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抗Mouse (Murine) DIO3 抗体:
抗Rat (Rattus) DIO3 抗体:
抗Human DIO3 抗体:
Hamster Polyclonal DIO3 Primary Antibody for FACS, IHC (p) - ABIN446380
Kalló, Mohácsik, Vida, Zeöld, Bardóczi, Zavacki, Farkas, Kádár, Hrabovszky, Arrojo E Drigo, Dong, Barna, Palkovits, Borsay, Herczeg, Lechan, Bianco, Liposits, Fekete, Gereben: A novel pathway regulates thyroid hormone availability in rat and human hypothalamic neurosecretory neurons. in PLoS ONE 2012
Show all 9 Pubmed References
Hamster Polyclonal DIO3 Primary Antibody for ICC, IF - ABIN410067
Freitas, Gereben, Castillo, Kalló, Zeöld, Egri, Liposits, Zavacki, Maciel, Jo, Singru, Sanchez, Lechan, Bianco: Paracrine signaling by glial cell-derived triiodothyronine activates neuronal gene expression in the rodent brain and human cells. in The Journal of clinical investigation 2010
Show all 6 Pubmed References
Hamster Polyclonal DIO3 Primary Antibody for IHC (p), WB - ABIN446381
Jo, Kalló, Bardóczi, Arrojo e Drigo, Zeöld, Liposits, Oliva, Lemmon, Bixby, Gereben, Bianco: Neuronal hypoxia induces Hsp40-mediated nuclear import of type 3 deiodinase as an adaptive mechanism to reduce cellular metabolism. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2012
Show all 4 Pubmed References
Polyclonal DIO3 Primary Antibody for WB - ABIN540383
Baqui, Botero, Gereben, Curcio, Harney, Salvatore, Sorimachi, Larsen, Bianco: Human type 3 iodothyronine selenodeiodinase is located in the plasma membrane and undergoes rapid internalization to endosomes. in The Journal of biological chemistry 2003
Show all 3 Pubmed References
Polyclonal DIO3 Primary Antibody for WB - ABIN540382
Huang, Fish, Dorfman, Salvatore, Kozakewich, Mandel, Larsen: A 21-year-old woman with consumptive hypothyroidism due to a vascular tumor expressing type 3 iodothyronine deiodinase. in The Journal of clinical endocrinology and metabolism 2002
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Paternal inheritance of IG-DMR-Rep deletion allele resulted in loss of methylation imprints at IG-DMR through embryonic development and maternalization of the paternal Dlk1-Dio3 domain, indicating that IG-DMR-Rep is essential for paternal-derived imprinting status of the domain through maintenance of DNA methylation at paternal IG-DMR.
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.
long noncoding RNAs in the Dlk1-Dio3 locus, particularly Meg3, play a critical role in maintaining postmitotic motor neuron cell fate.
Results demonstrate that DIO3 is essential for normal aggression and maternal behaviors, and indicate that abnormal local regulation of thyroid hormone action in the brain may contribute to the social deficits associated with neurodevelopmental disorders.
Functional analysis revealed that ground-state miRNAs embedded in the Dlk1-Dio3 locus (miR-541-5p, miR-410-3p, and miR-381-3p) promoted pluripotency via inhibition of multi-lineage differentiation and stimulation of self-renewal
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)
Cardiac D3 is induced in a mouse model of dilated cardiomyopathy, indicating that D3 induction may be a general response to diverse forms of cardiomyopathy.
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.
A critical role for reduced intracellular TH concentrations in neutrophil function during infection, for which the TH inactivating enzyme D3 appears essential.
Gene body methylation of noncoding RNA genes was observed and among these microRNA genes were prominent. Of particular note, observed only in hyperphenylalaninemic animals, was hypomethylation of miRNA genes within the imprinted Dlk1-Dio3 locus on chromosome 12.
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 marked phenotypic abnormalities observed in the D3-deficient mouse, including perinatal mortality, growth retardation, and central hypothyroidism in adult animals, require expression of MCT8, confirming the interdependent relationship between the TH transport into cells and the deiodination processes.
The brain-specific miR-379/miR-410 gene cluster at the imprinted Dlk1-Dio3 domain is implicated in several aspects of brain development and function.
DNA methylation regulates genomic imprinted DLK1-Dio3 miRNAs in autoimmune lupus
identify the molecular regulators involved in the recruitment of AFF3 to gDMRs and provide mechanistic insight into the requirement of AFF3 at an enhancer for the expression of an approximately 200-kb polycistronic transcript within the imprinted Dlk1-Dio3 locus
Dppa3 has a critical role in generation of fully reprogrammed iPS cells and maintenance of Dlk1-Dio3 imprinting
Gtl2((-/+)) teratomas have decreased expression of 28 miRNAs encoded by the Dlk1-Dio3 domain
This study provides the spatiotemporal expression and dynamic changes of lncRNAs from Dlk1-Dio3 imprinted region in mouse preimplantation stage embryos and offers insight into the potential mechanisms responsible for Gtl2 activation.
The existence of unidentified epigenetic determinants of tissue-specific Dio3 imprinting.
DNA methylation dynamics of a maternally methylated DMR in the mouse Dlk1-Dio3 domain
No changes in TRb or DI-2 and DI-3 expression in tail tissue collected from Triclosan exposure larvae were found.
A direct relationship between DLK1-DIO3 deregulation and replicative senescence of adipose-derived stem cells is reported, involving upregulation of a very significant fraction of its largest miRNA cluster (14q32.31), paralleled by the progressive overexpression of the lncRNA MEG3.
The expression of DIO3 on mRNA/protein levels in the depressive disorders patients was increased in comparison to the control subjects.
The expression of piRNAs encoded at DLK1-DIO3 enhances the prognostic potential of small non-coding RNAs specific to this locus in predicting lung cancer patient outcome.
In neonatal skin, DIO3 exhibited a high degree of monoallelic expression from the paternal allele.
Presence and subcellular location of D3 in human neutrophils for the first time and propose a model, in which D3 plays a role in the bacterial killing capacity of neutrophils either through generation of iodide for the myeloperoxidase system or through modulation of intracellular Thyroid hormone bioavailability.
MAPK and SHH pathways modulate type 3 deiodinase expression in papillary thyroid carcinoma
D3 is a critical factor in testis development and in testicular protection from thyrotoxicosis.
Thyroid hormone deiodinases D1, D2, and D3 are differentially expressed in endothelial cells following thyroid hormone exposure.
the microRNA cluster at the Dlk1-Dio3 locus is upregulated in lung adenocarcinoma
[review] D3 polymorphisms show no relationship with inter-individual variation in serum thyroid hormone parameters.
Overall, the data suggest that active expression of the DLK1-DIO3 cluster represents a new biomarker for epigenetic stability of hESCs and indicates the importance of using a proper physiological oxygen level during the derivation and culture of hESCs.
the imprinted DLK1-DIO3 locus is regulated by noncoding RNA IPW in an induced pluripotent stem cell model of Prader-Willi syndrome
Data indicate that Na+/I- symporter and type 3 iodothyronine deiodinase genes are expressed in term placenta and amniotic membrane.
Treatment with high affinity amyloidbeta42 oligomer-binding enantiomeric D3 peptide significantly decreases amyloidbeta deposits and the associated inflammatory response and improves cognition, even when applied only at late stages and high age.
D3 expression is re-activated in various types of human cancers. It may play a role in carcinogenesis and neoplastic cell proliferation. Review.
Reviewed are the microRNAs within the DLK1-DIO3 genomic region, their role in controlling tissue homeostasis and in the pathogenesis of some human diseases, mostly cancer, when aberrantly expressed. [review]
Deiodinase iodothyronine type III activity was increased in all papillary thyroid carcinomas as compared with that in adjacent thyroid tissue, parallel with ~ 5 times increase in deiodinase iodothyronine type III mRNA levels.
D3 expression in perinatal pancreatic beta-cells prevents untimely exposure to thyroid hormone, the absence of which leads to impaired beta-cell function and subsequently insulin secretion and glucose homeostasis
coordinate up-regulation of the DLK1-DIO3 miRNA cluster at 14q32.2 may define a novel molecular (stem cell-like) subtype of hepatocellular carcinoma associated with poor prognosis
The imprinted gene DIO3 is a candidate gene for litter size in pigs
DIO3 gene polymorphism was significantly associated with almost all fat deposition and carcass traits.
expression of D3 was observed in cerebrum and was positively regulated by thyroid state.
An allele-specific expression analysis-based SNP method revealed that DIO3 and DIO3OS genes exhibited monoallelic expression in the eight tissues, indicating that DIO3 and DIO3OS are imprinted in cattle.
The protein encoded by this intronless gene belongs to the iodothyronine deiodinase family. It catalyzes the inactivation of thyroid hormone by inner ring deiodination of the prohormone thyroxine (T4) and the bioactive hormone 3,3',5-triiodothyronine (T3) to inactive metabolites, 3,3',5'-triiodothyronine (RT3) and 3,3'-diiodothyronine (T2), respectively. This enzyme is highly expressed in the pregnant uterus, placenta, fetal and neonatal tissues, suggesting that it plays an essential role in the regulation of thyroid hormone inactivation during embryological development. This protein contains a selenocysteine (Sec) residue, which is essential for efficient enzyme activity. The selenocysteine is 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.
type III iodothyronine deiodinase
, Type 3 DI
, Type-III 5'-deiodinase
, type 3 iodothyronine deiodinase
, deiodinase, iodothyronine, type III
, gene 15
, type 3 deiodinase
, iodothyronine 5-deiodinase type III
, type 3 DI
, type-III 5'-deiodinase
, deiodinase, iodothyronine, type 3
, iodothyronine deiodinase, placental type
, thyroxine deiodinase type III (selenoprotein)
, type 3 iodothyronine selenodeiodinase
, type-III 5' deiodinase
, iodothyronine deiodinase type III