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Статті в журналах з теми "Lipid signal":
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Eyster, Kathleen M. "The membrane and lipids as integral participants in signal transduction: lipid signal transduction for the non-lipid biochemist." Advances in Physiology Education 31, no. 1 (January 2007): 5–16. http://dx.doi.org/10.1152/advan.00088.2006.
Анотація:
Reviews of signal transduction have often focused on the cascades of protein kinases and protein phosphatases and their cytoplasmic substrates that become activated in response to extracellular signals. Lipids, lipid kinases, and lipid phosphatases have not received the same amount of attention as proteins in studies of signal transduction. However, lipids serve a variety of roles in signal transduction. They act as ligands that activate signal transduction pathways as well as mediators of signaling pathways, and lipids are the substrates of lipid kinases and lipid phosphatases. Cell membranes are the source of the lipids involved in signal transduction, but membranes also constitute lipid barriers that must be traversed by signal transduction pathways. The purpose of this review is to explore the magnitude and diversity of the roles of the cell membrane and lipids in signal transduction and to highlight the interrelatedness of families of lipid mediators in signal transduction.
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Lee, Seung-Cheol, Hari Hariharan, Fernando Arias-Mendoza, Gabor Mizsei, Kavindra Nath, Sanjeev Chawla, Mark A. Elliott, Ravinder Reddy, and Jerry D. Glickson. "Coherence pathway analysis of J-coupled lipids and lactate and effective suppression of lipids upon the selective multiple quantum coherence lactate editing sequence." Biomedical Physics & Engineering Express 8, no. 3 (March 8, 2022): 035004. http://dx.doi.org/10.1088/2057-1976/ac57ad.
Анотація:
Abstract Objective. The selective multiple quantum coherence (Sel-MQC) sequence is a magnetic resonance spectroscopy (MRS) technique used to detect lactate and suppress co-resonant lipid signals in vivo. The coherence pathways of J-coupled lipids upon the sequence, however, have not been studied, hindering a logical design of the sequence to fully attenuate lipid signals. The objective of this study is to elucidate the coherence pathways of J-coupled lipids upon the Sel-MQC sequence and find a strategy to effectively suppress lipid signals from these pathways while keeping the lactate signal. Approach. The product operator formalism was used to express the evolutions of the J-coupled spins of lipids and lactate. The transformations of the product operators by the spectrally selective pulses of the sequence were calculated by using the off-resonance rotation matrices. The coherence pathways and the conversion rates of the individual pathways were derived from them. Experiments were performed on phantoms and two human subjects at 3 T. Main results. The coherence pathways contributing to the various lipid resonance signals by the Sel-MQC sequence depending on the gradient ratios and RF pulse lengths were identified. Theoretical calculations of the signals from the determined coherence pathways and signal attenuations by gradients matched the experimental data very well. Lipid signals from fatty tissues of the subjects were successfully suppressed to the noise level by using the gradient ratio −0.8:−1:2 or 1:0.8:2. The new gradient ratios kept the lactate signal the same as with the previously used gradient ratio 0:−1:2. Significance. The study has elucidated the coherence pathways of J-coupled lipids upon the Sel-MQC sequence and demonstrated how lipid signals can be effectively suppressed while keeping lactate signals by using information from the coherence pathway analysis. The findings enable applying the Sel-MQC sequence to lactate detection in an environment of high concentrations of lipids.
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Torres, Manuel, Catalina Ana Rosselló, Paula Fernández-García, Victoria Lladó, Or Kakhlon, and Pablo Vicente Escribá. "The Implications for Cells of the Lipid Switches Driven by Protein–Membrane Interactions and the Development of Membrane Lipid Therapy." International Journal of Molecular Sciences 21, no. 7 (March 27, 2020): 2322. http://dx.doi.org/10.3390/ijms21072322.
Анотація:
The cell membrane contains a variety of receptors that interact with signaling molecules. However, agonist–receptor interactions not always activate a signaling cascade. Amphitropic membrane proteins are required for signal propagation upon ligand-induced receptor activation. These proteins localize to the plasma membrane or internal compartments; however, they are only activated by ligand-receptor complexes when both come into physical contact in membranes. These interactions enable signal propagation. Thus, signals may not propagate into the cell if peripheral proteins do not co-localize with receptors even in the presence of messengers. As the translocation of an amphitropic protein greatly depends on the membrane’s lipid composition, regulation of the lipid bilayer emerges as a novel therapeutic strategy. Some of the signals controlled by proteins non-permanently bound to membranes produce dramatic changes in the cell’s physiology. Indeed, changes in membrane lipids induce translocation of dozens of peripheral signaling proteins from or to the plasma membrane, which controls how cells behave. We called these changes “lipid switches”, as they alter the cell’s status (e.g., proliferation, differentiation, death, etc.) in response to the modulation of membrane lipids. Indeed, this discovery enables therapeutic interventions that modify the bilayer’s lipids, an approach known as membrane-lipid therapy (MLT) or melitherapy.
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Maccarrone, Mauro. "Deciphering Complex Interactions in Bioactive Lipid Signaling." Molecules 28, no. 6 (March 14, 2023): 2622. http://dx.doi.org/10.3390/molecules28062622.
Анотація:
Lipids are usually viewed as metabolic fuel and structural membrane components. Yet, in recent years, different families of lipids able to act as authentic messengers between cells and/or intracellularly have been discovered. Such lipid signals have been shown to exert their biological activity via specific receptors that, by triggering distinct signal transduction pathways, regulate manifold pathophysiological processes in our body. Here, endogenous bioactive lipids produced from arachidonic acid (AA) and other poly-unsaturated fatty acids will be presented, in order to put into better perspective the relevance of their mutual interactions for health and disease conditions. To this end, metabolism and signal transduction pathways of classical eicosanoids, endocannabinoids and specialized pro-resolving mediators will be described, and the intersections and commonalities of their metabolic enzymes and binding receptors will be discussed. Moreover, the interactions of AA-derived signals with other bioactive lipids such as shingosine-1-phosphate and steroid hormones will be addressed.
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Woscholski, Rüdiger, and Peter J. Parker. "Inositol lipid 5-phosphatases-traffic signals and signal traffic." Trends in Biochemical Sciences 22, no. 11 (November 1997): 427–31. http://dx.doi.org/10.1016/s0968-0004(97)01120-1.
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Simons, Kai, and Derek Toomre. "Lipid rafts and signal transduction." Nature Reviews Molecular Cell Biology 1, no. 1 (October 2000): 31–39. http://dx.doi.org/10.1038/35036052.
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Mehta, Sahil, Amrita Chakraborty, Amit Roy, Indrakant K. Singh, and Archana Singh. "Fight Hard or Die Trying: Current Status of Lipid Signaling during Plant–Pathogen Interaction." Plants 10, no. 6 (May 30, 2021): 1098. http://dx.doi.org/10.3390/plants10061098.
Анотація:
Plant diseases pose a substantial threat to food availability, accessibility, and security as they account for economic losses of nearly $300 billion on a global scale. Although various strategies exist to reduce the impact of diseases, they can introduce harmful chemicals to the food chain and have an impact on the environment. Therefore, it is necessary to understand and exploit the plants’ immune systems to control the spread of pathogens and enable sustainable agriculture. Recently, growing pieces of evidence suggest a functional myriad of lipids to be involved in providing structural integrity, intracellular and extracellular signal transduction mediators to substantial cross-kingdom cell signaling at the host–pathogen interface. Furthermore, some pathogens recognize or exchange plant lipid-derived signals to identify an appropriate host or development, whereas others activate defense-related gene expression. Typically, the membrane serves as a reservoir of lipids. The set of lipids involved in plant–pathogen interaction includes fatty acids, oxylipins, phospholipids, glycolipids, glycerolipids, sphingolipids, and sterols. Overall, lipid signals influence plant–pathogen interactions at various levels ranging from the communication of virulence factors to the activation and implementation of host plant immune defenses. The current review aims to summarize the progress made in recent years regarding the involvement of lipids in plant–pathogen interaction and their crucial role in signal transduction.
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De Biasio, Alfredo, Alain Ibáñez de Opakua, Mark J. Bostock, Daniel Nietlispach, Tammo Diercks, and Francisco J. Blanco. "A generalized approach for NMR studies of lipid–protein interactions based on sparse fluorination of acyl chains." Chemical Communications 54, no. 53 (2018): 7306–9. http://dx.doi.org/10.1039/c8cc02483a.
Анотація:
Sparse lipid fluorination enhances the lipids' 1H signal dispersion, enables clean molecular distinction by 19F NMR, and evinces micelle insertion of proteins via fluorine induced signal shifts.
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Kook, Eunjin, and Do-Hee Kim. "Elucidating the Role of Lipid-Metabolism-Related Signal Transduction and Inhibitors in Skin Cancer." Metabolites 14, no. 6 (May 28, 2024): 309. http://dx.doi.org/10.3390/metabo14060309.
Анотація:
Lipids, as multifunctional molecules, play a crucial role in a variety of cellular processes. These include regulating membrane glycoprotein functions, controlling membrane trafficking, influencing apoptotic pathways, and affecting drug transport. In addition, lipid metabolites can alter the surrounding microenvironment in ways that might encourage tumor progression. The reprogramming of lipid metabolism is pivotal in promoting tumorigenesis and cancer progression, with tumors often displaying significant changes in lipid profiles. This review concentrates on the essential factors that drive lipid metabolic reprogramming, which contributes to the advancement and drug resistance in melanoma. Moreover, we discuss recent advances and current therapeutic strategies that employ small-molecule inhibitors to target lipid metabolism in skin cancers, particularly those associated with inflammation and melanoma.
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Bickel, Perry E. "Lipid rafts and insulin signaling." American Journal of Physiology-Endocrinology and Metabolism 282, no. 1 (January 1, 2002): E1—E10. http://dx.doi.org/10.1152/ajpendo.2002.282.1.e1.
Анотація:
Lipid rafts are domains within the plasma membrane that are enriched in cholesterol and lipids with saturated acyl chains. Specific proteins, including many signaling proteins, segregate into lipid rafts, and this process is important for certain signal transduction events in a variety of cell types. Within the past decade, data have emerged from many laboratories that implicate lipid rafts as critical for proper compartmentalization of insulin signaling in adipocytes. A subset of lipid rafts, caveolae, are coated with membrane proteins of the caveolin family. Direct interactions between resident raft proteins (caveolins and flotillin-1) and insulin-signaling molecules may organize these molecules in space and time to ensure faithful transduction of the insulin signal, at least with respect to the glucose-dependent actions of insulin in adipocytes. The in vivo relevance of this model remains to be determined.
Дисертації з теми "Lipid signal":
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Frangioudakis, Georgia St Vincent's Clinical School UNSW. "Insulin signal transduction in vivo in states of lipid-induced insulin resistance." Awarded by:University of New South Wales. St Vincent's Clinical School, 2004. http://handle.unsw.edu.au/1959.4/27419.
Анотація:
Insulin resistance is the major metabolic defect in obesity and Type 2 diabetes. Increased lipid accumulation is strongly associated with insulin resistance. A significant component of insulin resistance is thought to be a reduced ability of insulin to activate the cascade of phosphorylation events that lead to the metabolic effects of this hormone. The broad aims of this thesis were to examine the effect of high-fat diets containing different fat subtypes on in vivo insulin signalling, under conditions normally used to detect whole body insulin resistance, and to compare the effects of acute and chronic lipid oversupply on insulin signalling in vivo. Time-course and dose-response effects of insulin stimulation on site-specific phosphorylation of key signalling proteins were studied in rat tissues in vivo, to establish an appropriate experimental system to examine the onset of activation of the insulin signalling pathway. It was determined that short insulin infusions with concurrent glucose infusion, similar to the beginning of a euglycaemic-hyperinsulinaemic clamp, significantly increased the phosphorylation of major intermediates of the insulin signalling pathway in important tissues of insulin action (skeletal muscle [RQ], liver [LIV] and white adipose tissue [EPI]). These experiments provided a platform to study insulin signalling under the same conditions used to study lipid-induced insulin resistance. The provision of diets enriched in polyunsaturated or saturated fatty acids (FA) resulted in the corresponding enrichment of these fat subtypes in rat plasma and tissues. However, the effects on insulin signalling were essentially the same. Both fat diets induced defects in sitespecific phosphorylation of insulin receptor substrate (IRS)-1 and protein kinase B (PKB) in RQ and LIV, but not EPI. This suggests that the amount of fat in the diet, rather than enrichment in a particular fat subtype, had a greater impact on the development of signalling defects and that the response to high-fat feeding was tissue-specific. A 3hr elevation of circulating FA (using a lipid/heparin infusion), to a level that is relevant in clinical Type 2 diabetes, impaired insulin-stimulated PKB phosphorylation with no significant effect on IRS-1 phosphorylation. This suggests that there may be differences in the way acute and chronic exposure to increased FA impair insulin signalling. The phosphorylation defects observed in both chronic and acute studies did not seem to be associated with activation of major stress signalling pathways (JNK and NFkB), which have been suggested to have a role in lipidinduced insulin resistance. In conclusion, these studies demonstrate that impaired IRS-1 and PKB phosphorylation do have a role in the reduced insulin action observed with lipid oversupply in vivo, because the changes were detected under similar conditions as those used to determine whole body insulin resistance.
2
Pott, Markus Philipp. "Organic hydroperoxide-induced lipid peroxidation (LPO) and signal transduction pathways in human keratinocytes." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=96545293X.
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FEZZA, FILOMENA. "Regulation of endocannabinoid system by lipid rafts along the neuroimmune axis." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2006. http://hdl.handle.net/2108/202611.
Анотація:
L’anandamide (arachidonoiletanolammide, AEA), insieme con l’altro endocannabinoide 2arachidonoilglicerolo (2-AG), lega ed attiva i due recettori accoppiati a proteine G inibitorie, (GPCR), chiamati recettori dei cannabinoidi di tipo-1 (CB1R) e di tipo-2 (CB2R). I CB1R sono localizzati principalmente nel sistema nervoso centrale, ma sono anche espressi in tessuti periferici come le cellule immunitarie. Mentre i CB2R sono maggiormente espressi a livello periferico, ma sono anche presenti nel cervello. Quindi l’attivazione dei recettori CB1 o CB2 da parte dell’AEA e del 2-AG ha molti effetti sia a livello centrale che periferico. Queste azioni sono controllate attraverso un non ancora caratterizzato meccanismo cellulare, che regola il rilascio degli endocannabinoidi da precursori di membrana, il loro trasporto all’interno delle cellule, ed infine la loro eliminazione. L’agente chiave nella sintesi dell’AEA è la N-acilfosfatidiletanolammine (NAPE)-fosfolipasi D (NAPE-PLD), mentre la sua degradazione avviene attraverso un trasportatore di membrana per AEA (AMT), ed una fatty acid amide hydrolase (FAAH). Oltre i recettori CB, l’AEA lega anche il recettore dei vanilloidi di tipo 1 (TRPV1). Il 2-AG è invece rilasciato da lipidi di membrana per azione di una lipasi specifica, sn-1-diacilglicerolo (DAGL), ed è idrolizzato da una specifica monoacilglicerolo lipasi (MAGL). E’ stato dimostrato che il trasporto del 2-AG attraverso la membrana cellulare è saturabile ed energia-indipendente e che può occorrere attraverso lo stesso trasportatore dell’AEA. L’AEA ed il 2-AG, con altri congeneri, le proteine che legano, trasportano, sintetizzano ed idrolizzano questi lipidi formano il “sistema endocannabinoide”. I lipid rafts sono subdomini della membrana plasmatica che contengono alte concentrazioni di colesterolo e di sfingolipidi, e sono ben conosciuti modulatori dell’attivitità di un numero di GPCR. Infatti, essi modulano il segnale ed il “trafficking” in molti tipi cellulari. La crescente evidenza che i lipid rafts possono modulare il segnale degli endocannabinoidi ci ha spinto ad investigare il possibile effetto della loro integrità sui recettori CB, sul metabolismo dell’AEA e del 2-AG in cellule neuronali e del sistema immunitario. A tale scopo abbiamo utilizzato la metil-β-ciclo destrina (MCD), un depletore del colesterolo, un composto largamente utilizzato per distruggere l’integrità dei lipid rafts. Abbiamo utilizzato le cellule di glioma di ratto C6, perché esse hanno un ben caratterizzato sistema endocannabinoide. Abbiamo poi esteso lo studio alla linea cellulare di neuroblastoma umano CHP100, la quale ha la stessa abilità delle cellule C6 di metabolizzare l’AEA, ma sono prive del CB1R e quindi sono più sensibili all’attività pro-apoptotica dell’AEA. Abbiamo inoltre esteso lo studio agli enzimi che degradano e sintetizzano il 2-AG. Inoltre, abbiamo studiato la linea cellulare umana DAUDI, perché possiede l’AMT e l’enzima FAAH ed esprime un CB2R funzionale. Le cellule DAUDI, inoltre, regolano importanti funzione in cui sono coinvolti i lipid rafts, come la secrezione di esosomi e l’arresto della crescita indotta dai farmaci antitumorali. Inoltre abbiamo valutato l’effetto della deplezione e dell’arrichimento di colesterolo sul metabolismo degli endocannabinoidi. In conclusione, questo studio ha monitorato l’effetto dell’integrità dei lipid rafts sulle principali proteine che legano e metabolizzano l’AEA ed il 2-AG, sia in cellule neuronali che in cellule del sistema immunitario. Tale studio indica che il CB1R ed il trasportatore degli endocannabinoidi sono probabilmente localizzati all’interno dei lipid rafts a differenza del CB2R e delle altre proteine che compongono il sistema endocannabinoide.Anandamide (arachidonoylethanolamide, AEA) and the other endocannabinoid 2-arachidonoylglycerol (2-AG) bind to and activate two G protein-coupled receptors (GPCR), namely type-1 (CB1R) and type-2 (CB2R) cannabinoid receptors. CB1R are localized mainly in the central nervous system, but are also expressed in peripheral tissues like immune cells. Conversely CB2R are predominantly expressed peripherally, but they are also present in the brain. Therefore, activation of CB1 or CB2 receptors by AEA or 2-AG has many central and peripheral effects. These actions are controlled through not yet fully characterized cellular mechanisms, that regulate the release of endocannabinoids from membrane precursors, their uptake by cells, and finally their intracellular disposal. The key agent in AEA synthesis is the N-acylphosphatidylethanolamines (NAPE)-hydrolyzing phospholipase D (NAPE-PLD), whereas degradation occurs through an AEA membrane transporter (AMT), and a fatty acid amide hydrolase (FAAH). Besides CB receptors, AEA binds also to type 1 vanilloid receptors (now called transient receptor potential channel vanilloid receptor subunit 1, TRPV1). On the other hand, 2-AG is released from membrane lipids by means of a sn-1-specific diacylglycerol lipase (DAGL), and is hydrolyzed by a specific monoacylglycerol lipase (MAGL). The transport of 2-AG through the cellular membrane has been shown to be saturable and energyindependent, and might occur through the same AMT that transports AEA. Altogether AEA and 2-AG, with other congeners, the proteins that bind, transport, synthesize and hydrolyze these lipids, form the “endocannabinoid system”. Lipid rafts are subdomains of the plasma membrane that contain high concentrations of cholesterol and glycosphingolipids, and are well-known modulators of the activity of a number of GPCR. In fact, they modulate signaling and membrane trafficking in many cell types. The growing evidence suggesting that lipid rafts might modulate the endocannabinoid signaling prompted us to investigate also the possible effect of lipid rafts integrity on CB receptors, on AEA metabolism in neuronal and immune cells and on the proteins that synthesize, transport and degrade 2-AG. We have used the methyl--cyclodextrin (MCD), a membrane cholesterol depletor that is widely used to disrupt the integrity of lipid rafts. We have chosen rat C6 glioma cells, because they have a well characterized endocannabinoid system. We extended the study to human CHP100 neuroblastoma cells, which have the same ability as C6 cells to metabolize AEA, but are devoid of CB1R and hence are more sensitive to the pro-apoptotic activity of AEA. We did not further extend this study to 2-AG and the enzymes that degrade and synthesize it, because 2-AG does not have pro-apoptotic activity toward C6 cells or CHP100 cells, in keeping with the observation that it does not activate TRPV1 receptors. Furthermore, we have chosen human DAUDI leukemia cells, because they have active AMT and FAAH, and express functional CB2R. On the other hand, in DAUDI cells lipid rafts regulate important functions like exosome secretion, or growth arrest induced by antitumor drugs. In addition, we checked for the first time the effect of membrane cholesterol depletion or enrichment on 2-AG metabolism in C6 cells and DAUDI cells. In conclusion, this study monitor the effect of lipid rafts integrity on all the major proteins that bind and metabolize AEA and 2-AG, both in neuronal and immune cells. The results point out that CB1R and endocannabinoid transporters are probably localized within lipid rafts, at variace with CB2R and the other proteins of the endocannabinoid system.
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Sampey, Brante P. "Studies of the adduction of hepatocellular proteins by 4-HNE in animals [sic] models of alcoholic liver disease : systematic analysis of hepatocellular Erk 1/2 modulation and dysregulation of the Erk-Elk-AP1 signal transduction pathway /." Connect to full text via ProQuest. IP filtered, 2005.
Анотація:
Thesis (Ph.D. in Toxicology) -- University of Colorado, 2005.Typescript. Includes bibliographical references (leaves 141-156). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Metcalfe, Maureen Grage. "Two-dimensional crystallization of archaeal signal peptide peptidases for structural studies by electron crystrallography." Thesis, Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53984.
Анотація:
The membrane proteins signal peptide peptidase, signal peptide peptidase like and presenilin are intramembrane aspartyl proteases located in the endoplasmic reticulum, plasma membrane and organelle. These membrane proteins are able to catalyze a hydrolytic reaction in a hydrophobic space. The downstream consequences of these reactions impact a variety of cellular functions such as cytokine production, inflammatory responses, embryogenesis, and immune system regulation. Additionally, the aspartyl proteases such as signal peptide peptidase and presenilin, a part of the γ-secretase complex, hydrolyze peptides leading to pathogen maturation and Alzheimer’s disease, respectively.
Electron crystallography offers the unique aspect of studying membrane proteins in a near native state. Determining the structures of Haloarcula morismortui and Methanoculleus marisnigri JR1 signal peptide peptidases by electron crystallography may provide insight into how a hydrolysis reaction occurs in a hydrophobic environment and how the protein determines which transmembrane signal peptides to cleave. Additionally, structure determination may help answer questions regarding why human presenilin, part of the γ-secretase complex, incorrectly processes amyloid precursor protein into amyloid-beta peptides leading to Alzheimer’s disease. Such structural data may not only shed light on how amyloid precursor protein is processed but how other proteins are processed by signal peptide peptidase leading to immune responses, cell signaling, and pathogen maturation. In addition, structure-function data may have an impact on pharmaceutical drug designs that targets signal peptide peptidase, signal peptide peptidase like, and/or presenilin.
To determine the structure of aspartyl proteases, two archaeal signal peptide peptidases were used for two-dimensional crystallization trials to be able to study their structure by electron crystallography. Haloarcula morismortui and Methanoculleus marisnigri JR1 signal peptide peptidases, both human signal peptide peptidase homologues, were recombinantly over-expressed and purified. During dialysis trials, various lipid-to-protein ratios, sodium chloride concentrations, temperatures, detergents and a variety of other variables were tested.
Methanoculleus marisnigri JR1 signal peptide peptidase showed the most promising results in terms of crystallinity. Optimizing dialysis conditions, specifically narrowing the lipid to protein ratio, resulted in two-dimensional crystals. Ordered arrays measuring up to 200 nm x 200 nm were observed. These ordered arrays have been shown to be reproducible amongst multiple batches of purified Methanoculleus marisnigri JR1 signal peptide peptidase. Preliminary projection maps of negatively stained ordered arrays show unit cell dimensions of a = 178 Å, b = 160 Å, γ = 92.0 Å and a = 175 Å, b = 167 Å, γ = 92.0 Å. The monomer measurements are approximately 70 Å by 80 Å. This is the first time a signal peptide peptidase homologue has been crystallized by two-dimensional crystallization.
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Lautscham, Lena Astrid [Verfasser], and Ben [Akademischer Betreuer] Fabry. "Cell migration and mechanosensitive signal transduction on 2-dimensional biomembrane-mimicking lipid bilayer stacks and in confined 3-dimensional microstructures / Lena Astrid Lautscham. Gutachter: Ben Fabry." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2015. http://d-nb.info/1076166105/34.
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Casiraghi, Marina. "Functional modulation of a G protein-coupled receptor conformational landscape in a lipid bilayer." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC138/document.
Анотація:
Les récepteurs couplés aux protéines G (GPCRs en anglais) représentent la famille de récepteurs intégrales de membrane plus vaste dans la majorité des cellules eucaryotes. Ils jouent un rôle clé dans la transduction de signal, ainsi que la compréhension de leur mécanisme de signalisation représente une des questions principales dans la biologie d'aujourd'hui. Dans la caractérisation du paysage énergétique de ces récepteurs à l'échelle atomique, les structures cristallographiques publiées pendant la décennie dernière par cristallographie aux rayons X représentent la percée scientifique majeure et donnent une contribution fondamentale dans la biologie structurelle de GPCRS. Ces structures représentent un point de départ précieux dans la compréhension du mécanisme de transduction de signal, en plaçant des structures dans l'ensemble conformationnel de ces récepteurs le long du processus d'activation. Pour compléter ce cadre de structures statiques qui correspondent aux états à basse l'énergie et fortement peuplés, une caractérisation de l'ensemble conformationnel et des barrières cinétiques qui sont associées est un point nécessaire et fondamentale. À ce but nous proposons une approche innovant avec la finalité d'observer le paysage conformationnel dynamique des GPCR et étudier la modulation de ces récepteurs par des ligands et des lipides, qui sont connus pour jouer un rôle clé dans la structure et les fonctions des protéines de membrane (e.g.). Un des outilles le plus approprié pour explorer les barrières cinétiques de GPCR c'est la résonance magnétique nucléaire (RMN) en solution. Pour tirer profit au mieux de cette technique, nous avons utilisé des sondes marqués 13CH3 immergées dans un environnement perdeuteré, qui constitue le marquage isotopique le plus approprié en RMN pour examiner les paysages conformationnels des protéines de grosses dimensionnes ou des complexes de protéines. Nous avons choisi Escherichia coli comme système d'expression pour sa capacité de pousser dans des conditions très hostiles comme des solutions 100%-D2O. Pour surmonter les difficultés habituellement rencontrées lors de l'expression des GPCRs, nous avons appliqué un protocole innovant qui cible l'expression de GPCRs directement aux corps d'inclusion. Ceci permet la production des bonnes quantités de protéines (jusqu’à 6 mg/litres de culture de pur 13CH3-u-2H-GPCRs). Une fois purifié, le récepteur est foldé en amphipols et transféré ensuite à une double couche lipidique appelée nanometric lipid bilayer ou nanodisc (NLB). De façon très important, les mesures pharmacologiques quantitatives indiquent que les récepteurs incorporés dans des NLBs après ce protocole sont stables et entièrement actifs dans les conditions des expériences de NMR.Les investigations par RMN conduites sur le GPCR en NLB ont donné lieu à une résolution jamais obtenue dans le domaine, grâce à la biochimie finement accordée et à la perdeuteration du récepteur. Selon les données obtenues, notre récepteur modèle, le récepteur 2 pour le leukotriene B4 (BLT2), est capable d'explorer plusieurs conformations différentes, même dans l'état pas lié aux ligands, y compris l'état actif. Ce paysage conformationnel est également modulé par des ligands et des lipides. Dans le cas spécifiques, nous avons observé que un incrément dans le contenu de stérol dans la membrane modifie la distribution des différents états conformationnels du récepteur, en favorisant l'état actif, qui indique une régulation allosteric positif du stérol sur l'activation de ce récepteur, comme confirmé aussi par les mesures de liaison du GTP à la protéine G. Cette propriété du stérol est probablement importante pour le contrôle de mécanisme de signalisation de GPCRsG protein-coupled receptors (GPCRs) are the largest family of integral membrane protein receptors present in most eukaryotic cells. They play a key role in signal transduction and understanding their signalling mechanism represents one of the main issues in biology today. In the characterization of the energy landscape of these receptors, at the atomic scale, X-ray crystal atomic structures published during the last decade represent the major breakthrough and contribution in the structural biology of GPCRs. They represent a precious starting point in the understanding of the mechanism of signal transduction by placing structures in the conformational ensemble of these receptors along the activation pathway. To complete these static snapshots that correspond to low energy and highly populated states, a characterization of the whole conformational ensemble and associated kinetic barriers is fundamental to complete the picture. To this aim we proposed an innovative approach to observe GPCRs dynamic conformational landscape and how it is modulated by ligands and lipids, that are known to play a key role in membrane protein structures and functions (e.g.). One of the most appropriate tool to explore GPCR kinetic barriers is solution state NMR. To do so, we used 13CH3 probes immersed in a perdeuterated environment, the most appropriate isotope-labelling scheme to investigate conformational landscapes of large proteins or protein complexes with this spectroscopy. We chose Escherichia coli as expression system for its ability to grow in very hostile conditions like 100%-D2O solutions. In order to overcome the usual expression issues concerning GPCRs, we applied an innovative protocol which targets the expression directly to inclusion bodies. This allows the production of high amounts of proteins (up to 6 mg/litre of culture of pure 13CH3-u-2H-GPCRs). Once purified, receptors are folded in amphipols and then transferred to nanometric lipid bilayers or nanodiscs. Importantly quantitative pharmacological measurements indicate that receptors embedded in NLBs following this protocol are stable and fully active in the conditions of the NMR experiments. NMR investigation of a GPCR in a NLB gave rise to a resolution never achieved in the field thanks to a fine tuned biochemistry and a perdeuteration of the receptor. According to our data, the prototypical receptor, the leukotriene B4 receptor (BLT2), is able to explore multiple different conformations, even in the unliganded state, including the active state. This conformational landscape is further modulated by ligands and lipids. In particular, we observed that an increment in the sterol content of the membrane modifies the distribution of the different conformational states of the receptor in favour of the active one, indicating a positive allosteric regulation of the sterol on the activation of this receptor, as confirmed by GTP-to-G protein binding measurements. This property of the sterol is likely important for the control of the signalling properties of GPCRs
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Panakova, Daniela. "Lipoprotein particles associate with lipid-linked proteins and are required for long-range Wingless and Hedgehog signaling." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2005. http://nbn-resolving.de/urn:nbn:de:swb:14-1122025765300-27455.
Анотація:
Morphogens of the Wnt and Hedgehog families are secreted signaling molecules that coordinate growth and patterning of many different tissues. Both, Wingless and Hedgehog spread across long distances in developing wing of Drosophila melanogaster. However, both proteins are covalently modified with lipid moieties. The mechanisms that allow long-range movement of such hydrophobic molecules are unclear. Like Wingles and Hedgehog, glycosylphosphatidylinositol (gpi)-linked proteins also transfer between cells with their lipid anchor intact. It has been speculated that gpi-linked proteins and lipid-linked morphogens travel together on a membranous particle, which was termed an argosome. As yet however, no functional link between argosome production and dispersal of lipid-linked proteins has been established. The topic of this thesis is to understand the cell biological nature of the argosome and thus contribute to understanding of morphogen gradient formation. To address the question of argosome biosynthesis, at least two models have been proposed. One possibility is that argosomes are membranous exovesicles with a complete membrane bilayer. Alternatively, argosomes might resemble lipoprotein particles that comprise on of a family of apolipoproteins scaffolded around a phospholipid monolayer that surrounds a core of esterified cholesterol and triglyceride. Lipid-modified proteins of the exoplasmic face of the membrane (like GFPgpi, Wingless or Hedgehog) might fit well into the outer phospholipid monolayer of such a particle. Here, I utilize biochemical fractionation to determine the sort of particle that lipid-linked proteins associate with. I show that Wingless, Hedgehog and gpi-linked proteins bind Drosophila lipoprotein particles in vitro, and colocalize with them in wing imaginal discs. Next, I use genetic means to address the functional importance of this association. I demonstrate that reducing Lipophorin levels in Drosophila larvae perturbs long-range but not shor-range Wingless and Hedgehog signaling, and increases the sequestration of Hedgehog by Patched. I propose that Lipophorin particles are vehicles for the long-range movement of lipid-linked morphogens and gpi-linked proteins.
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Poidevin, Mickaël. "La synthèse d'acides gras dans des cellules spécialisées agit à distance sur le processus d'activation des ovocytes chez la drosophile." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL016.
Анотація:
Une étude statistique de l'organisation mondiale de la santé a révélé qu'un adulte sur six est concerné par des problèmes d'infertilité. Ce sujet majeur de nos sociétés est complexe, multifactoriel avec une évolution à l'échelle mondiale qui est difficile à évaluer. Il est donc essentiel de mener davantage de recherche pour mieux comprendre l'évolution de l'infertilité, mais aussi les mécanismes cellulaires et moléculaires conduisant à une bonne fertilité.Fortuitement, un crible génétique des enzymes responsables de la synthèse des acides gras dans des cellules spécialisées de la drosophile a déclenché un phénotype de stérilité. Ces cellules spécialisées que l'on nomme oenocytes sont essentielles aux métabolismes des acides gras et impliquées dans de nombreux processus tels que l'homéostasie lipidique, la protection contre la dessication et la communication phéromonale.Mes travaux montrent que la synthèse d'un ou plusieurs acides gras à très longue chaîne dans les oenocytes est indispensable à la fertilité des femelles et que le défaut de cette synthèse provoque une rétention des spermatozoïdes dans les organes de stockage, spermathèques et réceptacle séminal. J'ai montré que le phénotype de stérilité n'est pas lié à un défaut d'activité des spermatozoïdes et qu'ils fertilisent efficacement les ovocytes matures. En revanche mes résultats indiquent que les oeufs présentent un défaut d'activation empêchant leur développement.Chez les insectes l'activation de l'ovocyte mature qui permet le développement embryonnaire ne dépend pas de l'entrée du spermatozoïde comme chez les mammifères. Cette activation est déclenchée par un signal calcique lors du passage dans les voies génitales femelles. L'ensemble de mes résultats montrent pour la première fois qu'un signal lipidique extra-génital provoque l'activation des ovocytes matures permettant ainsi l'induction du développement embryonnaireA statistical study by the World Health Organization revealed that one adult over six is affected by infertility problems. This major social issue is complex and multifactorial, with worldwide trends that are difficult to assess. It is therefore essential to carry out more research to better understand not only the evolution of infertility, but also the cellular and molecular mechanisms leading to efficient fertility.Serendipitously, we discovered that a genetic screen to enzymes responsible for fatty acid synthesis in specialized Drosophila cells provoked a sterile phenotype. These specialized cells, called as oenocytes, are essential for fatty acid metabolism, and are involved in numerous processes, including lipid homeostasis, protection against desiccation and pheromonal communication.My work shows that the synthesis of one or more very long-chain fatty acids in oenocytes is essential for female fertility, and that a defect in this synthesis causes spermatozoa to be retaintion in the storage organs, spermathecae and seminal receptacle. I have shown that the sterility phenotype is not linked to a defect in sperm activity, and that sperm fertilize mature oocytes efficiently. On the other hand, my results indicate that the eggs show an activation defect preventing their development.In insects, activation of the mature oocyte, which leads to embryonic development, is not dependent on sperm entry as in mammals. This activation is triggered by a calcium signal while the oocyte moves through the female genital tract. Taken together, my results show for the first time that an extra-genital lipid-signal triggers the activation of mature oocytes, thus enabling the induction of embryonic development
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Waterstradt, Katja. "Der Einfluss des Cholesterolgehaltes der Diskmembranen des Stäbchenaußensegmentes auf die ersten Schritte der visuellen Signaltransduktion." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15949.
Анотація:
Das Außensegment der Stäbchenzelle ist aus einem Stapel von flachen Membransäckchen, den Diskmembranen, aufgebaut. Entlang dessen existiert ein Cholesterolgradient mit 24 mol% Cholesterol in den basalen Diskmembranen und 5 mol% in den apikalen. Das Außensegment enthält alle Proteine der Signaltransduktion. Der Photorezeptor Rhodopsin ist als integrales Membranprotein in die Diskmembran eingebettet. Das G-Protein Transducin und das Effektorprotein, die Phosphodiesterase (PDE), sind periphere Proteine mit Lipidankern und somit reversibel mit der Membranoberfläche assoziiert. Um den Einfluss des Cholesterolgehaltes der Diskmembranen auf diese drei Proteine zu untersuchen, wurden Diskmembranen mit unterschiedlichem Cholesterolgehalt präpariert (Simulation des Cholesterolgradienten). Die Untersuchungen zur transversalen Verteilung des Cholesterols in der Diskmembran ergaben eine schnelle Transmembranbewegung mit einer Halbwertzeit von weniger als einer Minute bei 35 °C. Desweiteren konnte gezeigt werden, dass es zu kopfgruppenspezifischen Wechselwirkungen von Cholesterol mit dem Phospholipid Phosphatidylcholin kommt. Cholesterol verschiebt das Meta I-Meta II-Gleichgewicht (nach Lichtaktivierung von Rhodopsin) auf die Seite von Meta I (inaktiv). In dieser Arbeit konnte jedoch gezeigt werden, dass durch die Anwesenheit des Transducins das Gleichgewicht vollständig auf die Seite von Meta II (aktiv) verschoben wird, da Transducin spezifisch die Meta-II-Form stabilisiert. Somit kann die verminderte Meta II-Bildung des Rezeptors in Diskmembranen mit hohem Cholesterolgehalt durch Transducin ausgeglichen werden. Lediglich die Geschwindigkeit der Transducinaktivierung ist verlangsamt. Durch den erhöhten Cholesterolgehalt werden die Membraneigenschaften für eine Bindung der beiden peripheren Proteine Transducin und PDE über deren Lipidanker optimiert. Somit kann die Signaltransduktion auch in den basalen Diskmembranen des Stäbchenaußensegmentes stattfinden.The rod outer segment consists of a stack of flat membrane saccules called disc membranes. Along this stack a cholesterol gradient exists with 24 mol% cholesterol in the basal and only 5 mol% in the apical disc membranes. The outer segment contains all the proteins necessary for signal transduction. The photoreceptor rhodopsin as integral membrane protein is embedded in the disc membrane. The G protein transducin and the effector protein phosphodiesterase (PDE) are soluble proteins with lipid modifications, which are associated reversibly to the membrane surface. Disc membranes with different cholesterol contents were prepared to simulate the cholesterol gradient along the rod outer segment and to investigate the influence of disc membrane cholesterol content of these three proteins. Investigations of the transversal distribution of cholesterol in the disc membrane revealed a fast transmembrane movement with a half life of less than one minute at 35 °C. Further, head group specific interactions between cholesterol and phosphatidylcholine could be shown. The Meta I Meta II equilibrium after light activation of rhodopsin was shifted to the Meta I (inactive) site in membranes with high cholesterol. In this work it was shown that in the presence of transducin this equilibrium is shifted completely to the Meta II (active) site because transducin stabilizes specifically the Meta II form of the receptor. Hence the reduced Meta II formation in disc membranes with high cholesterol could be compensated by transducin. The speed of transducin activation is decelerated. By the increased cholesterol content membrane properties are optimized to the binding of transducin and PDE via their lipid modifications. Thus the signal transduction can take place also in disc membranes with high cholesterol.
Книги з теми "Lipid signal":
1
Larijani, Banafshé. Lipid signaling protocols. New York, N.Y: Humana, 2009.
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Banafshé, Larijani, Woscholski Rudiger, and Rosser Colin A, eds. Lipid signaling protocols. New York, N.Y: Humana, 2009.
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S, Bell Robert M., Exton John H. 1933-, and Prescott Stephen M, eds. Lipid second messengers. New York: Plenum Press, 1996.
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G, Laychock Suzanne, and Rubin Ronald P, eds. Lipid second messengers. Boca Raton: CRC Press, 1999.
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G, Laychock Suzanne, and Rubin Ronald P, eds. Lipid second messengers. Boca Raton, Fla: CRC Press, 1998.
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Munnik, Teun. Lipid Signaling in Plants. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.
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1963-, Murphy Eric J., and Rosenberger Thad A, eds. Lipid-mediated signaling. Boca Raton: CRC Press/Taylor & Francis, 2009.
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Murphy, Eric J. Lipid-mediated signaling. Boca Raton, FL: CRC Press/Taylor & Francis, 2010.
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Raeburn, David, and Mark A. Giembycz, eds. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7504-2.
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1953, Raeburn D., and Giembycz M. A. 1961-, eds. Airways smooth muscle: Neurotransmitters, amines, lipid mediators, and signal transduction. Basel: Birkhauser Verlag, 1995.
Частини книг з теми "Lipid signal":
1
Zheng, Ning, Joanna L. Feltham, and Lila M. Gierasch. "In Vitro Studies of the Interactions Between Signal Peptides and Signal Recognition Factors." In Lipid and Protein Traffic, 125–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-51463-0_11.
2
Scherer, Günther F. E. "Phospholipase A in Plant Signal Transduction." In Lipid Signaling in Plants, 3–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_1.
3
Duckworth, Brian C., and Lewis C. Cantley. "PI 3-Kinase and Receptor-Linked Signal Transduction." In Lipid Second Messengers, 125–75. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1361-6_4.
4
Li, Li. "Active Targeting: Mitochondria-Targeting Signal Peptides." In Functional Lipid Nanosystems in Cancer, 471–81. New York: Jenny Stanford Publishing, 2021. http://dx.doi.org/10.1201/9781003056997-18.
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Pérez-Sancho, Jessica, Arnaldo L. Schapire, Miguel A. Botella, and Abel Rosado. "Analysis of Protein–Lipid Interactions Using Purified C2 Domains." In Plant Signal Transduction, 175–87. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3115-6_14.
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Scherer, Günther F. E. "Biologically Active Lipids and Lipid-modulated Protein Kinase in Plants." In Signal Transduction in Plant Growth and Development, 197–215. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-7474-6_8.
7
Wardle, E. Nigel. "Lipid Products and Cell Signaling." In Guide to Signal Pathways in Immune Cells, 101–9. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_7.
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Roberts, Mary F. "Phospholipases: Generation of Lipid-Derived Second Messengers." In Introduction to Cellular Signal Transduction, 89–146. Boston, MA: Birkhäuser Boston, 1999. http://dx.doi.org/10.1007/978-1-4612-1990-3_6.
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Sandra, Alex, Wouter van’t Hof, Ida van Genderen, and Gerrit van Meer. "Lipid Synthesis and Targeting to the Mammalian Cell Surface." In Phospholipids and Signal Transmission, 13–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02922-0_2.
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Murphy, Eric J., and Lloyd A. Horrocks. "CDPcholine, CDPethanolamine, Lipid Metabolism and Disorders of the Central Nervous System." In Phospholipids and Signal Transmission, 353–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02922-0_28.
Тези доповідей конференцій з теми "Lipid signal":
1
Hernandez, Christopher, Jacob L. Lilly, Pinunta Nittayacharn, Judy Hadley, Robert Coyne, Michael Kolios, and Agata A. Exner. "Ultrasound signal from sub-micron lipid-coated bubbles." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8091670.
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Hernandez, Christopher, Jacob Lilly, Gabriellla Fioravanti, Judy Hadley, and Agata A. Exner. "Ultrasound signal from sub-micron lipid-coated bubbles." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092139.
3
Hernando, Diego, Justin Haldar, Bradley Sutton, and Zhi-pei Liang. "REMOVAL OF LIPID SIGNAL IN MRSI USING SPATIAL-SPECTRAL CONSTRAINTS." In 2007 4th IEEE International Symposium on Biomedical Imaging: From Nano to Macro. IEEE, 2007. http://dx.doi.org/10.1109/isbi.2007.357113.
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Ji, Yulin, Yujuan Wang, Wei Si та Yunfei Chen. "Molecular dynamics study on the effect of lipid membrane mechanical properties on the interaction between β-amyloid and lipid membrane". У 2020 14th International Conference on Signal Processing and Communication Systems (ICSPCS). IEEE, 2020. http://dx.doi.org/10.1109/icspcs50536.2020.9310006.
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Park, Sang Min, Seongjin Bak, Gyeong Hun Kim, Soon-Woo Cho, Hyung-Hoi Kim, Yeong Jin Kim, and Chang-Seok Kim. "Multi-wavelength Raman fiber laser for photoacoustic signal sensing of lipid." In Optical Sensors. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/sensors.2023.stu5d.5.
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Pan, Min-chun, Chien-hung Chen, and Min-cheng Pan. "NIR Optical-Property Images of Heterogeneous Intra-lipid Phantom." In 2006 IEEE International Symposium on Signal Processing and Information Technology. IEEE, 2006. http://dx.doi.org/10.1109/isspit.2006.270767.
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Yingchun, Lv, Ma Fuchang, and Ma Jun. "The research of modified solid supported bilayer lipid membrane electrode characteristics." In 2010 2nd International Conference on Signal Processing Systems (ICSPS). IEEE, 2010. http://dx.doi.org/10.1109/icsps.2010.5555817.
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Taylor, Graham, Donald Leo, and Andy Sarles. "Detection of Botulinum Neurotoxin/A Insertion Using an Encapsulated Interface Bilayer." In ASME 2012 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/smasis2012-8101.
Анотація:
Many signaling mechanisms in living cells occur at biological boundaries via cell surface receptors and membrane proteins embedded in lipid bilayers. The coordination of actions of sensory and motor neurons in the nervous system represents one example of many that heavily depends on lipid membrane bound receptor mediated signaling. As a result, chemical and biological toxins that disrupt these neural signals can have severe physiological effects, including paralysis and death. Botulinum neurotoxin Type A (BoNT/A) is a proteolytic toxin that inserts through vesicle membranes and cleaves membrane receptors involved with synaptic acetylcholine uptake and nervous system signal conduction. In this work, we investigate the use of a Bioinspired liquid-supported interface bilayer for studying the insertion of BoNT/A toxin molecules into synthetic lipid bilayers. DPhPC lipid bilayers are formed using the regulated attachment method (RAM), as developed by Sarles and Leo, and we perform current measurements on membranes exposed to BoNT/A toxin to characterize activity of toxin interacting with the synthetic bilayer. Control tests without toxin present are also presented. The results of these tests show an increase in the magnitude of current through the bilayer when the toxin is included. We interpret these initial results to mean that incorporation of BoNT/A toxin at a high concentration in an interface bilayer increases the permeability of the membrane as a result of toxin molecules spanning the thickness of the bilayer.
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Lee, HeaYeon, and JuKyung Lee. "Advanced Biomimetic Nanodevice Using Nanotechnology Addressable Lipid Rafts Nanoarrays Toward Advanced Nanomaterials." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93286.
Анотація:
In recent years, a new paradigm of nanobiomedical devices combining miniaturization and integration has been exploited in areas such as combinational chemistry, biotechnology, engineering, proteomics and clinical diagnostics. One of the critical issues in the development of nanobiomedical system is how to differentiate signal-to-noise ratio per very small amount of signal. Biocompatible integrated nanopattern requires the fabrication of appropriately designed nanomatrix for high sensitivity homogenous assays, which are capable of ultimately mimic the physiological environment. We reported the nanomatrix geometry of a well-oriented nanowell array derived from nanofabrication technology which can easily be employed for digital detection with a high S/N ratio, miniaturization, integrated assays and single molecule analysis. In this present, we describe a nano(submicro) array of tethered lipid bilayer raft membranes comprising a biosensing platform.
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Shamitko-Klingensmith, Nicole, Kelley M. Wambaugh, Kathleen A. Burke, George J. Magnone, and Justin Legleiter. "Correlation of Atomic Force Microscopy Tapping Forces to Mechanical Properties of Lipid Membranes." In ASME 2012 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/detc2012-70233.
Анотація:
There is considerable interest in measuring, with nanoscale spatial resolution, the physical properties of lipid membranes because of their role in the physiology of living systems. Due to its ability to nondestructively image surfaces in solution, tapping mode atomic force microscopy (TMAFM) has proven to be a useful technique for imaging lipid membranes. However, further information concerning the mechanical properties of surfaces is contained within the time-resolved tip/sample force interactions. The tapping forces can be recovered by taking the second derivative of the cantilever deflection signal and scaling by the effective mass of the cantilever; this technique is referred to as scanning probe acceleration microscopy. Herein, we describe how the maximum and minimum tapping forces change with surface mechanical properties. Furthermore, we demonstrate how these changes can be used to measure mechanical changes in lipid membranes containing cholesterol.
Звіти організацій з теми "Lipid signal":
1
Brown Horowitz, Sigal, Eric L. Davis, and Axel Elling. Dissecting interactions between root-knot nematode effectors and lipid signaling involved in plant defense. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598167.bard.
Анотація:
Root-knot nematodes, Meloidogynespp., are extremely destructive pathogens with a cosmopolitan distribution and a host range that affects most crops. Safety and environmental concerns related to the toxicity of nematicides along with a lack of natural resistance sources threaten most crops in Israel and the U.S. This emphasizes the need to identify genes and signal mechanisms that could provide novel nematode control tactics and resistance breeding targets. The sedentary root-knot nematode (RKN) Meloidogynespp. secrete effectors in a spatial and temporal manner to interfere with and mimic multiple physiological and morphological mechanisms, leading to modifications and reprogramming of the host cells' functions, resulted in construction and maintenance of nematodes' feeding sites. For successful parasitism, many effectors act as immunomodulators, aimed to manipulate and suppress immune defense signaling triggered upon nematode invasion. Plant development and defense rely mainly on hormone regulation. Herein, a metabolomic profiling of oxylipins and hormones composition of tomato roots were performed using LC-MS/MS, indicating a fluctuation in oxylipins profile in a compatible interaction. Moreover, further attention was given to uncover the implication of WRKYs transcription factors in regulating nematode development. In addition, in order to identify genes that might interact with the lipidomic defense pathway induced by oxylipins, a RNAseq was performed by exposing M. javanicasecond-stage juveniles to tomato protoplast, 9-HOT and 13-KOD oxylipins. This transcriptome generated a total of 4682 differentially expressed genes (DEGs). Being interested in effectors, we seek for DEGs carrying a predicted secretion signal peptide. Among the DEGs including signal peptide, several had homology with known effectors in other nematode species, other unknown potentially secreted proteins may have a role as root-knot nematodes' effectors which might interact with lipid signaling. The molecular interaction of LOX proteins with the Cyst nematode effectors illustrate the nematode strategy in manipulating plant lipid signals. The function of several other effectors in manipulating plant defense signals, as well as lipids signals, weakening cell walls, attenuating feeding site function and development are still being studied in depth for several novel effectors. As direct outcome of this project, the accumulating findings will be utilized to improve our understanding of the mechanisms governing critical life-cycle phases of the parasitic M. incognita RKN, thereby facilitating design of effective controls based on perturbation of nematode behavior—without producing harmful side effects. The knowledge from this study will promote genome editing strategies aimed at developing nematode resistance in tomato and other nematode-susceptible crop species in Israel and the United States.
2
Philosoph-Hadas, Sonia, Richard Crain, Shimon Meir, Nehemia Aharoni, and Susan Lurie. Calcium-Mediated Signal Transduction during Leaf Senescence. United States Department of Agriculture, November 1995. http://dx.doi.org/10.32747/1995.7604925.bard.
Анотація:
We have examined the possibility that modulation of [Ca2+]cyt may represent a signal which induces senescence processes in leaves, through triggering of lipid hydrolysis leading to the cascade of detriorative events. Characterization of the signal transduction components operating during leaf senescence was gained by studying various Ca2+-dependent activities of parsley and chrysanthemum leaves, in relation to several senescence functions, and in response to senescence-modulating hormones (ethylene,ABA, BA and IAA). Some innovative findings regarding the control of senescence processes by [Ca2+]cyt were established: Several Ca2+-or CaM-related compounds were shown to modulate [Ca2+]cyt and action, thereby affecting whole leaf senescence. The involvement of [Ca2+]cyt in mediating the effects of senescence-modulating hormones has been demonstrated. Loss of energized Ca2+-transport capability of PM was found to an early event in leaf senescence, which occurs before changes in senescence parameters are observed, and while other PM ATPase enzymes still retain about 50% of their activities. A general pattern of increased phosphorylation of PM proteins with advanced senescence, which could be modified by plant hormones applied in vivo (BA) or in vitro (ABA), sa found. Taken together, all this indirect evidence indicate that [Ca2+]cyt is elevated due to the senescence-induced decrease in the ability to extrude Ca2+, which results particularly from reduced PM Ca2++-transport capability rather than increased operation of Ca2+ channels or elevated Ins(1,4,5)P3 levels. The direct proof for such a senescence-related elevation in [Ca2+]cyt was provided for the first time by the Ca2+ imaging measures with fura-2, showing a rise in [Ca2+]cyt of mesophyll cells upon senescence induction, which preceeded changes in typical senescence characteristics. This research provides strong evidence for regarding the rise in [Ca2+]cyt as a primary event in induction of the senescence syndrome in detached leaves. The findings have also broad implications for postharvest handling of leafy crops and ornamentals, and open new avenues for employing Ca2+-related inhibitors to delay leaf senescence.
3
O'Neill, Sharman, Abraham Halevy, and Amihud Borochov. Molecular Genetic Analysis of Pollination-Induced Senescence in Phalaenopsis Orchids. United States Department of Agriculture, 1991. http://dx.doi.org/10.32747/1991.7612837.bard.
Анотація:
The project investigated the molecular genetic and biochemical basis of pollination-induced senescence of Phalaenopsis flowers. This experimental system offered unique advantages in that senescence is strictly regulated by pollination, providing the basis to experimentally initiate and synchronize senescence in populations of flowers. The postpollination syndrome in the Phalaenopsis orchid system was dissected by investigating the temporal and spatial regulation of ACC synthase gene expression. In the stigma, pollen-borne auxin induces the expression of the auxin-regulated ACC synthase (PS-ACS2) gene, resulting in ACC synthesis within 1 h following pollination. Newly formed ACC is oxidized by basal constitutive ACC oxidase to ethylene, which then induces the expression of the ethylene-regulated ACC synthase(PS-ACS1) and oxidase (ACO1) genes for further autocatalytic production of ethylene. It is speculated that during the 6-h period following pollination, emasculation leads to the production or release of a sensitivity factor that sensitizes the cells of the stigma to ethylene. ACC and ethylene molecules are translocated from the stigma to the labellum and perianth where ethylene induces the expression of PS-ACS1 and ACO1 resulting in an increased production of ACC and ethylene. Organ-localized ethylene is responsible for inrolling and senescence of the labellum and perianth. The regulation of ethylene sensitivity and signal transduction events in pollinated flowers was also investigated. The increase in ethylene sensitivity appeared in both the flower column and the perianth, and was detected as early as 4 h after pollination. The increase in ethylene sensitivity following pollination was not dependent on endogenous ethylene production. Application of linoleic and linoleic acids to Phalaenopsis and Dendrobium flowers enhanced their senescence and promoted ethylene production. Several major lipoxygenase pathway products including JA-ME, traumatic acid, trans-2-hexenal and cis-3-hexenol, also enhanced flower senescence. However, lipoxygenase appears to not be directly involved in the endogenous regulation of pollination-induced Phalaenopsis and Dendrobium flower senescence. The data suggest that short-chain saturated fatty acids may be the ethylene "sensitivity factors" produced following pollination, and that their mode of action involves a decrease in the order of specific regions i the membrane lipid bilayer, consequently altering ethylene action. Examination of potential signal transduction intermediates indicate a direct involvement of GTP-binding proteins, calcium ions and protein phosphorylation in the cellular signal transduction response to ethylene following pollination. Modulations of cytosolic calcium levels allowed us to modify the flowers responsiveness to ethylene.
4
Dickman, Martin B., and Oded Yarden. Regulation of Early Events in Hyphal Elongation, Branching and Differentiation of Filamentous Fungi. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7580674.bard.
Анотація:
In filamentous fungi, hyphal elongation, branching and morphogenesis are in many cases the key to successful saprophytic and pathogenic fungal proliferation. The understanding of the fungal morphogenetic response to environmental cues is in its infancy. Studies concerning the regulation of fungal growth and development (some of which have been obtained by the participating collaborators in this project) point to the fact that ser/thr protein kinases and phosphatases are (i) involved in the regulation of such processes and (ii) share common structural and functional features between saprophytes and pathogens. It is our objective to combine a pharmaceutical and a genetic approach in order to identify, characterize and functionally dissect some of the regulatory factors involved in hyphal growth, branching and differentiation. Using an immunohistochemical approach, a ser/thr protein kinase involved in hyphal elongation in both Neurospora crassa and Colletotrichum trifolii has been localized in order to identify the physical arena of regulation of hyphal elongation. The analysis of additional kinases and phosphatases (e.g. Protein kinase C, cAMP-dependent kinase, lipid-activated protein kinase, components of the type 2A protein phosphatase) as well as a RAS-related gene (an additional key participant in signal transduction) has been performed. In order to succeed in advancing the goals of this project, we have taken advantage of available elongation/branching mutants in N. crassa and continuously combined the accumulated information obtained while studying the two systems in order to dissect the elements involved in these processes. The various inhibitors/effectors analyzed can serve as a basis for modification to be used as anti-fungal compounds. Understanding the regulation of hyphal proliferation is a key requirement for identifying novel target points for either curbing fungal growth (as in the case of pathogenesis) or affecting growth patterns in various biotechnological processes. The major objective of our joint project was to advance our understanding of regulation of hyphal growth, especially during early events of fungal germination. Towards achieving this goal, we have coupled the analysis of a genetically tractable organism (N. crassa) with a plant pathogen o economic importance (C. trifolii). As the project progressed we believe that the results obtained have provided a reinforcement to our basic approach which called for combining the two fungal systems for a joint research project. On the one hand, we feel that much of the advance made was possible due to the amenability of N. crassa to genetic manipulations. The relevance of some of the initial findings obtained in Neurospora have been proven to be relevant to the plant pathogen while unique features of the pathogen have been identified in Colletotrichum. Most of the results obtained from this research project have been published. Thus, the main volume of this report is comprised of the relevant publications describing the research and results obtained.
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Laxmi Prasanna, Porandla, B. Anil kumar, and Macha Sahithi. A STUDY TO EVALUATE THE TEAR FILM CHANGES IN PATIENTS WITH PTERYGIUM. World Wide Journals, February 2023. http://dx.doi.org/10.36106/ijar/3408221.
Анотація:
Introduction: Pterygium is a degenerative condition of the subconjunctival tissues which proliferate as vascularized granulation tissue to invade the cornea, destroying the supercial layers of the stroma and bowmans membrane, the whole being covered by conjunctival epithelium.The tear lm consists of three layers, the most supercial layer of tear lm is lipid layer produced by meibomian glands. The middle layer is the aqueous layer produced by the main lacrimal gland as well as accessory lacrimal glands of Krause and Wolfring. Aqueous layer constitutes over 90% of the tear lm. The layer closest to the cornea is the mucin layer produced by conjunctival goblet cells. Tear function abnormalities have been proposed as an etiologic factor for pterygium due to observation that a pterygium is exacerbated by dryness and dellen formation. Whether tear dysfunction is a precursor to pterygium growth or pterygium causes tear dysfunction is still not clear. The present study was taken up to study the tear lm changes in patients presenting with pterygium. Materials and methods: The present prospective study was conducted at the Department of Ophthalmology, Chalmeda Anand Rao Institute of Medical Sciences from Jan 2021- July 2022. 75 patients satisfying inclusion and exclusion criteria were included in the study. The eye with pterygium was considered as case and the normal eye of the same patient was considered as controls. The data was recorded for 150 eyes. All patients underwent visual acuity assessment, a detailed slit-lamp examination and ophthalmoscopy to rule out adnexal, anterior segment and posterior segment diseases. Patients were evaluated for tear lm changes using Schirmer's test(with anesthesia),Tear lm breakup time and Tear lm meniscus height. The mean age of the study population was 34.7±4.98 years, with 56% of ma Results: les and 44% of females. Pterygium was present in right eye in 73.33% (n=55) cases and 26.66% (n=20) had it in the left eye. All were on the nasal conjunctiva. Schirmer's test was signicantly lower in eyes with pterygium with P value of <0.001. Tear Film Break Up time and Tear Film meniscus height was signicantly lesser in the eyes with pterygium with P=<0.001. From the present study, we ca Conclusion: n suggest that unstable tear lm is found to a greater extent in eyes with pterygium than in eyes without pterygium. Pterygium is one of the most common ocular surface disorders which results in instability of tear lm indices and thus lead to dysfunctional tear lm and development of dry eye.
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Keshav, Dr Geetha, Dr Suwaibah Fatima Samer, Dr Salman Haroon, and Dr Mohammed Abrar Hassan. TO STUDY THE CORRELATION OF BMI WITH ABO BLOOD GROUP AND CARDIOVASCULAR RISK AMONG MEDICAL STUDENTS. World Wide Journals, February 2023. http://dx.doi.org/10.36106/ijar/2405523.
Анотація:
Introduction: Advancements and increase in access to healthcare have increased the life expectancy in India from 32 years in 1947 to almost 70 years currently. Due to robust vaccination and basic health programs, most of the communicable diseases are kept under control. The disease burden is now skewed towards non-communicable diseases. It is an established fact that body mass index (BMI) is a reliable predictor of cardiovascular disease (CVD) later in life. Early prediction can decrease the disease load and enable early preventative measures. A more novel approach of connecting it with blood groups would yield profound results in predictability and subsequent management. This study was done to see correlation between BMI and known blood groups in order to predict the potential incidence of CVDs in medical students. Material and Method - A cross-sectional descriptive study was conducted in Bhaskar Medical College from September 2022 - November 2022. The sample population included 150- 1st year medical students chosen by Randomized sampling method. BMI was calculated based as weight in kilograms divided by the square of the height in meters (kg/m2). Discussion - Many studies conducted on the association of Blood groups with BMI yielded mixed and inconclusive results. On analysis of the data obtained from this study, O- positive blood group showed the highest inclination towards obesity i.e. 30 of the total participants. A-positive and B- positive blood groups were shown to have a lesser association with obesity i.e. 11 participants of the 150. These results were in accordance with a study done among female students by Shireen Javad et.al, nding blood group O to be the most prone to obesity.8 Incompatible to our results, a study conducted by Samuel Smith Isaac Okai et.al. found no signicant association between blood groups and BMI.10 Another study conducted by Christina Ravillo et.al. found that blood group O had the highest and blood group AB with lowest prevalence of obesity9. These ndings were similar to the results obtained in our study. To study the correlation of BMI with ABO blood group and Cardiovascula AIMS and OBJECTIVES Aim: - r risk among medical students. 1. Calculate and segregate the participants according to BM Objectives: - I using the standard formula provided by the WHO. 1. Determine Blood group using antisera 2. Evaluation of Lipid prole in obese individuals