Genetic therapies to lower cholesterol.
London, United Kingdom. In Vascul Pharmacol, Jan 2015
Other strategies involve knocking down the expression of Apolipoprotein B100 (APOB100) and the protease PCSK9 which designates LDLR for degradation.
Hypermutation in human cancer genomes: footprints and mechanisms.
In Nat Rev Cancer, Dec 2014
This major expansion of cancer mutation data sets has provided unprecedented statistical power for the analysis of mutation spectra, which has confirmed several classical sources of mutation in cancer, highlighted new prominent mutation sources (such as apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) enzymes) and empowered the search for cancer drivers.
LOX-1 in atherosclerotic disease.
Matsumoto, Japan. In Clin Chim Acta, Dec 2014
We hypothesized that LOX-1 is a candidate risk factor beyond LDL cholesterol (LDLC) and developed a novel assay to quantify LOX-1 ligand containing apoB (LAB).
[Heterozygous familial hypercholesterolemia].
More papers using
In Turk Kardiyol Dern Ars, Oct 2014
New classes of drugs for the treatment of hypercholesterolemia include microsomal triglyceride transfer protein inhibitors, apolipoprotein B synthesis inhibitors, and pro-protein convertase subtilisin/kexin 9 inhibitors.