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Physiology and pathophysiology of the RANKL/RANK system
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Reiko Hanada
Published/Copyright:
November 18, 2010
Abstract
The TNF family molecule RANKL and its receptor RANK are key regulators of bone remodeling, lymph node formation, and mammary gland development during pregnancy. RANKL and RANK are also expressed in the central nervous systems (CNS). However, the functional relevance of RANKL/RANK in the brain was entirely unknown. Recently, our group reported that the RANKL/RANK signaling pathway has an essential role in the central regulation of body temperature via the prostaglandin axis. This review discusses novel aspects of the RANKL/RANK system as key regulators of fever and female basal body temperature in the CNS.
Received: 2010-7-21
Accepted: 2010-9-26
Published Online: 2010-11-18
Published in Print: 2010-12-01
©2010 by Walter de Gruyter Berlin New York
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Articles in the same Issue
- Minireview
- Physiology and pathophysiology of the RANKL/RANK system
- Genes and Nucleic Acids
- Murine aldo-keto reductase family 1 subfamily B: identification of AKR1B8 as an ortholog of human AKR1B10
- Characterization of plant miRNAs and small RNAs derived from potato spindle tuber viroid (PSTVd) in infected tomato
- Protein Structure and Function
- Characterization of a mutant R11H αB-crystallin associated with human inherited cataract
- Secretion of hepatoma-derived growth factor is regulated by N-terminal processing
- Twin arginine translocation (Tat)-dependent protein transport: the passenger protein participates in the initial membrane binding step
- Kinetic and structural characterization of bacterial glutaminyl cyclases from Zymomonas mobilis and Myxococcus xanthus
- Membranes, Lipids, Glycobiology
- Quantitative determination of haptoglobin glycoform variants in psoriasis
- Molecular Medicine
- Bile acid retention and activation of endogenous hepatic farnesoid-X-receptor in the pathogenesis of fatty liver disease in ob/ob-mice
- Cell Biology and Signaling
- Acute and long-term effects of metformin on the function and insulin secretory responsiveness of clonal β-cells
- Proteolysis
- Increase of SARS-CoV 3CL peptidase activity due to macromolecular crowding effects in the milieu composition
- Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin
- Acknowledgement
- Acknowledgement
