Abstract
The leptin receptor (OB-R) bears homology to members of the class I cytokine receptor family. We demonstrate that leptin binding to OB-R stimulates formation of STAT-1 and STAT-3 complexes, thereby defining transcriptional motifs for genes that are under leptin control. Transfected fa OB-R bound leptin with equal affinity to that of wild type OB-R. fa OB-R abundance was about 7 fold reduced compared to control cells. Surprisingly, the low level of fa OB-R is fully capable of activating the STAT signal transduction pathway. We discuss plausible explanations for the obese phenotype in Zucker fatty rats.
MeSH terms
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Animals
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Base Sequence
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COS Cells
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Carrier Proteins / biosynthesis*
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Carrier Proteins / physiology*
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Cell Line
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DNA Probes
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DNA-Binding Proteins / metabolism*
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Hypothalamus / metabolism
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Kinetics
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Leptin
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Mice
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Obesity
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Oligodeoxyribonucleotides
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Polymerase Chain Reaction
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Proteins / metabolism
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Proteins / pharmacology
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Rats
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Rats, Zucker
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Receptors, Cell Surface*
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Receptors, Leptin
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Recombinant Proteins / biosynthesis
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STAT1 Transcription Factor
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STAT3 Transcription Factor
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Signal Transduction*
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Trans-Activators / metabolism*
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Transfection
Substances
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Carrier Proteins
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DNA Probes
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DNA-Binding Proteins
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Leptin
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Oligodeoxyribonucleotides
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Proteins
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Receptors, Cell Surface
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Receptors, Leptin
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Recombinant Proteins
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STAT1 Transcription Factor
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STAT3 Transcription Factor
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Stat1 protein, mouse
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Stat1 protein, rat
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Stat3 protein, mouse
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Stat3 protein, rat
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Trans-Activators
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leptin receptor, mouse