Atherosclerosis and Lipoprotein Analysis Core (Core C). Jonathan Smith, Ph.D., Core Leader Project Summary/Abstract The Lipoprotein analysis portion of this Core's primary objective is to analyze lipid and lipoprotein levels in various mouse models produced by projects and to provide human lipoproteins as needed. Mouse lipoprotein analysis will be accomplished using two methods, one based on separation of HDL-C from non-HDL-C via ultracentrifugation or precipitation, and the other based on size exclusion chromatography by FPLC. The Atherosclerosis portion of this Core's primary objective is to train investigators how to sacrifice mice and prepare tissues for atherosclerosis assays, and to offer two separate quantitative atherosclerosis assays; 1) cross sectional lesion area at the aortic root, and 2) cross sectional brachiocephalic lesion area. We can also assist Project personnel by teaching them the assay of surface lesion area on en face preparations of the entire aorta. Standardization of the lipoprotein assays and atherosclerosis assays will facilitate inter-laboratory collaboration and data comparisons. In addition, the Core will relieve the individual laboratories from having to learn and perform the laborious assays for atherosclerosis quantification.
Atherosclerosis and Lipoprotein Analysis Core (Core C). Project Narrative Core C will provide services to all three projects to increase productivity. These services include providing lipoproteins, the determination of lipoprotein cholesterol and triglyceride levels by buoyant density and size (FPLC) fractionation, and the determination of mouse atherosclerotic lesion areas in the aortic root and brachiocephalic artery.
|Herjan, Tomasz; Hong, Lingzi; Bubenik, Jodi et al. (2018) IL-17-receptor-associated adaptor Act1 directly stabilizes mRNAs to mediate IL-17 inflammatory signaling. Nat Immunol 19:354-365|
|Robinet, Peggy; Milewicz, Dianna M; Cassis, Lisa A et al. (2018) Consideration of Sex Differences in Design and Reporting of Experimental Arterial Pathology Studies-Statement From ATVB Council. Arterioscler Thromb Vasc Biol 38:292-303|
|Zhang, Cun-Jin; Wang, Chenhui; Jiang, Meiling et al. (2018) Act1 is a negative regulator in T and B cells via direct inhibition of STAT3. Nat Commun 9:2745|
|Han, Juying; Enyindah-Asonye, Gospel; Lin, Feng et al. (2018) CD6 expression has no effect on atherosclerosis in apolipoprotein E-deficient mice. BMC Res Notes 11:229|
|Sarvestani, Samaneh K; Signs, Steven A; Lefebvre, Veronique et al. (2018) Cancer-predicting transcriptomic and epigenetic signatures revealed for ulcerative colitis in patient-derived epithelial organoids. Oncotarget 9:28717-28730|
|Arif, Abul; Yao, Peng; Terenzi, Fulvia et al. (2018) The GAIT translational control system. Wiley Interdiscip Rev RNA 9:|
|Hai, Qimin; Ritchey, Brian; Robinet, Peggy et al. (2018) Quantitative Trait Locus Mapping of Macrophage Cholesterol Metabolism and CRISPR/Cas9 Editing Implicate an ACAT1 Truncation as a Causal Modifier Variant. Arterioscler Thromb Vasc Biol 38:83-91|
|Eswarappa, Sandeep M; Potdar, Alka A; Sahoo, Sarthak et al. (2018) Metabolic origin of the fused aminoacyl-tRNA synthetase, glutamyl-prolyl-tRNA synthetase. J Biol Chem 293:19148-19156|
|Halawani, Dalia; Gogonea, Valentin; DiDonato, Joseph A et al. (2018) Structural control of caspase-generated glutamyl-tRNA synthetase by appended noncatalytic WHEP domains. J Biol Chem 293:8843-8860|
|Zhou, Hao; Bulek, Katarzyna; Li, Xiao et al. (2017) IRAK2 directs stimulus-dependent nuclear export of inflammatory mRNAs. Elife 6:|
Showing the most recent 10 out of 276 publications