SLC5A8 (solute carrier family 5 member 8)

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منابع مشابه

SLC 1 A 5 ( solute carrier family 1 ( neutral amino acid transporter ) , member 5 )

Review on human SLC1A5, with data on DNA/RNA, on the protein encoded and pathological and physiological implications.

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Silencing of solute carrier family 13 member 5 disrupts energy homeostasis and inhibits proliferation of human hepatocarcinoma cells.

The solute carrier family 13 member 5 (SLC13A5), a sodium-coupled citrate transporter, plays a key role in importing citrate from the circulation into liver cells. Recent evidence has revealed that SLC13A5 deletion protects mice from high-fat diet-induced hepatic steatosis and that mutation of the SLC13A5 orthologues in Drosophila melanogaster and Caenorhabditis elegans promotes longevity. Howe...

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PharmGKB update: III. Genetic variants of SLC22A1, solute carrier family 22 (organic cation transporter), member 1.

Publications: Shu Y, Leabman MK, Feng B, Mangravite LM, Huang CC, Stryke D, Kawamoto M, Johns SJ, DeYoung J, Carlson E, Ferrin TE, Herskowitz I, Giacomini KM. Pharmacogenetics Of Membrane Transporters Investigators. (2003) Evolutionary conservation predicts function of variants of the human organic cation transporter, OCT1. Proc Natl Acad Sci (USA) 100:5902–5907. Leabman MK, Huang CC, DeYoung J...

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Aberrant Hypomethylation of Solute Carrier Family 6 Member 12 Promoter Induces Metastasis of Ovarian Cancer

PURPOSE Ovarian cancer (OC) is the most fatal of gynecological malignancies with a high rate of recurrence. We aimed to evaluate the expression of solute carrier family 6, member 12 (SLC6A12) and methylation of its promoter CpG sites in a xenograft mouse model of metastatic OC, and to investigate the regulatory mechanisms that promote aggressive properties during OC progression. MATERIALS AND...

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Incomplete glycosylation and defective intracellular targeting of mutant solute carrier family 11 member 1 (Slc11a1).

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ژورنال

عنوان ژورنال: Atlas of Genetics and Cytogenetics in Oncology and Haematology

سال: 2011

ISSN: 1768-3262

DOI: 10.4267/2042/44829