Rabbit Anti-Human PACS2 (a.a. 22-181) Polyclonal antibody

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell (EC) apoptosis is the initial step of atherogenesis and associated with Ca2+ overload. Mitochondria-associated endoplasmic reticulum (ER) membrane (MAM), regulated by tethering proteins such as phosphofurin acidic cluster sorting protein 2 (PACS2), is essential for mitochondrial Ca2+ overload by mediating ER-mitochondria Ca2+ transfer. In our study, we aimed to investigate the role of PACS2 in ox-LDL-induced apoptosis in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms. Ox-LDL dose- and time-dependently increased cell apoptosis concomitant with mitochondrial Ca2+ elevation, mitochondrial membrane potential (MMP) loss, reactive oxygen species (ROS) production, and cytochrome c release. Silencing PACS2 significantly inhibited ox-LDL-induced cell apoptosis at 24 h in addition to the effects of ox-LDL on mitochondrial Ca2+, MMP, and ROS at 2 h. Besides, ox-LDL promoted PACS2 localization at mitochondria as well as ER-mitochondria contacts at 2 h. Not only that, ox-LDL upregulated PACS2 expression at 24 h. Furthermore, silencing PACS2 inhibited ox-LDL-induced mitochondrial localization of PACS2 and MAM formation at 24 h. Altogether, our findings suggest that PACS2 plays an important role in ox-LDL-induced EC apoptosis by regulating MAM formation and mitochondrial Ca2+ elevation, implicating that PACS2 may be a promising therapeutic target for atherosclerosis.

Chromosome 14q32.3 deletions are uncommon, with most described patients harboring a ring chromosome 14. Only 15 deletions have been described not associated with ring formation or other complex chromosomal rearrangements. Here, we describe a child with the smallest deletion of chromosome 14q32.3 reported in the literature. This child's deletion encompasses at most 0.305?Mb and six genes including NUDT14, BRF1, BTBD6, PACS2, MTA1, and TEX22. He has similar clinical findings, including mild facial dysmorphisms and intellectual disability, as other individuals with much larger deletions of the terminus of the long arm of chromosome 14. This suggests that the genes deleted in our patient contribute to the 14q32 deletion syndrome. (C) 2012 Wiley Periodicals, Inc.