DIO1 Antibodies

Type I iodothyronine deiodinase (DIO1)

Responsible for the deiodination of T4 (3,5,3',5'- tetraiodothyronine) into T3 (3,5,3'-triiodothyronine) and of T3 into T2 (3,3'-diiodothyronine).

Plays a role in providing a source of plasma T3 by deiodination of T4 in peripheral tissues like liver and kidney.

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Gene Information

Human
Gene Name:	DIO1
Uniprot:	P49895
Entrez:	1733

Family

Belongs to:
iodothyronine deiodinase family

Alternative Names

5DI; deiodinase, iodothyronine, type I; DIOI; EC 1.97.1; EC 1.97.1.10; ITDI1; MGC130050; thyroxine deiodinase type I (selenoprotein); TXDI1MGC130051; Type 1 DI; type I iodothyronine deiodinase; Type-I 5'-deiodinase

Molecular Weight

Mass (kDA):
28.924 kDA

Genomic Context

Human
Location:	1p32.3
Sequence:	1; NC_000001.11 (53894187..53911086)

Subcellular Localizations

Endoplasmic reticulum membrane; Single-pass membrane protein.

Diseases

• Malignant Neoplasms
• Neoplasms
• Pituitary Diseases
• Carcinoma
• Hypothyroidism
• Thyroid Neoplasm
• Thyroid Diseases
• Kidney Neoplasm
• Malignant Paraganglionic Neoplasm
• Hyperthyroidism
• Adenoma
• Renal Cell Carcinoma

• Follicular Adenoma
• Fatty Liver
• Follicular Thyroid Carcinoma
• Conventional (clear Cell) Renal Cell Carcinoma
• Heart Diseases
• Depressive Disorder

Pathways

• Cell Proliferation
• Secretion
• Transport
• Lactation
• Regulation Of Gene Expression
• Translation
• Pathogenesis
• Developmental Process
• Parturition
• Brain Development
• Aging
• Glycosylation

• Pigmentation
• Glucose Homeostasis
• Dna Replication
• Hatching
• Rna Interference
• Excretion
• Chromatin Remodeling

PTMs

• Deiodination
• Phosphorylation
• Carboxylation

• Glycosylation
• Acetylation
• Bromination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/DIO1

Best Uses of the DIO1 Marker

The DIO1 Marker is a versatile tool that is used to detect DNA damage in cancer cells. It is widely used to test the effects of certain drugs on the cells, and many clinical trials are being conducted to determine the effectiveness of these drugs. The following article will discuss the background of Steven Boster, the development of this marker, and the various uses for the DIO1 marker.

Background

The DIO1 marker is a protein found in hepatocytes. It inhibits the activity of deiodinase A. Its activities are negatively affected by uremic toxins. Inflammatory cytokines also negatively impact DIO1 activity. Inhibition of DIO1 has a role in preventing and treating a variety of diseases, including diabetes, heart disease, and cancer.

One such gene is DIO1. The D1 is responsible for converting T4 to T3, while D2 converts T3 into its active form. The DIO1 gene is polymorphic in two distinct regions, i.e., the G allele and the T allele. There are several possible DIO1 polymorphisms, but only one is associated with a particular symptom. In this study, the DIO1 polymorphism was associated with increased free T3 levels, while D2 and 3 were not.

A single variant in DIO1 causes hypersensitivity and an increased risk of developing type 1 diabetes. The rs2235544" SNP increases the expression of DIO1. However, there are mutations in the gene that cause high levels of T4 and a lower conversion of T3 to T4.

Although there is no homology between the DIO1 marker and DIO2 genes, the genetic sequences of both markers are related. Hence, it is necessary to obtain the raw data from the company to fully understand the mutation. The raw data for these two genes can be found in the raw data file. Then, type the rs number associated with the mutation and click on 'find'. In this way, the mutation is identified.

Early studies

The DIO1 marker is a molecule that is detected in the serum of patients with ESRD. It is also associated with the presence of cytokines such as IL-1b, IL-6, and TNF-a. However, its precise clinical application remains to be determined. The goal of future studies is to better understand the biological functions of the DIO1 marker. Here, we will discuss some of the findings and potential clinical applications of the DIO1 marker.

The DIO1 protein was isolated from HepG2 cells after transfection using Lipofectamine 2000. Six hours after transfection, the cells were collected. The DIO1 siRNAs were chemically synthesized by Sangon Biotech. The sequences were:

Several researchers have confirmed that DIO1 is localized to the plasma membrane. Furthermore, uremic toxins increased the expression of TNF-a and IL-1b mRNAs, which were not decreased by siRNA. These findings indicate that the DIO1 marker may have a contrasting role from the uremic toxins. To further explore the potential of DIO1 as a biomarker, additional studies are necessary to determine its role in inflammatory diseases.

The DIO1 gene polymorphisms associated with the levels of T3, fT4, and (ln)-rT3 are closely related to cardiac mortality. Other SNPs on chromosome 9p21 have also been associated with cardiovascular mortality, but more research is needed. In addition, the polymorphisms of the DIO1 gene rs1515777-AG have been associated with lower fT4 levels.

However, further studies are needed to determine the relationship between DIO-1 and oxidative stress in patients with ESRD. Additionally, further research is needed to determine how DIO1 and TNF-a levels are related in patients with both conditions. It is still unclear whether DIO-1 is an effective biomarker in evaluating the toxicity of NSAIDs. So far, however, this is promising and is a valuable step in assessing patients' risk for developing the disease.

There are several SNPs that may be associated with the DIO1 gene polymorphism. However, these polymorphisms have not been associated with the T4 and fT3 levels in individuals with a normal thyroid. However, the genetic variations are likely to affect the function of the thyroid. As such, this marker has significant implications for thyroid disease. This gene is known to be associated with a number of other risk factors for ES.

Adjuvants

The effect of adjuvants on the expression of CD80 and CD86 was studied in cancer patients and healthy subjects. In both groups, RNAdjuvant(r) caused statistically significant increases in the expression of these activation markers. However, no significant effect was found on the expression of CD86 and HLA-DR. The results of this study are interpreted with caution because the results were not reproducible.

SE adjuvants induced increased generation of follicular helper T cells and the frequency of germinal center B cells. SE adjuvants also induced apoptosis in lymph node macrophages. These cells then cross-present the antigen to CD8+ T cells, which show a RIP3K-dependent response. The effect of squalene on CD8+ T cell responses was less obvious. It was concluded that squalene-based adjuvants enhanced B cell response without affecting CD8+ T cells.

The RIPK3 protein has multiple functions, including necroptosis, the induction of inflammatory cytokines, and scaffolding functions. The RIPK3 kinase activity of DIO1 was required for optimal CD8 T cell responses to SE-adjuvanted immunization. Therefore, this type of adjuvant is not suitable for patients with severe allergies, such as diabetes, asthma, or rheumatoid arthritis.

In this study, RNAdjuvant(r) produced high levels of Th2 IFN-g in cancer patients but not in healthy subjects. In healthy subjects, the cytokine levels were comparable with those of post-chemotherapy samples. However, none of the adjuvants induced Th2 IL-4. In addition, the effects of RNAdjuvant(r) on immune cells were not correlated with chemotherapy treatment, but this does not necessarily rule out the possibility that RNAdjuvants may have a therapeutic effect in cancer patients.