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Facts about Tumor necrosis factor receptor superfamily member 12A.
Promotes angiogenesis and the proliferation of endothelial cells. May modulate cellular adhesion to matrix proteins.
Mouse | |
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Gene Name: | Tnfrsf12a |
Uniprot: | Q9CR75 |
Entrez: | 27279 |
Belongs to: |
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No superfamily |
CD266 antigen; CD266; FGF-inducible 14; Fibroblast growth factor-inducible immediate-early response protein 14; Fn14; FN14tumor necrosis factor receptor superfamily member 12A; TNFRSF12; TNFRSF12A; tumor necrosis factor receptor superfamily, member 12A; TWEAK R; TWEAKR; tweak-receptor; type I transmembrane protein Fn14
Mass (kDA):
13.641 kDA
Mouse | |
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Location: | 17|17 A3.3 |
Sequence: | 17; |
Highly expressed in fetal heart, intestine, kidney, liver, lung and skin, and in adult heart and ovary. Intermediate expression in adult kidney, lung and skin.
The TNFRSF12A markers can be used for validation of a variety if samples, including plasma or HGSCs. It can also be used to validate any sample type that cannot be routinely validated by Boster Bio. Here are some of most common uses of TNFRSF12A. If you're a scientist, you may benefit from this marker.
This protein causes lysosomal degradation, activates caspases, promotes cell death and promotes cell death when cultured myotubes. It also inhibits PGC1a, which is required for mitochondrial biogenesis. TRAF (TNF receiver-associated protein), cIAP cellular inhibitors of apoptosis, and FOXO, which stands Forkheadbox O.
Tnfrsf12a was expressed in VSMCs and were cultured using transwell cell culture inserts measuring 8 mm. The culture medium contained 0.2% BSA. Cells were seeded into the chemotaxis chambers at a density of 70 x 104/well. Lower wells were stocked with rTWEAK and 0.5% FBS. FBS containing 10% was used as a positive indicator of migration. After 4 h, nonmigrating cells were removed and the number of migrated cells counted in randomly chosen fields.
TWEAK has been implicated in multiple human neuroinflammatory diseases. Studies performed on postmortem brain sections from MS patients have revealed that the protein is involved in the development of neuroinflammatory disease. FluoroJade B+ also caused neuronal damage. The study also shows that MS progression is influenced by the TNFSF12/TWEAK pathway.
In addition to regulating TNFSF12, TWEAK also regulates angiogenesis and endothelial cell proliferation. It may also modulate cellular adhesions to matrix proteins. TNFSF12 is a weak inducer for apoptosis but promotes angiogenesis as well as the proliferation of endothelial cell.
TWEAK binds IKK2 the transcriptional regulator and is implicated as regulating gene Expression. IKK2 regulates the expression of TWEAK in KIM2 mammary endothelial cell cells. The expression of TWEAK is upregulated during involution, suggesting that it is regulated by IKK2.
RN was extracted from the brain tissues using the RNeasy Lipid Tissue Midi Kit (Life Technologies). One micrograms of purifiedRNA were reverse-transcribed. The cDNA could then be used to amplify TWEAK (FN14), and GAPDH with the QuantiTect RNA DNA Polymerase kits.
Tnfrsf12a mice produced murine VSMCs. They were cultured with ice-cold buffer. The cell extracts were then normalized to equal protein levels and were resuspended again in SDS sample broth. The cell lysates were then separated using SDS-PAGE. After the membrane had been fixed, the cell lysates could be immunoblotted for fusion proteins.
TNFRSF12A is upregulated mainly in HGSC plasma and is associated with cytokine and growth factor signaling pathways. These pathways are associated with several biological processes, including immune cell functions and metastasis-associated processes. The growth factors, cytokinases and other proteins are involved in this process. These proteins also activate integrin signals, which are triggered by the presence of extracellular components such as collagen, fibronectin, and laminin. This protein is also involved in protease activity.
Although most HGSCs can be treated with chemotherapy, a large percentage of patients experience relapses. It is vital to identify novel molecules that may be associated with these cells. TNFRSF12A has been shown to be upregulated in plasma of HGSCs, and may be associated with a subtype of the disease. To improve diagnosis and treatment of this disease, it is important to discover new molecules that are associated with HGSC plasma.
Numerous proteins have been linked with ovarian tumor progression and survival, including IL-6 (GDF15), OPN/SST1, VEGFA, and GDF15. However, SPINT2 has never been linked to HGSC before. Future studies could reveal the role SPINT2 plays in tumor progression. The potential for discovering new biomarkers is also evident in the data from this study.
TNFRSF12A monoclonal antibodies bind with high affinity to TWEAK/TNFSF12A. This binding triggers a signal-transduction cascade that produces distinct cellular responses. These responses can range from cell death to proliferation and angiogenesis. For validation of any type of sample, there are several types of antibodies as well as ELISA kits.
PMID: 10551889 by Meighan-Mantha R.L., et al. The mitogen-inducible Fn14 gene encodes a type I transmembrane protein that modulates fibroblast adhesion and migration.