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- Data for: High uric acid promotes dysfunction in pancreatic β cells by blocking IRS2/AKT signalingThese data,including,ros level,insulin secretion,the expression of genes associated with glycolysis, was exhibited.
- Data for: Extracellular cyclophilin A induces cardiac hypertrophy via the ERK/p47phox pathwayRaw data of western blot and fluorescent probe are included, other data such as HE and Masson (TIF), we originally prepared to upload, but we do not know why it keeps showing errors, we feel sorry for that.
- Data for: L-type amino acid transporter 1, LAT1, in growth hormone-producing pituitary tumor cellsThe data show the roles of LAT1 in growth hormone (GH)-producing pituitary tumor cells, GH4 cells. Briefly, GH4 cells express higher LAT1 gene levels compared to rat normal pituitary tissues (Fig. 1A). A selective LAT1 inhibitor, JPH203, does not change LATs expression profiles in GH4 cells (Fig.1B and C), and pharmacological LAT1 inhibition by JPH203 suppresses leucine uptake and cell growth in GH4 cells (Fig. 2A and C, and Supplemental Fig. 1). Deprivation of leucine reduces cell growth in GH4 cells (Fig 2B). JPH203 suppresses GH production and secretion in GH4 cells (Fig. 3A, B, and C). JPH203 also reduces prolactin gene expression levels. Genetic downregulation of LAT1 shows similar effects on cell growth and hormone production (Fig. 4A, B, and C, and Supplemental Fig 3). JPH203 does not alter the activity of the mTOR pathway (Fig. 5A, B, and C). Pharmacological mTOR inhibition by rapamycin suppresses cell growth but does not alter GH production in GH4 cells (Fig. 6A, B, and C). JPH203 does not induce apoptosis in GH4 cells (Fig. 7). A combination of JPH203 and rapamycin shows additive anti-tumor effects on cell growth in GH4 cells (Supplemental Fig. 4) .
- Data for: Modulation of RXR-DNA complex assembly by DNA contextReagent and Ressources, DNA Deposited data Sofwares