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anti-Human SLC13A5 Anticorps:
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SLC13A5 is the second major gene associated with the clinical diagnosis of KTZS.
Data suggest that SLC13A5 plays a role in progression/cell proliferation of human hepatocellular carcinoma cells; here, RNA interference using shRNA against SLC13A5 decreased tumor burden in treatment of hepatocarcinoma in a xenograft tumor model in nude mice.
Data suggest that SLC13A5 plays a role in progression/proliferation of human hepatocellular carcinoma cells; RNA interference using shRNA against SLC13A5 decreased tumor burden in treatment of hepatocarcinoma in a xenograft tumor model in nude mice. [REVIEW]
Study identified additional SLC13A5 mutations in patients with chronic epilepsy starting in the neonatal period, with the mutations producing inactive Na+/citrate transporters.
Studies show that SLC13A5 is a transporter in the plasma membrane that mediates the uptake of citrate into cells. It is expressed in hepatocytes, neurons, and spermatozoa. Its loss-of-function mutations are associated with neonatal epilepsy in humans. This is a single-gene disease with epilepsy resulting solely from the inactivity of SLC13A5. [review]
In infants presenting with therapy resistant seizures in the first days after birth, without a clear history of hypoxic-ischemic encephalopathy, but with Punctate White Matter Lesions on their neonatal MRI, a diagnosis of SCL13A5 related epileptic encephalopathy should be considered.
Discovery and characterization of novel inhibitors of the sodium-coupled citrate transporter (NaCT or SLC13A5).
Eight patients from four families with SLC13A5 mutation are described. They have neonatal epilepsy, tooth hypoplasia, and developmental delay.
SLC13A5 is a novel target gene of PXR and may contribute to drug-induced steatosis and metabolic disorders in humans.
Screening of 68 additional unrelated individuals with early-onset epileptic encephalopathy for SLC13A5 mutations led to identification of one additional subject with heterozygous mutations of SLC13A5 and a similar clinical presentation as index subjects
This paper describes the cloning and functional characterization of the human Na(+)-coupled citrate transporter (NaCT).
mediates the utilization of extracellular citrate for fat synthesis in human liver cells, and that the process is stimulated by lithium
Expression and function of NaCT in a cell line and in primary hepatocytes.
The findings revealed the potentially important role of citrate and Slc13a5 in the development and function of teeth and bone.
Our studies demonstrate a profound effect of mIndy on mammalian energy metabolism.
Molecular cloning and transport properties of NaCT.
Na+ -coupled di/tricarboxylate transport system expressed in neurons as NaC2/NaCT, which can transport the tricarboxylate citrate as well as dicarboxylates such as succinate, alpha-ketoglutarate, and malate.
SLC13A5 is a tricarboxylate plasma transporter with a preference for citrate.
solute carrier family 13 (sodium-dependent citrate transporter), member 5
, solute carrier family 13 member 5
, Na(+)/citrate cotransporter
, sodium-coupled citrate transporter
, sodium-dependent citrate transporter
, solute carrier family 13, member 5
, novel solute carrier family 13 (sodium-dependent dicarboxylate transporter) (Slc13a2 or 3) member