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The Full-Length Leptin Receptor has Signaling Capabilities of Interleukin 6-Type Cytokine Receptors
Heinz Baumann, Karen K. Morella, David W. White, Marlene Dembski, Pascal S. Bailon, Hongkyun Kim, Chun-Fai Lai and Louis A. Tartaglia
Proceedings of the National Academy of Sciences of the United States of America
Vol. 93, No. 16 (Aug. 6, 1996), pp. 8374-8378
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/39869
Page Count: 5
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The leptin receptor (OB-R) is a single membrane-spanning protein that mediates the weight regulatory effects of leptin (OB protein). The mutant allele (db) of the OB-R gene encodes a protein with a truncated cytoplasmic domain that is predicted to be functionally inactive. Several mRNA splice variants encoding OB-Rs with different length cytoplasmic domains have been detected in various tissues. Here we demonstrate that the full-length OB-R (predominantly expressed in the hypothalamus), but not a major naturally occurring truncated form or a mutant form found in db/db mice, can mediate activation of signal transducer and activator of transcription (STAT) proteins and stimulate transcription through interleukin 6 responsive gene elements. Reconstitution experiments suggest that, although OB-R mediates intracellular signals with a specificity similar to interleukin 6-type cytokine receptors, signaling appears to be independent of the gp130 signal transducing component of the interleukin 6-type cytokine receptors.
Proceedings of the National Academy of Sciences of the United States of America © 1996 National Academy of Sciences