increase in membrane conductance in mammalian cells
AU - Van Der Goot, F. Gisou
AU - Pugin, Jérôme
AU - Hribar, Marusa
AU - Fransen, Lucie
AU - Dunant, Yves
AU - De Baetselier, Patrick
AU - Bloc, Alain
AU - Lucas, Rudolf
N1 - Funding Information:
This work was supported by grants from the Swiss National Foundation for Scientific Research (32-50764 to J.P., 3100-49195.96 to F.G.V.D.G., 3147268.96 to A.B., and to Y.D.). J.P. is the recipient of a fellowship from the Prof. Dr. Max Cloëtta Foundation. M.H. was supported by the Slovenian Ministry of Science.
Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1999/10/22
Y1 - 1999/10/22
N2 - 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. Copyright (C) 1999 Federation of European Biochemical Societies.
AB - 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. Copyright (C) 1999 Federation of European Biochemical Societies.
KW - Channel
KW - Membrane
KW - Tumor necrosis factor
KW - Unfolding
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U2 - 10.1016/S0014-5793(99)01294-6
DO - 10.1016/S0014-5793(99)01294-6
M3 - Article
C2 - 10571070
AN - SCOPUS:0032833505
SN - 0014-5793
VL - 460
SP - 107
EP - 111
JO - FEBS Letters
JF - FEBS Letters
IS - 1
ER -