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anti-Human DIO2 Antibodies:
anti-Mouse (Murine) DIO2 Antibodies:
anti-Rat (Rattus) DIO2 Antibodies:
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Mouse (Murine) Polyclonal DIO2 Primary Antibody for ELISA, IHC - ABIN314280
Langford, Baron, Joy, Del Valle, Shack: Contributions of HIV infection in the hypothalamus and substance abuse/use to HPT dysregulation. in Psychoneuroendocrinology 2011
Show all 5 Pubmed References
Human Polyclonal DIO2 Primary Antibody for ELISA, FACS - ABIN190862
Gumieniak, Perlstein, Williams, Hopkins, Brown, Raby, Williams: Ala92 type 2 deiodinase allele increases risk for the development of hypertension. in Hypertension 2007
Show all 2 Pubmed References
TSHR mutations along with DIO2 T92A SNP ("double hit") may lead to a significant reduction in DIO2 activity stimulated by TSH, and thereby may have clinical relevance in a select population of hypothyroidism patients who might benefit from a T3/T4 combination therapy.
D2-Thr92Ala polymorphism in hypothyroid patients can be related to lower levels of intracellular T3 and consequently to a peripheral hypothyroidism. D2-Thr92Ala polymorphism has been related to more severe type 2 diabetes. [review]
DIO2 catalytic activity is lower in carriers of Thr92Ala polymorphism, who also exhibit localized or systemic hypothyroidism. DIO2 Thr92Ala also localizes abnormally to the Golgi apparatus. African American carriers of Thr92Ala-DIO2 exhibit an about 30% higher risk of developing Alzheimer's disease.
type II iodothyronine deiodinase polymorphism Thr92Ala (DII-Thr92-Ala, rs225014) is a risk plays a role in glycosylated hemoglobin metabolism
adipocyte-derived DIO2 may play a role in weight maintenance but is likely not a major contributor to obesity-related insulin resistance
Thr92AlaD2 was associated with molecular markers known to underlie Alzheimer disease (AD) pathogenesis in African Americans (AAs), translating to an observed phenotype of increased odds of developing AD/dementia in AAs in these populations. Thr92AlaD2 might represent one factor contributing to racial discrepancies in incident AD.
In vitro, GH significantly increased D2 expression at the mRNA level in HTC/C3 cells, as well as D2 protein and its activity. GH increased serum fT3 level and decreased serum fT4 level in humans. Our results suggest that its mechanism involves D2 upregulation.
the low frequency of the TT genotype D2 rs225014 polymorphism was associated with the development of AITD and severity of HD.
Expression of DIO2 mRNA/protein was reduced in recurrent depressive disorders.
The Thr92Ala polymorphism of D2 was not associated with thyroid parameters, HRQoL, and cognitive functioning in the general population and in participants on thyroid hormone replacement therapy.
Thyroidectomized patients carrying DIO2 Thr92Ala are at increased risk of reduced intracellular and serum T3 concentrations that are not adequately compensated for by LT4, thus providing evidence in favor of customized treatment of hypothyroidism in athyreotic patients.
D2-Thr92Ala genetic variant is associated with the severity and the obstetric outcome of preeclampsia, and it also influences thyroid hormone levels.
Homozygosity for the Dio2 Thr92Ala polymorphism is associated with higher HbA1C levels in type 2 diabetes patients. [Meta-Analysis]
the reduction of SAT DIO2 expression is negatively correlated with DBP and TG levels that are associated with the MetS. This might have an effect on developing MetS.
In subjects who are alcohol dependent, the rs225014 DIO2 gene was associated with significant differences in the amount of naturalistic alcohol drinking.
Data provide evidence in humans that genetic predisposition combined with early osteoarthritis-related changes results in loff of epigenetic silencing of DIO2.
DIO2 gene plays a role in the etiology of recurrent depressive disorder.Association of the DIO2 gene single nucleotide polymorphisms with recurrent depressive disorder.
DIO2 gene polymorphisms may play a role in the incidence of MCI in male patients.
conversion of T4 to T3 by D2 is required for TRalpha1/PI3K-mediated nongenomic actions of T4 in HUVECs, including stimulation of Akt phosphorylation and Rac activation, which result in cell migration.
Thyroid hormone deiodinases D1, D2, and D3 are differentially expressed in endothelial cells following thyroid hormone exposure.
Type 2 deiodinase polymorphism causes ER stress and hypothyroidism in the brain.
Upregulation of DIO2 in CRC.
Mice experiencing a 3 hours of status epilepticus exhibit a rapid increase in expression of Dio2 and a decrease in the expression of Dio3 gene in hippocampus, amygdala and prefrontal cortex. Dio2 induction caused by SE accelerates production of T3 in different areas of the central nervous system and modifies the hippocampal gene expression profile, affecting the balance between adaptive and maladaptive mechanisms.
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.
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)
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.
Two mouse models of early developmental disruption of Dio2 in myocyte precursor exhibit no significant skeletal muscle phenotype.
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.
The consistent association between Calr and Dio2 expression suggests that enhanced expression of these two genes facilitate detrimental effects on cartilage integrity.
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
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.
Perinatal deiodinase 2 expression in hepatocytes defines epigenetic susceptibility to liver steatosis and obesity.
Data show that type 2 deiodinase (Dio2) inactivation in skeletal myocytes preserves T3 thyroid hormone content and only mildly disrupts thyroid hormone signaling.
D2KO mice do have normal articular cartilage and no other features of spontaneous joint damage, but exhibit increased subchondral bone mineral content
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.
These studies reveal that tissue-specific differences in D2 ubiquitination are an inherent property of the TRH/TSH feedback mechanism
congenital severe reduction of thyrotroph Dio2 causes a major impairment of the TSH response to hypothyroidism
Within the supportive environment of a research vivarium, mice lacking all three deiodinases can be bred and survive.
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.
Data indicate that deiodinase Dio2 was mainly localized in stroma cells before implantation, whereas deiodinase Dio3 was highly expressed in stromal cells after implantation.
In zebrafish embryos, D2 knockdown increased mortality during pneumococcal meningitis.
essential to assure normal development
Knockdown of D1+D2 (D1D2MO) and knockdown of D3 (D3MO) both resulted in transcriptional regulation of energy metabolism and (muscle) development in abdomen and tail
This study investigated deiodinase 1 (Dio1), deiodinase 2 (Dio2), and deiodinase 3 (Dio3) mRNA expression at the several zebrafish life stages and found life stage specific expression of these genes that were highly localized.
role in zebrafish embryonic development
The expression of D2 activity in thyroid and skeletal muscle is of particular interest for studies on the importance of this enzyme in hypothyroidism
Increased expression of mammary TRbeta1 and DIO2, and decreased RXRalpha, provide a mechanism to increase thyroid hormone activity within the mammary gland during lactation.
No changes in TRb or DI-2 and DI-3 expression in tail tissue collected from Triclosan exposure larvae were found.
converts thyroxine to the active hormone 3,5,3'-triiodothyronine in peripheral tissues
The protein encoded by this gene belongs to the iodothyronine deiodinase family. It activates thyroid hormone by converting the prohormone thyroxine (T4) by outer ring deiodination (ORD) to bioactive 3,3',5-triiodothyronine (T3). It is highly expressed in the thyroid, and may contribute significantly to the relative increase in thyroidal T3 production in patients with Graves disease and thyroid adenomas. This protein contains selenocysteine (Sec) residues encoded by the UGA codon, which normally signals translation termination. The 3' UTR of Sec-containing genes have a common stem-loop structure, the sec insertion sequence (SECIS), which is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Alternative splicing results in multiple transcript variants encoding different isoforms.
thyroxine deiodinase, type II
, type 2 DI
, type 2 iodothyronine deiodinase
, type II iodothyronine deiodinase
, type-II 5'-deiodinase
, type-II 5'deiodinase
, iodothyronine type II deiodinase
, type-II 5' deiodinase
, deiodinase, iodothyronine, type 2
, deiodinase, iodothyronine, type II
, deiodinase 2
, type 2 deiodinase