The TFRC gene encodes the protein Transferrin Receptor 1 (TFRC), which is a cell surface receptor involved in the uptake of iron from the bloodstream. Iron is an essential mineral required for various biological processes, including oxygen transport, energy production, and DNA synthesis.
TFRC is primarily expressed in cells with high iron requirements, such as hepatocytes, enterocytes, and erythroid cells. The receptor binds to transferrin, a protein that transports iron in the blood, and facilitates the internalization of iron into the cell. Once inside the cell, iron is either stored for future use or used for various metabolic processes.
Dysregulation of the TFRC gene and its encoded protein can lead to iron-related disorders. For example, mutations in the TFRC gene can result in a condition called hereditary hemochromatosis, which is characterized by excessive iron absorption and accumulation in the body. This can lead to organ damage and dysfunction, particularly in the liver, pancreas, and heart.
Additionally, TFRC has been found to be involved in the pathogenesis of certain diseases, such as cancer and infection. For example, increased expression of TFRC has been associated with tumor growth and progression, while altered TFRC expression has been observed in various microbial infections, including HIV and malaria.
In summary, the TFRC gene and its encoded protein, TFRC, play a crucial role in the regulation of iron homeostasis and the maintenance of cellular iron levels. Dysregulation of this gene and protein can lead to iron-related disorders and the development of various diseases. Further research into the role and regulation of the TFRC gene may contribute to the development of novel diagnostic and therapeutic strategies for the treatment of these conditions.
Iron-dependent ferroptosis causes lipid peroxidation and cell death. Hepatocellular carcinoma (HCC) overproduces the transferrin receptor (TFRC), which is essential for ferroptosis. The post-translational modifications (PTMs) of TFRC—especially O-GlcNAcylation—which influences hepatocyte susceptibility to Erastin-induced ferroptosis were examined by the researchers. Erastin they found causes de-O-GlcNAcylation at serine 687, which lowers ubiquitin E3 ligase MARCH8's binding capacity. This process decreases polyubiquitination at lysine 665, enhancing the stability of TFRC and promoting the accumulation of labile iron. These findings shed light on the intricate regulatory mechanisms of ferroptosis in HCC and highlight the significance of iron metabolism pathways.
Figure 1. The researchers transfected HEK293T cells with pcDNA3.1, pcDNA3.1-TFRC, and pcDNA3.1-OGA to evaluate how global O-GlcNAcylation alterations influence TFRC protein levels, revealing increased TFRC expression following co-transfection. (Zhou X, et al., 2024)
Creative Biogene's Human TFRC Stable Cell Line - HEK293T can serve as a valuable tool for further investigations into ferroptosis and related pathways in cancer research.
The TFRC gene, Transferrin Receptor 1, plays a crucial role in iron homeostasis and cellular metabolism. It is the transferrin receptor, a protein that binds to transferrin, the main iron carrying protein in the blood. The interaction between transferrin and its receptor is critical for cellular uptake of iron, which is an essential component of various biological processes such as oxygen transport, energy production and cell growth.
Mutations in the TFRC gene can lead to abnormal iron metabolism, resulting in conditions such as iron deficiency anaemia or iron overload. Iron deficiency anaemia is a common type of anaemia characterised by a reduction in the number of red blood cells or the amount of haemoglobin in the blood, which can lead to fatigue, weakness and other symptoms. Iron overload, on the other hand, is a condition in which too much iron builds up in the body, which can damage organs and tissues.
The application of TFRC gene-targeted therapies is important for the treatment and prevention of these diseases. For example, inhibition of the TFRC gene or its protein products has the potential to reduce the uptake and accumulation of iron in cells, thereby preventing iron-related diseases.
In summary, the TFRC gene is a key regulator of iron homeostasis and cellular metabolism. Dysregulation of this gene can lead to a variety of iron-related diseases and is therefore a promising target for the development of novel therapies to modulate iron metabolism and improve patient prognosis.
Customer Q&As
What is the TFRC gene and its function?
A: The TFRC gene encodes for the transferrin receptor 1 (TfR1), which is a cell surface protein that binds transferrin (Tf), the primary iron-carrying protein in the blood. This receptor is essential for the cellular uptake of iron, a vital nutrient for many metabolic processes. By mediating the endocytosis of Tf, TfR1 plays a key role in iron homeostasis and cell growth.
How does the TFRC gene contribute to iron homeostasis and cell growth?
A: The TFRC gene contributes to iron homeostasis and cell growth by ensuring the efficient uptake of iron into cells. TfR1 facilitates the internalization of iron-loaded Tf, which is then released into the cytoplasm. This process is crucial for the production of hemoglobin in red blood cells and for the synthesis of essential proteins and enzymes in other cell types.
Are there any diseases associated with mutations in the TFRC gene?
A: Mutations in the TFRC gene can lead to disorders affecting iron homeostasis and cellular iron utilization. These include hereditary hemochromatosis type 1, a condition characterized by excessive iron accumulation, and anemia of inflammation, where iron absorption is impaired. These mutations can alter the function of TfR1, leading to impaired iron regulation and cellular metabolism.
How is the expression of the TFRC gene regulated?
A: The expression of the TFRC gene is regulated by various factors, including iron availability and cellular demand. Iron deficiency can lead to increased expression of TfR1 to enhance iron uptake. Conversely, iron excess can downregulate TfR1 expression to prevent further iron accumulation. Transcription factors, such as IRP1 and IRP2, also play a role in regulating TFRC expression in response to iron levels.
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Ethical and safety concerns
The Human TFRC Stable Cell Line - HEK293T is derived from a well-characterized human cell line, addressing ethical concerns associated with animal testing. However, proper safety protocols should be followed to handle the cell line, ensuring researcher safety and preventing unintended consequences.
Sustainability and environmental impact
The use of a stable cell line like Human TFRC Stable Cell Line - HEK293T can contribute to sustainable research practices. By providing a renewable source of cells for experimentation, it helps reduce the environmental impact associated with continuous animal sourcing and tissue harvesting.
Global accessibility
The Human TFRC Stable Cell Line - HEK293T is made accessible to researchers worldwide, enabling collaboration and reproducibility of research findings across different geographical locations. This global availability facilitates the advancement of scientific knowledge and promotes international research partnerships.
Functional validation
The Human TFRC Stable Cell Line - HEK293T undergoes rigorous functional validation, including assays to confirm the expression and activity of TFRC. Researchers can trust the reliability and consistency of the cell line for their experiments, allowing for accurate interpretation of results and meaningful data analysis.
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