Anti-ARPC3 (aa 165-177) polyclonal antibody

Aims: To test the potential association of cytosine-phosphate- guanine dinucleotides (CpG)-single-nucleotide polymorphisms (SNPs) located within actin-related protein 2/3 complex subunit 3 (ARPC3), a gene recently linked to adipogenesis and lipid accumulation, with metabolic syndrome (MetS) features in severely obese patients. Methods: Prioritized SNPs within the ARPC3 locus were genotyped and tested for associations with MetS features in a cohort of 1,749 obese patients with and without MetS. Association testing with CpG methylation levels was performed in a methylation sub-cohort of 16 obese men. Results: A significant association was found between the CpG-SNP rs3759384 (C>T) and plasma triglyceride (TG) levels (false discovery rate-corrected p = 3.5 x 10(-2)), with 0.6% of the phenotypic variance explained by the CpG-SNP, and with TT homozygotes showing the highest plasma TG levels (1.89 mmol/l). The carriers of the rs3759384 T allele also showed a significant decrease in methylation levels of the ARPC3 promoter-associated CpG site cg10738648 in both visceral adipose tissue and blood. ARPC3 expression levels showed a strong correlation with plasma TG levels (r = 0.70; p = 0.02). Conclusions: The increased plasma TG levels found in homozygous rs3759384 T allele carriers argue for a relevant role of this CpG-SNP in lipid management among obese individuals, which may be driven by an epigenetic-mediated mechanism. (C) 2016 S. Karger AG, Basel

Genetic contribution has been consistently implicated in several neurological disorders, however only a fraction of candidate genes can be directly linked to these disorders. Many known risk factors for psychiatric diseases are related to the enzymatic regulatory machinery of the actin based cytoskeleton of neuronal cells. Synaptic plasticity which is fundamental for neuronal function heavily relies on actin-polymerization. To gain insight into the neuronal architecture during actin-related pathologic conditions, using quantitative electron-microscopy, the authors investigated a conditional knock-out mice breed, in which they studied the result of the postnatal loss of ArpC3 subunit of the Arp2/3 complex an evolutionary conserved final output of actin signalling pathways that orchestrates de novo actin polymerization. They found, that in the hippocampus which is a particularly favourable model for synaptic plasticity and believed to play a key role in learning and memory and neocortex, synaptic architecture is significantly altered compared to the wild-type. Their results suggest that dysregulation of the actin cytoskeleton results in pathologic neuronal architecture which may contribute to the ethiology of complex neurological disorders.