Molecular and Cellular Biology · 2006 · 100 citations · 50 references
Life SciencesGeneticsMolecular GeneticsCell SignalingMolecular PhysiologySignal TransductionHormone Binding ProteinsRodent EndocrinologyThyroid EndocrinologyThyroid Hormone BiochemistryWnt SignalingDeiodinase EnzymesDeiodinase RegulationDickkopf ProteinsIodothyronine DeiodinaseThyroid Hormone Binding ProteinsThyroid Hormone Metabolism AlterationsThyroid Hormone PhysiologyWnt Antagonists
dickkopf (dkk) genes encode a small family of secreted Wnt antagonists, except for dkk3, which is divergent and whose function is poorly understood. Here, we describe the generation and characterization of dkk3 mutant mice. dkk3-deficient mice are viable and fertile. Phenotypic analysis shows no major alterations in organ morphology, physiology, and most clinical chemistry parameters. Since Dkk3 was proposed to function as thyroid hormone binding protein, we have analyzed deiodinase activities, as well as thyroid hormone levels. Mutant mice are euthyroid, and the data do not support a relationship of dkk3 with thyroid hormone metabolism. Altered phenotypes in dkk3 mutant mice were observed in the frequency of NK cells, immunoglobulin M, hemoglobin, and hematocrit levels, as well as lung ventilation. Furthermore, dkk3-deficient mice display hyperactivity.
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