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anti-Human SLC13A5 Antikörper:
anti-Mouse (Murine) SLC13A5 Antikörper:
anti-Rat (Rattus) SLC13A5 Antikörper:
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SLC13A5 is the second major gene associated with the clinical diagnosis of KTZS (zeige ROGDI Antikörper).
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 (zeige C7ORF49 Antikörper), 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 (zeige NR1I2 Antikörper) 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
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