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murine D2 knockout macrophages exhibited impaired phagocytosis and partially reduced cytokine response to stimulation with bacterial endotoxin. These effects are presumably due to reduced intracellular T3 availability.
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Regulation of the expression and activity of the deiodinases constitutes a cell-autonomous, pre-receptor mechanism that controls crucial steps during the various phases of myogenesis. (Review)
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Results indicate that basal cell carcinoma cells constitute an example in which the thyroid hormone signal is finely tuned by the concerted expression of opposite-acting deiodinases. The dual regulation of Dio2 and Dio3 expression plays a critical role in cell cycle progression and cell death by influencing cyclin D1-mediated entry into the G1-S phase.
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Two mouse models of early developmental disruption of Dio2 in myocyte precursor exhibit no significant skeletal muscle phenotype.
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Dio3-/- mice display degeneration of retinal cones, the photoreceptors that mediate daylight and color vision. In Dio2-/- mice, cone function was largely normal but deletion of Dio2 in Dio3-/- mice markedly recovered cone numbers and electroretinogram responses, suggesting counterbalancing roles for both enzymes in cone survival.
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The consistent association between Calr and Dio2 expression suggests that enhanced expression of these two genes facilitate detrimental effects on cartilage integrity.
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mice with astrocyte-specific Dio2 inactivation (Astro-D2KO) have normal serum T3 but exhibit anxiety-depression-like behavior as found in open field and elevated plus maze studies and when tested for depression using the tail-suspension and the forced-swimming tests
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Mice subjected to a running regime have significant increased cartilage damage and synovitis scores. Lack of Dio2 protected against cartilage damage in this model and was reflected in a specific gene expression profile.
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Perinatal deiodinase 2 expression in hepatocytes defines epigenetic susceptibility to liver steatosis and obesity.
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Data show that type 2 deiodinase (Dio2) inactivation in skeletal myocytes preserves T3 thyroid hormone content and only mildly disrupts thyroid hormone signaling.
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D2KO mice do have normal articular cartilage and no other features of spontaneous joint damage, but exhibit increased subchondral bone mineral content
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The motor alterations observed in D2KO mice indicate an important role for D2 in T3 availability to maintain motor function and muscle strength. Our results suggest a possible implication of D2 in motor disorders.
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These studies reveal that tissue-specific differences in D2 ubiquitination are an inherent property of the TRH/TSH feedback mechanism
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congenital severe reduction of thyrotroph Dio2 causes a major impairment of the TSH response to hypothyroidism
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Within the supportive environment of a research vivarium, mice lacking all three deiodinases can be bred and survive.
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Systemic changes in thyroid hormone economy as a result of acute food deprivation are not dependent on the deiodinases D1 or D2 but are mediated in part by sequestration of type 4 and type 3 in tissues and their enhanced metabolism by deiodinase D3.
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Data indicate that deiodinase Dio2 was mainly localized in stroma cells before implantation, whereas deiodinase Dio3 was highly expressed in stromal cells after implantation.
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Data suggest that hepatic deiodinase type 2 (D2) favors the innate immune response by specifically regulating cellular thyroid hormone levels in macrophages.
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Data suggest that type 2 deiodinase is induced in inflammation of tanycytes (as in inflammation of periventricular area, arcuate nucleus, and median eminence of hypothalamus); this enzyme induction appears to involve NFkappaB signaling.
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Data suggest that type 2 deiodinase induction (and kinetics of induction) in animal models of inflammation of leptomeninges, choroid plexus, and brain blood vessels is tissue specific and species specific.
