Cardiac Fas-Dependent and Mitochondria-Dependent Apoptotic Pathways in a Transgenic Mouse Model of Huntington's Disease.
Wuxue, China. In Cardiovasc Toxicol, 24 Apr 2015
The key components of Fas-dependent apoptosis (TNF-alpha, TNFR1, Fas ligand, Fas death receptors, FADD, activated caspase-8, and activated caspase-3) and the key components of mitochondria-dependent apoptosis (Bax, Bax-to-Bcl-2 ratio, cytosolic cytochrome c, activated caspase-9, and activated caspase-3) increased significantly in the hearts of the HD group.
Role of oxidative stress in endothelial insulin resistance.
Stockholm, Sweden. In World J Diabetes, 15 Apr 2015
Complex molecular circuits including endothelial nitric oxide synthase, prostacyclin synthase, mitochondrial adaptor p66(Shc), nicotinamide adenine dinucleotide phosphate-oxidase oxidase and nuclear factor kappa-B are discussed.
Large-scale genetic analysis of chloroplast biogenesis in maize.
Eugene, United States. In Biochim Biophys Acta, 25 Mar 2015
We include a summary of mutant phenotypes for 20 previously unstudied maize genes, including genes encoding chloroplast ribosomal proteins, a PPR protein, tRNA synthetases, proteins involved in plastid transcription, a putative ribosome assembly factor, a chaperonin 60 isoform, and a NifU-domain protein required for Photosystem I biogenesis.
Heat shock proteins in obesity: links to cardiovascular disease.
In Horm Mol Biol Clin Investig, 01 Mar 2015
Several members of the heat shock protein (HSP) family have been identified as novel adipokines released upon cellular stress, which might be a molecular link from adipose tissue inflammation to the cardiovascular system.
The role of heat shock proteins in atherosclerosis.
Innsbruck, Austria. In Nat Rev Cardiol, Sep 2014
These T cells recognize heat shock protein (HSP)60, which is expressed together with adhesion molecules by endothelial cells in response to classic risk factors for atherosclerosis.
TNF receptor 1 genetic risk mirrors outcome of anti-TNF therapy in multiple sclerosis.
More papers using
Oxford, United Kingdom. In Nature, 2012
analysis of multiple sclerosis GWAS data in conjunction with the 1000 Genomes Project data, shows genetic evidence that strongly implicates SNP rs1800693 as the causal variant in the TNFRSF1A region; further functional studies show that this MS risk allele directs expression of a novel, soluble form of TNFR1 that can block TNF
Lipopolysaccharide-induced increase in signalling in hippocampus is abrogated by IL-10–a role for IL-1 beta?
In Journal of Neuroinflammation, 2003
... anti-phospho-JAK1, anti-phospho-STAT1, STAT1, anti-phospho-IκBα and anti-SOCS3 (Cell Signalling, Danvers, MA, USA), anti-phospho-c-jun and anti-TNFα receptor (TNFR1) (Santa Cruz Biotechnology, Heidelberg, Germany, and anti-actin ...