Spelling suggestions: "subject:"[een] LIPIDS"" "subject:"[enn] LIPIDS""
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The relation of environment to lipid and protein synthesis by a species of cladosporium /Abou el Seoud, Mohamed Osman January 1964 (has links)
No description available.
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The changes in the lipid components of broccoli as the result of various heat treatments /Dahlke, Lorraine Carolyn January 1966 (has links)
No description available.
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Aspects of decreased all cis 5, 8, 11-eicosatrienoic acid deposition in tissue lipids of the fat deficient rat /Ullman, Myron Davis January 1971 (has links)
No description available.
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Placental lipid metabolism : I. Palmityl-coa: carnitine palmityltransferase identification in human placental tissue ; II. Incorporation of radioactive precursors into the neutral lipids and phospholipids of human placental tissue /Karp, Warren B. January 1971 (has links)
No description available.
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Synthesis and antilipolytic activity of phenoxyacetic acid derived compounds /Stratford, Eugene Scott,1942- January 1970 (has links)
No description available.
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The application of surface area measurements for the quantitative microdetermination of lipids /Burke, Lester Irwin January 1971 (has links)
No description available.
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A study of the components of the lipid fraction of rifle peat /Braids, O. C. January 1966 (has links)
No description available.
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Utilization of acetate-1-14C? in the synthesis of lipid by Acholeplasmas /Herring, Patricia Kay January 1974 (has links)
No description available.
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New Roles for PagP in the Bacterial Outer Membrane Stress Response / The Multifunctional Enzymology of PagPDixon, Charneal Latoye 22 November 2018 (has links)
The ability of Gram-negative bacteria to modulate outer membrane (OM)
composition in response to stressful environments is essential for their survival
and replication within host tissues. The OM enzyme PagP catalyzes the transfer of
palmitate from a glycerophospholipid to lipid A. Lipid A is the endotoxic portion
of LPS responsible for transmembrane signalling to initiate the immune response.
Palmitoylation of lipid A can either attenuate or stimulate the immune response
depending on where the palmitate chain is attached to a specific lipid A molecule.
Here we report that the Escherichia coli PagP homolog is a multifunctional
enzyme, which displays two distinct active sites exposed on either side of the
bacterial OM. E. coli PagP converts phosphatidylglycerol (PG) to palmitoyl-PG
(PPG) using the same cell surface active site involved in the palmitoylation of
lipid A. PPG is then serially degraded to bis(monoacylglycero)phosphate (BMP)
and either lyso-PG or lyso-BMP by a novel lipase active site located in PagP on
the periplasmic side of the OM. The periplasmic lipase active site can be
inactivated with the Y87F amino acid substitution. BMP is a novel
glycerophosphoglycerol (GPG) that has not previously been reported in bacterial
lipid metabolism. Not all PagP homologs have this ability to remodel GPGs. We
have identified a divergent lipid A palmitoyltransferase in Pseudomonas
aeruginosa that does not palmitoylate PG. The P. aeruginosa homolog also has
different lipid A regiospecificity, adding palmitate on the opposite glucosamine at the 3’-position compared to the 2-position of the proximal sugar observed for the
E. coli homolog. We have determined that P. aeruginosa PagP is representative of
a distinct clade of PagP evolved to fulfill different functions. Although this minor
clade is inclusive of homologs that lack obvious sequence similarity with the
major clade enterobacterial PagP, we have identified conserved catalytic and
structural elements within the minor clade that contribute to our growing
understanding of homologous PagP structure/function relationships. A
comparative analysis of all available sequences of minor clade PagP homologs has
revealed invariant His, Ser, and Tyr residues that are necessary for catalysis.
Additionally, a 4-amino acid conserved signature indel or CSI is unique to
bacteria clustered phylogenetically within the γ-subclass of Proteobacteria. / Thesis / Doctor of Philosophy (PhD)
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An Examination of the Role of Sphingosine-1-Phosphate in High Density Lipoprotein Mediated Protection of Macrophages Against Apoptosis / Role of HDL and S1P in Macrophage SignalingChathely, Kevin January 2019 (has links)
Prevention of macrophage apoptosis in advanced atherosclerotic lesions can help stop atherosclerosis progression to vulnerable plaques. High density lipoprotein (HDL) can protect macrophages from apoptosis that has been induced by a variety of agents. We hypothesize that this is the consequence of the sphingolipid, sphingosine-1-phosphate (S1P), specifically carried by HDL, and transferred to S1P receptor 1 (S1P1) on the cells via the HDL receptor, scavenger receptor class B type 1 (SR-B1).
Apoptosis was induced in murine peritoneal macrophages from wild type and different knockout mice with, tunicamycin, thapsigargin, staurosporine, or UV irradiation. Apoptosis was measured by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) or with cleaved caspase-3 (CC3) staining. Treatment of cells with HDL or S1P protected them against apoptosis induced by a variety of stimuli. In contrast, pre-treatment of HDL with S1P lyase, which irreversibly cleaves S1P, eliminated the ability of HDL to protect macrophages. Inhibition of SR-B1’s lipid transport activity reduced HDL dependant protection against apoptosis. Furthermore, HDL dependent protection against apoptosis induced by tunicamycin was prevented when the S1P receptor S1P1 was knocked out. However, this protection was not prevented when apoptosis was induced by staurosporine.
These results suggest that the HDL mediated protection of macrophages against apoptosis is multi-faceted and one approach may involve SR-B1 mediated delivery of S1P from HDL to the S1P1. Understanding the mechanisms by which HDL elicits atheroprotective signalling in macrophages will provide insight into new targets for therapeutic intervention in atherosclerotic disease. / Thesis / Master of Science in Medical Sciences (MSMS) / Atherosclerosis, is a disease where in the artery walls thicken due to cholesterol build-up, is the major underlying cause for cardiovascular diseases, which is currently a leading cause of death in many populations. We believe that HDL, the “good” cholesterol and S1P, a small molecule carried by HDL, can help prevent the progress of atherosclerosis by preventing macrophages, cells that absorb the cholesterol, from dying. We attempt to prove this by providing S1P or HDL to macrophages that are made to undergo cell death. Results show that both HDL and S1P can protect cells against cell death induced by many factors. However, HDL can protect against certain cell death inducing stimuli without the need for S1P and more research is required to fully understand HDL’s protective role in atherosclerosis. Understanding how HDL elicits atheroprotective signalling in macrophages will help in finding new drugs and therapies to reduce atherosclerosis-based deaths across the world.
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