SFPQ interacts with two FGFR I fusion partners, ZNF 198 and CPSF6

SFPQ interacts with two FGFR I fusion partners, ZNF 198 and CPSF6, that are functionally related to the recurrent PDGFR alpha partner FIP1L1. Our findings thus identify a group of proteins that are important check details for pre-mRNA processing as fusion partners for tyrosine kinases in hematological malignancies. (C) 2008 Wiley-Liss, Inc.”
“We aimed to characterize the primary abnormalities associated with fat accumulation and vulnerability to hepatocellular injury of obesity-related fatty liver. We performed

functional analyses and comparative transcriptomics of isolated primary hepatocytes from livers of obese insulin-resistant Zucker rats (comprising mild to severe hepatic steatosis) and age-matched lean littermates, searching for novel genes linked to chronic hepatic steatosis. Of the tested genome, 1.6% was identified as steatosis linked. Overexpressed genes were mainly dedicated to primary metabolism (100%), signaling, and defense/acute phase (similar to 70%); detoxification, steroid, and sulfur metabolism (similar to 65%) CB-839 as well as cell growth/proliferation and protein synthesis/transformation (similar to 70%) genes were downregulated. The overexpression of key genes involved in de

novo lipogenesis, fatty acid and glycerolipid import and synthesis, as well as acetyl-CoA and cofactor provision was paralleled by enhanced hepatic lipogenesis and production of large triacylglycerol-rich VLDL. Greatest changes in gene expression were seen in those encoding the lipogenic malic enzyme (up to 7-fold increased) and cell-to-cell interacting cadherin 17 (up to 8-fold decreased). Among validated genes, fatty acid synthase, stearoyl-CoA desaturase 1, fatty acid translocase/Cd36, malic enzyme, cholesterol-7 alpha hydroxylase, cadherin 17, and peroxisome proliferator-activated receptor alpha significantly correlated with severity compound inhibitor of hepatic steatosis. In conclusion, dysregulated expression of metabolic and survival genes accompany hepatic steatosis in obese insulin-resistant rats and may render steatotic hepatocytes more vulnerable to cell injury in progressive nonalcoholic fatty liver disease.-Buque,

X., M. J. Martinez, A. Cano, M. E. Miquilena-Colina, C. Garcia-Monzon, P. Aspichueta, and B. Ochoa. A subset of dysregulated metabolic and survival genes is associated with severity of hepatic steatosis in obese Zucker rats. J. Lipid Res. 2010. 51: 500-513.”
“Mn2+-assisted catalysis by B. stearothermophilus TrpRS parallels that in polymerases and reduces specificity in amino acid activation. As predicted by nonequilibrium molecular dynamics simulations, multivariant thermodynamic cycles with [ATP]dependent Michaelis-Menten kinetics and Mn2+ for Mg2+ substitution demonstrate energetic coupling of ATP affinities to the metal; to lysines K111 and K192, which interact via the PPi leaving group; and to K195, which couples differently to the metal via the a-phosphate.

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