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30 Citations 10 Q&As
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Facts about Tumor necrosis factor receptor superfamily member 11B.
Bone homeostasis appears to be based on the local ratio between TNFSF11 and TNFRSF11B. May also play a role in preventing arterial calcification.
Human | |
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Gene Name: | TNFRSF11B |
Uniprot: | O00300 |
Entrez: | 4982 |
Belongs to: |
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No superfamily |
OCIF; OCIFMGC29565; OPGtumor necrosis factor receptor superfamily member 11B; Osteoclastogenesis inhibitory factor; Osteoprotegerin; TNFRSF11B; TR1; tumor necrosis factor receptor superfamily, member 11b
Mass (kDA):
46.026 kDA
Human | |
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Location: | 8q24.12 |
Sequence: | 8; |
Highly expressed in adult lung, heart, kidney, liver, spleen, thymus, prostate, ovary, small intestine, thyroid, lymph node, trachea, adrenal gland, testis, and bone marrow. Detected at very low levels in brain, placenta and skeletal muscle. Highly expressed in fetal kidney, liver and lung.
Secreted.
The TNFRSF11B marker is an intracellular protein that regulates thyroid metabolism cells. It is also an RNA gene. Boster scientists worldwide can use it to present results from their species or applications. They also can earn product credits. The benefits are similar for scientists from all over the world. Continue reading to learn more. This article explains how this gene operates and what scientists are able to do do with it.
CPDD cases in families have been connected to mutations in TNFRSF11B genes. This gene codes osteoprotegerin, and is the target tissue of CPDD. The symptoms of CPDD appear very similar to sporadic cases of CPDD. Further studies on this mutation could uncover drugs that could treat CPDD. Numerous mutations have been observed in chromosome 8.
The TNFRSF11B gene gives instructions to produce the membrane protein osteoprotegerin which plays a critical role in bone remodeling. Osteoprotegerin regulates osteoclasts, which are cells that are responsible for breaking down bone tissue during the process of remodeling bone. It also regulates insulin signaling in the body. But, despite the importance of this gene further research must be conducted to determine how it plays a role in the process of reshaping bones.
We designed a network of computational computers for analyzing frontal cortex samples taken from HIV encephalitis patients in order to understand the molecular function and evolution of TNFRSF11B. It was previously demonstrated to have mutations in the codon ending Stop402Leu. This mutation is unique to this family, and is related to a component of the PGOA/CPDD gene.
The TNFRSF11B gene encodes osteoprotegerin. Mesenchymal stem cells osteoprotegerin is expressed, which functions as a decoy to TRANCE. Osteoprotegerin regulates TRANCE expression on the cell surface. In turn, the deficiency of this protein could result in osteoporosis, loss of bone, and juvenile Paget's Disease.
The TSHR membrane protein is synthesized as a single, monopeptide polypeptide, which has an extracellular domain as well as seven transmembrane pass areas, and an intracellular tail. Autoantibodies against this receptor target the ECD, which is expressed on the cell surface by a glycophosphatinositol anchor sequence. Both experimental and pathological antibodies recognize the TSHR protein at levels ten times greater than the full-length receptor clone.
Antibody studies have demonstrated that TSHR material is widely expressed on the cell surface. In a study with the GPIA6 cell line, the fluorescence signal was between three and ten times higher in cells with GPI-anchored TSHR. In a study similar to this using monoclonal antibodies to detect the TSHR molecules were identified in cells that express the surface of the GPI-anchored molecule.
Comparing the structure of the TSHR and FSHR TMDs was carried out. The TM1 and TM3 the helices move inwards while the TM6 and TSHR-Ac display small inward and lateral movements. In its inactive state, the TSHR has an operational 'ioniclock'. These three membrane proteins have similar TMDs to other GPCRs.
Similar models were developed for FSHR and LHR TMDs. Templates for the TMD of TSHR were developed from inactive GPCR structures. This model has been compared with the structures of active and inactive TSHR. The next step is to compare TMDs to find out their structural differences. This model has provided the most comprehensive explanation of the structure of TSHR to date.
Human TSHR has been studied in mouse models to study the effects of autoimmune TED. A plasmid that expresses human thyroid hormone (TSHRYFP) was reported. A plasmid expressing the Gas subunit, which is a component of thyroid hormone, was also made. This plasmid is designed express EYFP and TSHR. Both plasmids share a similar sequence. It is important to determine the TSHR subunit and Gas subunit in patients suffering from TED.
The TSHR is a crucial component of thyroid hormone metabolism and regulates thyroid cell growth and function. Its mutations are associated with various thyroid disorders, the most commonly hyperthyroidism. Although genetic modifications of TSHR do not directly contribute to carcinogenesis however, the hormone plays an important role in tumor growth and is a target for a variety of oncogenes. Here are a few mechanisms that TSHR can affect thyroid metabolism.
TSH is a hormone that acts on the TSHR in thyroid tissues and the hypothalamus. It is located in the basolateral cell membrane in the thyroid the follicular cell. The TSHR also binds with a G protein subunit, Gaq or Gas. This activates intracellular signaling through the G proteins. Gs and Gaq are two of the most important signal subtypes. G proteins (Gas, Gaq) activate the TSHR. This triggers a sequence of events that includes the phospholipase C and cyclic Adenosine Monphosphate (cAMP). The cAMP and PLC cascades begin by activating the G protein which leads to the production of cyclic adeno
TSH/TSHR is essential in regulating the organization of thyroid follicles throughout embryogenesis. When you reach adulthood, TSH and Tshr signaling are essential for proper thyroid development. Mutations that inhibit Tshr result in severe hypothyroidism. Functional Tshr isn't necessary for the final stage in follicular cell differentiation during early development. Tshr signaling is not required for the expression of NIS or TPO.
TSHR is expressed in follicular cells in the thyroid. It has also found in the pituitary testis, kidney, and brain. It is also believed to be involved in Graves' disease extrathyroidal manifestations. The expression of TSHR is a reliable predictor of thyroid cancer. The upregulation of this gene slows tumor cell spread. TSHR upregulation also significantly reduced distant metastasis. Additionally, the TSH-TSHR signal transduction pathway didn't affect the growth of thyroid cancer cells.
Researchers have identified TSHR as susceptibility to GD-1 as a gene. It is closely connected to the NRXN3 gene, which is responsible for insulin resistance. TSHR stimulates the production of cAMP. The receptors stimulate TSH and bTSH expression in COS-7 cells. Their cAMP production activities were affected by mutations in the TSHR gene.
There are various species of beta subunits in human thyroid tissue. The most frequent beta subunit is about 50 kD in molecular mass. These subunits play a role in posttranslational processing. There are numerous cleavage sites in TSHR. This could explain the inconsistent results across studies. The authors believe that the lack of consistency in the results could be due to differences in the stratification of populations and ethnicity.
The D727E polymorphism in the TSHR gene has been linked to toxic thyroid adenomas and multinodular gonosis, as well as other types of goiter. A high risk of developing autoimmune Thyroiditis is also associated with a D727E polymorphism. However these associations aren't yet confirmed. Further research is needed to prove the connection between TSHR, GD.
The TSHR is a gene with an enviable association with Graves' disease. Studies on the TSHR gene have concentrated on the underlying molecular mechanisms. The TSHR gene has been the focus of intense research for more than two decades. Genome-wide studies revealed that there was a strong connection between TSHR gene, GD and fine mapping studies further defined the genetic region that is associated with the disease. In addition, at least five SNPs were identified in close linkage disequilibrium. The next step is to unravel the mechanisms that underlie the polymorphisms.
Boster Bio's TNFRSF-11B marker detects the protein known as TSHR. This protein can be utilized in gene therapy trials for various indications. It is also used in screening of a wide range of diseases. Boster scientists may submit their results to species or applications. Credits for their work are granted for their work. This is a process that is applicable to scientists across the globe.
TSHR is a membrane protein that regulates thyroid cell metabolism. It acts as an thyropin receptor and Thyrostimulin. It is controlled by adenylate cycling enzyme. Hyperthyroidism is a disease caused by defects in the TSHR. There are three types of TSHR, each with distinct functional characteristics.
The TSHR gene encodes a transmembrane receiver in the G protein-coupled family. It is located in fat cells and adipocytes. This protein has been linked to adipogenesis as well as the differentiation of preadipocytes. It was found in human embryonic stem cells and human orbital preadipocytes fibroblasts.
PMID: 9108485 by Simonet W.S., et al. Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.
PMID: 9492069 by Yasuda H., et al. Identity of osteoclastogenesis inhibitory factor (OCIF) and osteoprotegerin (OPG): a mechanism by which OPG/OCIF inhibits osteoclastogenesis in vitro.
*Showing only the more recent 20. More publications can be found for each product on its corresponding product page