Mouse Anti-Human CAPN1 Hybridoma [Q-0]

Diacylglycerol acyltransferase1 (DGAT1) plays an important role in the metabolism of triglycerides which catalyze the final step of triglyceride synthesis in animals. The objective of this study was to investigate the single-nucleotide polymorphisms (SNPs) in 5'UTR, exon-1, and exon-2 of DGAT1 in two Iranian indigenous sheep breeds. A total of 309 animals including fat-tailed Lori-Bakhtiari (n=152) and thin-tailed Zel (n=157) were used in this study. The genotypic patterns were detected by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). Five SSCP patterns were detected for 5'UTR and exon-1 fragment by PCR-SSCP and subsequently confirmed by sequencing PCR products. The sequencing results revealed that there are three novel polymorphisms in 5'UTR and exon-1fragment of DGAT1 at the studied breeds. Out of the detected polymorphisms only A277G substitution in exon-1 of DGAT1 leads to the changes in amino acids (p.Arg26Gly). There was significant correlation (P<0.05) between fat-tail weight (FTW) and back-fat thickness (BFT) and the observed genotypes in Lori-Bakhtiari breed; therefore, animals with G5 pattern had higher FTW and BFT compared to G1 pattern. The G1 and G5 genotypic patterns or haplotypes were different at their position 101 of 5'UTR region. No significant relationship (P<0.05) was found between the detected genotypes of 5'UTR and exon-1 fragment of DGAT1 in Zel breed and carcass traits. These results revealed that detected DGAT1 novel SNPs had significant effects on carcass traits and they can be used as a marker for these traits.

Cardiovascular system is demonstrated the main target of PM2.5 and the objective of this study was to explore the toxic effect and molecular mechanisms caused by PM2.5 in primary human umbilical vein endothelial cells (HUVECs) using microarray and bioinformatics analysis. The results showed that 591 genes were differentially expressed triggered by PM2.5, of which 174 genes were down-regulated, while 417 genes were up-regulated. Gene ontology analysis revealed that PM2.5 caused significant changes in gene expression patterns, including response to stimuli, immune response, and cellular processes. Pathway analysis and Signal-net analysis suggested that endocytosis, chemokine signaling pathway, RNA transport, protein processing in endoplasmic reticulum (ER) and autophagy regulation were the most critical pathways in PM2.5-induced toxicity in HUVECs. Moreover, gene expression confirmation of LIF, BCL2L1, CSF3, HMOX1, RPS6, PFKFB, CAPN1, HSPBPI, MOGS, PREB, TUBB2A, GABARAP by qRT-PCR indicated that endocytosis might be involved in the cellular uptake of PM2.5 by forming phagosomes, and subsequently inflammation, hypoxia and ER stress was occurred, which finally activated autophagy after PM2.5 exposure in HUVECs. In summary, our data can serve as fundamental research clues for further studies of PM2.5-induced toxicity in HUVECs. (C) 2017 Elsevier Ltd. All rights reserved.