Introduction of SLC7A7
SLC7A7 (solute carrier family 7 member 7), also known as Y+L amino acid transporter 1 or monocyte amino acid permease 2 (MOP-2), is encoded by the gene SLC7A7. SLC7A7 is a member of catalytic chains of the hetero(di)meric amino acid transporters (HATs) subgroup of SLC7 family, and its structure is characterized with 12 transmembrane domains (12TM) with two conserved cysteine residues between TM3 and TM4 and a cytoplasmic N and C termini. The SLC7A7 gene, containing 11exons, is mapped to chromosome 14q11.2. The sodium-independent SLC7A7 transporter is combined with the 4F2hc protein encoded by SLC3A2 to form the cationic amino acid transport system Y+L on the basolateral cell membrane of epithelial cells, which exports cationic amino acids (arginine, lysine and ornithine) out of the cell while importing a large neutral amino acid and a Na+ ion into the cell. It is reported that SLC7A7 expression is regulated by an alternative, TATA-box-containing promoter in specific tissues.
|Basic Information of SLC7A7|
|Protein Name||Y+L amino acid transporter 1|
|Organism||Homo sapiens (Human)|
Function of SLC7A7 Membrane Protein
The most well-known role of SLC7A7 is acting as a transporter to take part in the sodium-independent uptake of dibasic amino acids and sodium-dependent uptake of some neutral amino acids. Defects in SLC7A7 gene may cause lysinuric protein intolerance (LPI), which is a severe multisystem disorder characterized by protein-rich food intolerance with secondary urea cycle disorders. Moreover, mutations in SLC7A7 cause cation transporter dysfunction, which is associated with various disorders, such as renal dysfunction, high blood ammonia, gastrointestinal symptoms, and abnormal hematopoiesis, growth retardation, osteoporosis, and pulmonary symptoms. It is reported that in human umbilical vein endothelial cells (HUVECs), SLC7A7 contributes to nitric oxide synthesis via transport of L-arginine. Strong evidence shows that prognosis of malignant glioma and multiple myeloma and drug resistance in ovarian cancer is related to SLC7A7 high expression. In T-cell acute lymphoblastic leukemia, downregulation of SLC7A7 increases cell apoptosis rate, but decreases the G1 phase ratio, cell migration, and invasion, suggesting a significant role in the pathogenesis of T-cell acute lymphoblastic leukemia.
Fig.1 The pathogenic model for pulmonary complications in LPI. (Rotoli, 2018)
Application of SLC7A7 Membrane Protein in Literature
The authors analyzed the role of the SLC7A7 in the cell cycle and cell proliferation, apoptosis, migration, and invasion of Jurkat cells (derived from a 14-year-old T-cell lymphoblastic leukemia patient) and revealed that SLC7A7 contributed to the pathogenesis of T-cell acute lymphoblastic leukemia.
This article utilized short interference RNA (siRNA) in macrophages and airway epithelial cells to demonstrate that SLC7A7 knockdown can induce the expression and release of inflammatory mediators IL1β and TNFα, indicating a potential role of SLC7A7 in inhibition of inflammation.
The authors studied the expression profiles in basal cell carcinoma (BCCs) to find the differences in tumour metabolism, mainly focusing on the SLC 7A5, SLC 7A7, SLC 7A8 and the enzyme TDO2. SLC7A5, SLC7A8 and TDO2 were upregulated in BCCs compared to non-tumour skin.
The authors discovered two heterozygous mutations in the SLC7A7 gene of two Chinese sisters with lysinuric protein intolerance, deletion of c.1387: del C and IVS4+1C>T.
The authors investigated the association of SLC7A7 polymorphisms (rs12888930, rs12436190, and rs2065134) and the development of glioma in a Chinese population and they found that SLC7A7 rs12436190 was responsible for the high risk of glioma.
SLC7A7 Preparation Options
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Over years, Creative Biolabs has successfully generated massive functional membrane proteins for our customers. We are happy to provide one-stop, custom-oriented service packages regarding a variety of membrane protein targets. Please contact us for more information if you need.