SLC1A5
SLC1A5 is a gene that encodes the amino acid transporter ASCT2 in humans. This transporter is primarily involved in the transport of neutral amino acids across the cell membrane, playing a crucial role in both amino acid metabolism and the regulation of cell growth.
Function[edit | edit source]
SLC1A5, also known as the solute carrier family 1 (neutral amino acid transporter), member 5, is a system ASC transporter responsible for the sodium-dependent transport of small neutral amino acids such as glutamine, serine, and threonine. These amino acids are critical for various cellular processes, including protein synthesis and the production of metabolites that fuel other biochemical pathways.
The transporter is particularly important in rapidly dividing cells, such as cancer cells, which require a high influx of nutrients to support rapid growth and proliferation. SLC1A5 has been identified as a key player in the transport of glutamine, which is often referred to as a "fuel" for cancer cells due to its role in supporting anabolic processes that lead to cell growth and survival.
Clinical Significance[edit | edit source]
Research has shown that SLC1A5 is upregulated in several forms of cancer, including breast cancer, lung cancer, and prostate cancer. Its role in facilitating glutamine uptake makes it a potential target for cancer therapy. Inhibiting SLC1A5 function has been proposed as a strategy to cut off the supply of nutrients to tumor cells, thereby inhibiting their growth and proliferation.
Furthermore, the expression levels of SLC1A5 have been correlated with the prognosis in certain cancers, suggesting that it could serve as a biomarker for disease progression and response to therapy.
Genetic Structure[edit | edit source]
The SLC1A5 gene is located on chromosome 19 and consists of multiple exons that encode the transporter protein. Variations in this gene may affect the efficiency and regulation of amino acid transport, potentially impacting cellular metabolism and growth.
See Also[edit | edit source]
References[edit | edit source]
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