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The protein encoded by Slc7a7 is the light subunit of a cationic amino acid transporter. Zusätzlich bieten wir Ihnen Solute Carrier Family 7 (Amino Acid Transporter Light Chain, Y+L System), Member 7 Kits (16) und Solute Carrier Family 7 (Amino Acid Transporter Light Chain, Y+L System), Member 7 Antikörper (14) und viele weitere Produktgruppen zu diesem Protein an.
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At present, 51 kinds of SLC7A7 gene mutations causing lysinuric protein intolerance have been found worldwide, including insert (C.1384-1385 ins (zeige INS Proteine) ACTA (zeige ACTA1 Proteine)), delete (C.1185-1188 del TTCT) and point mutations (P.R410X, P.Y457X, P.R 468X, P.L124p, etc).3, 4 In our cases, there were two heterozygous mutations in the SLC7A7 gene of the two sisters: C.1387 del C and IVS4+1C>T, which has never been reported worldwide.
The study reports a significant association between SLC7A7 rs12436190 and the risk of glioma in a Chinese population.
heteromerization of y+LAT1 and 4F2hc (zeige SLC3A2 Proteine) within the cell is not disrupted by any of the tested LPI mutations
SLC7A7 genetic variants are associated with increase risk for glioma in a Chinese population.
SLC7A7 plays a critical role in glioblastoma carcinogenesis and overexpression of SLC7A7 is correlated with worse outcomes in patients
SLC7A7/y+LAT1 mutations lead to a defective phenotype of macrophages resulting in lysinuric Protein Intolerance.
during differentiation of human monocytes from peripheral blood, SLC7A7 mRNA and system y(+)L activity are increased
novel SLC7A7 mutations in patients with lysinuric protein intolerance
expression levels and putative 5' promoter elements of the SLC7A7 gene
putative multiheteromeric structure of both [4F2hc/y(+)LAT-1] and [4F2hc/y(+)LAT-2], and the interference between y(+)LAT-1 and y(+)LAT-2 proteins may have a role in the pathogenesis of lysinuric protein intolerance
The expression of Mct8 and L-type amino acid transporters Lat2 and Lat1 are determined in brain neurons during development.
Increased LAT1 expression can be induced by lipid oxidation products relevant to inflammatory responses in atherogenesis. LAT1 mediates lysophosphatidylcholine-enhanced cytokine production by endothelial cells.
selective regulation of SNAT3 (zeige SLC38A3 Proteine) and y(+)LAT1 expression may serve a major role in the renal adaptation to acid secretion and thus for systemic acid-base balance.
The Slc7a7(-/-) mouse displayed intrauterine growth restriction, leading to neonatal lethality. After heavy protein ingestion, the surviving adult animals presented metabolic derangement consistent with lysinuric protein intolerance.
LAT1, and LAT2 (zeige SLC7A8 Proteine) mRNAs were detected in fetal and postnatal femurs and in MC3T3-E1 cells, while OATP1 and NTCP (zeige SLC10A1 Proteine) mRNAs were not.
The protein encoded by this gene is the light subunit of a cationic amino acid transporter. This sodium-independent transporter is formed when the light subunit encoded by this gene dimerizes with the heavy subunit transporter protein SLC3A2. This transporter is found in epithelial cell membranes where it transfers cationic and large neutral amino acids from the cell to the extracellular space. Defects in this gene are a cause of lysinuric protein intolerance (LPI). Alternative splicing results in multiple transcript variants.
Y+L amino acid transporter 1
, monocyte amino acid permease 2
, solute carrier family 7 (cationic amino acid transporter, y+ system), member 7
, y(+)L-type amino acid transporter 1
, solute carrier family 7 member 7