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Your search keyword '"Slotte, J."' showing total 2 results
2 results on '"Slotte, J."'

1. Autocrine sphingosine-1-phosphate signalingloop enhances NF-kB-activation and survival.

Author

Blom, Tomas, Bergelin, Nina, Meinander, Annika, Löf, Christoffer, Slotte, J. Peter, Eriksson^1,3, John E., and Törnquist, Kid

Subjects
SPHINGOSINE, BIOACTIVE compounds, CELL proliferation, G proteins, CARCINOGENESIS
Abstract

Background: Sphingosine-1-phosphate (S1P) is a bioactive lipid that regulates a multitude of cellular functions, including cell proliferation, survival, migration and angiogenesis. S1P mediates its effects either by signaling through G protein-coupled receptors (GPCRs) or through an intracellular mode of action. In this study, we have investigated the mechanism behind S1P-induced survival signalling. Results: We found that S1P protected cells from FasL-induced cell death in an NF-?B dependent manner. NF-?B was activated by extracellular S1P via S1P2 receptors and Gi protein signaling. Our study also demonstrates that extracellular S1P stimulates cells to rapidly produce and secrete additional S1P, which can further amplify the NF-?B activation. Conclusions: We propose a self-amplifying loop of autocrine S1P with capacity to enhance cell survival. The mechanism provides increased understanding of the multifaceted roles of S1P in regulating cell fate during normal development and carcinogenesis. [ABSTRACT FROM AUTHOR]

Published
2010
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2. An autocrine sphingosine-1-phosphate signaling loop enhances NF-kappaB-activation and survival.

Author

Blom T, Bergelin N, Meinander A, Löf C, Slotte JP, Eriksson JE, and Törnquist K

Subjects
Adaptor Proteins, Signal Transducing genetics, Adaptor Proteins, Signal Transducing metabolism, Autocrine Communication, Calcium-Calmodulin-Dependent Protein Kinases antagonists & inhibitors, Cell Line, Tumor, Cell Survival drug effects, Cell Survival genetics, Enzyme Activation drug effects, Enzyme Activation genetics, Fas Ligand Protein metabolism, Feedback, Physiological, Flavonoids pharmacology, Humans, Lysophospholipids antagonists & inhibitors, Lysophospholipids genetics, Pyrazoles pharmacology, Pyridines pharmacology, RNA, Small Interfering genetics, Receptors, Lysosphingolipid genetics, Signal Transduction drug effects, Signal Transduction genetics, Sphingosine antagonists & inhibitors, Sphingosine biosynthesis, Sphingosine genetics, Transgenes genetics, Lysophospholipids biosynthesis, NF-kappa B metabolism, Receptors, Lysosphingolipid metabolism, Sphingosine analogs & derivatives
Abstract

Background: Sphingosine-1-phosphate (S1P) is a bioactive lipid that regulates a multitude of cellular functions, including cell proliferation, survival, migration and angiogenesis. S1P mediates its effects either by signaling through G protein-coupled receptors (GPCRs) or through an intracellular mode of action. In this study, we have investigated the mechanism behind S1P-induced survival signalling., Results: We found that S1P protected cells from FasL-induced cell death in an NF-kappaB dependent manner. NF-kappaB was activated by extracellular S1P via S1P2 receptors and Gi protein signaling. Our study also demonstrates that extracellular S1P stimulates cells to rapidly produce and secrete additional S1P, which can further amplify the NF-kappaB activation., Conclusions: We propose a self-amplifying loop of autocrine S1P with capacity to enhance cell survival. The mechanism provides increased understanding of the multifaceted roles of S1P in regulating cell fate during normal development and carcinogenesis.

Published
2010
Full Text
View/download PDF

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