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SLC6A19 encodes a system B(0) transmembrane protein that actively transports most neutral amino acids across the apical membrane of epithelial cells. Zusätzlich bieten wir Ihnen SLC6A19 Antikörper (8) und SLC6A19 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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analysis of the interaction of amino acid transporters B0AT1 and B0AT3 with their ancillary protein collectrin (zeige TMEM27 ELISA Kits)
Slc6a19 expression in the intestine is regulated at three different levels involving promoter methylation, histone modification, and opposing transcription factors.
the presence of digestive protein complexes in the intestinal brush-border containing the peptidases APN (zeige ANPEP ELISA Kits) and ACE2 (zeige ACE2 ELISA Kits) and the neutral amino acid transporter B0AT1
Impaired nutrient signaling and body weight control in a Na+ neutral amino acid cotransporter (Slc6a19)-deficient mouse.
Average loss of solute carrier expression was similar in acute tubular necrosis (77%) and T cell-mediated rejection (75%) with high correlation of individual transcripts.
Glucocorticoid inducible kinase isoforms SGK1 (zeige SGK1 ELISA Kits)-3 are novel potent stimulators of Slc6a19 and may thus participate in the regulation of neutral amino acid transport in vivo.
We isolated the human homolog of B(0)AT1, called SLC6A19, and determined its size and molecular organization. We then identified mutations in SLC6A19 in members of the original family in whom Hartnup disorder was discovered
The mechanism of the mouse (m)B0AT1 (slc6a19) transporter was studied in detail using two electrode voltage-clamp techniques and tracer studies in the Xenopus oocyte expression system.
The relatively constant [Na(+)] along the renal proximal tubule both drives the uptake of neutral amino acids via B(0)AT1 thermodynamically and ensures that, upon binding, these are translocated efficiently into the cell.
This study shows the luminal brush-border localization of the Na(+)-dependent amino and imino acid transporters B degrees AT1 and XT3s1/SIT1 in kidney and intestine.
SIT1, B(0)AT1 and ACE2 (zeige ACE2 ELISA Kits) were co-localized in the brush-border membrane of small intestine enterocytes.
PKB/Akt (zeige AKT1 ELISA Kits) up-regulates SLC6A19 activity, which may foster amino acid uptake into PKB/Akt (zeige AKT1 ELISA Kits)-expressing epithelial and tumor cells.
JAK2 (zeige JAK2 ELISA Kits) up-regulates SLC6A19 activity which may foster amino acid uptake into JAK2 (zeige JAK2 ELISA Kits) expressing cells.
A novel SLC6A19 gene mutation is associated with late-onset seizures in a Korean patient with Hartnup disorder.
We identified six mutations in SLC6A19 that cosegregated with disease in the predicted recessive manner, with most affected individuals being compound heterozygotes.
Hartnup disorder is allelically heterogeneous with two mutated SLC6A19 allele.
These findings suggest that the rare SLC6A19-MS7 allele may be a risk factor for hypertension.
Suggest that amino acid transporters B(0)AT1 and b(0,+)AT are involved in the reabsorption of L-citrulline in the kidney, at least in part, by mediating the apical membrane transport of L-citrulline in renal tubule cells.
novel homozygous mutation of G284R in the transmembrane domain of the SLC6A19 transporter found in the proband, with typical dermatologic and neurologic manifestations and increased levels of urinary neutral amino acids
This gene encodes a system B(0) transmembrane protein that actively transports most neutral amino acids across the apical membrane of epithelial cells. Mutations in this gene result in Hartnup disorder.
, sodium-dependent neutral amino acid transporter B(0)AT1
, solute carrier family 6 member 19
, system B(0) neutral amino acid transporter AT1
, sodium-dependent amino acid transporter system B0
, solute carrier family 6 (neurotransmitter transporter), member 19
, system B0 neutral amino acid transporter
, neutral amino acid transporter
, solute carrier family 6, member 19
, system B0 neutral amino acid transporter SLC6A19
, sodium-dependent neutral amino acid transporter B(0)