A5048641079- Nuclear Structure and Function
- RNA Research and Splicing
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Lipid metabolism and disorders
- Genomics and Chromatin Dynamics
- Parvovirus B19 Infection Studies
- Educational Systems and Policies
- Technology and Data Analysis
- Metabolism, Diabetes, and Cancer
- Adipose Tissue and Metabolism
University of California, Los Angeles
2023-2024
Progerin, the protein that causes Hutchinson–Gilford progeria syndrome, triggers nuclear membrane (NM) ruptures and blebs, but mechanisms are unclear. We suspected expression of progerin changes overall structure lamina. High-resolution microscopy smooth muscle cells (SMCs) revealed lamin A B1 form independent meshworks with uniformly spaced openings (~0.085 µm 2 ). The in SMCs resulted formation an irregular meshwork clusters large (up to 1.4 acted a dominant-negative fashion disrupt...
Why apolipoprotein AV (APOA5) deficiency causes hypertriglyceridemia has remained unclear, but we suspected that the underlying cause was reduced amounts of lipoprotein lipase (LPL) in capillaries. By routine immunohistochemistry, observed LPL staining heart and brown adipose tissue (BAT) capillaries Apoa5–/– mice. Also, after an intravenous injection LPL-, CD31-, GPIHBP1-specific monoclonal antibodies, binding antibodies to BAT (relative CD31 or GPIHBP1 antibodies) levels postheparin plasma...
Lipoprotein lipase (LPL) is secreted into the interstitial spaces by parenchymal cells and then transported capillaries GPIHBP1. LPL carries out lipolytic processing of triglyceride (TG)-rich lipoproteins (TRLs), but tissue-specific regulation incompletely understood. Plasma levels TG hydrolase activity after heparin injection are often used to draw inferences about intravascular levels, validity these unclear. Moreover, plasma not helpful for understanding in specific tissues. Here, we...
The Lmna knockout mouse (Lmna–/–) created by Sullivan and coworkers in 1999 has been widely used to examine lamin A/C function. allele contains a deletion of intron 7–exon 11 sequences was reported be null allele. Later, Jahn discovered that the mutant produces 54-kDa truncated A identified, RT-PCR, cDNA containing exon 1–7 + 12 sequences. Because encodes prelamin A's CaaX motif, is assumed farnesylated. In current study, we found Lmna–/– embryonic fibroblasts (MEFs) predominantly...
Lipoprotein lipase (LPL) and multiple regulators of LPL activity (e.g., APOC2 ANGPTL4) are present in all vertebrates, but GPIHBP1-the endothelial cell (EC) protein that captures within the subendothelial spaces transports it to its site action capillary lumen-is mammals not chickens or other lower vertebrates. In mammals, GPIHBP1 deficiency causes severe hypertriglyceridemia, maintain low triglyceride levels despite absence GPIHBP1. To understand intravascular lipolysis we examined...
Abstract Hutchinson-Gilford progeria syndrome (HGPS) is a progeroid disorder characterized by multiple aging-like phenotypes, including disease in large arteries. HGPS caused an internally truncated prelamin A (progerin) that cannot undergo the ZMPSTE24-mediated processing step converts farnesyl-prelamin to mature lamin A; consequently, progerin retains carboxyl-terminal farnesyl lipid anchor. In cultured cells, and full-length (produced Zmpste24 −/– cells) form abnormal nuclear meshwork...