Bibliografias temáticas / Signaling lipid

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Literatura científica selecionada sobre o tema "Signaling lipid"

Autor: Grafiati

Publicado: 9 de novembro de 2024

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Artigos de revistas sobre o assunto "Signaling lipid"

Wang, Xuemin. "Lipid signaling". Current Opinion in Plant Biology 7, n.º 3 (junho de 2004): 329–36. http://dx.doi.org/10.1016/j.pbi.2004.03.012.

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Bickel, Perry E. "Lipid rafts and insulin signaling". American Journal of Physiology-Endocrinology and Metabolism 282, n.º 1 (1 de janeiro de 2002): E1—E10. http://dx.doi.org/10.1152/ajpendo.2002.282.1.e1.

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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.

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Junkins, Sadie, Gabrielle Westenberger, Jacob Sellers, Isabel Martinez, Nabin Ghimire, Cassandra Secunda, Morgan Welch, Urja Patel, Kisuk Min e Ahmed Lawan. "MKP-2 Deficiency Leads to Lipolytic and Inflammatory Response to Fasting in Mice". Journal of Cellular Signaling 5, n.º 1 (2024): 10–23. http://dx.doi.org/10.33696/signaling.5.108.

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The liver plays a crucial role in maintaining homeostasis for lipid and glucose. Hepatic lipid synthesis is regulated by nutritional signals in response to fasting and refeeding. It is known that overnutrition regulates MAPK-dependent pathways that control lipid metabolism in the liver by activating MAPK phosphatase-2 (MKP-2). Uncertainty still exists regarding the regulatory mechanisms and effects of MKP-2 on hepatic response to fasting. We investigated the effect of fasting on the expression of MKP-2 and the impact on hepatic inflammatory response to feeding a high-fat diet (HFD). In this study, we show that fasting stress led to an upregulation of hepatic MKP-2 expression and a corresponding decrease in phosphorylation of p38 MAPK in mouse livers. We discovered that hepatic steatosis brought on by fasting is not effective in MKP-2-deficient livers due in part to a decrease in lipolysis and GLUT2 expression. In response to refeeding a chow or HFD, MKP-2 exhibited differential regulation of hepatic inflammatory cytokines including IL-1β. It has been demonstrated that the mitochondrial carrier uncoupling protein 2 (UCP2) plays a significant role in immune function. We discovered that MKP-2 negatively controls the expression of the UCP2 protein in the liver, modulating the expression of inflammatory cytokines. These results lend credence to the idea that upregulation of MKP-2 is a physiologically relevant response and may help the liver better utilize hepatic lipids while fasting. Collectively, these findings show that MKP-2 modulates lipolysis and hepatic inflammatory response in response to alterations in nutritional status, such as excess nutrients and fasting.

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Bazan, Nicolas G. "Synaptic lipid signaling". Journal of Lipid Research 44, n.º 12 (16 de setembro de 2003): 2221–33. http://dx.doi.org/10.1194/jlr.r300013-jlr200.

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Irvine, R. "Nuclear Lipid Signaling". Science Signaling 2000, n.º 48 (5 de setembro de 2000): re1. http://dx.doi.org/10.1126/stke.2000.48.re1.

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Irvine, R. F. "Nuclear Lipid Signaling". Science Signaling 2002, n.º 150 (17 de setembro de 2002): re13. http://dx.doi.org/10.1126/stke.2002.150.re13.

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Höglinger, Doris, André Nadler, Per Haberkant, Joanna Kirkpatrick, Martina Schifferer, Frank Stein, Sebastian Hauke, Forbes D. Porter e Carsten Schultz. "Trifunctional lipid probes for comprehensive studies of single lipid species in living cells". Proceedings of the National Academy of Sciences 114, n.º 7 (2 de fevereiro de 2017): 1566–71. http://dx.doi.org/10.1073/pnas.1611096114.

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Lipid-mediated signaling events regulate many cellular processes. Investigations of the complex underlying mechanisms are difficult because several different methods need to be used under varying conditions. Here we introduce multifunctional lipid derivatives to study lipid metabolism, lipid−protein interactions, and intracellular lipid localization with a single tool per target lipid. The probes are equipped with two photoreactive groups to allow photoliberation (uncaging) and photo–cross-linking in a sequential manner, as well as a click-handle for subsequent functionalization. We demonstrate the versatility of the design for the signaling lipids sphingosine and diacylglycerol; uncaging of the probe for these two species triggered calcium signaling and intracellular protein translocation events, respectively. We performed proteomic screens to map the lipid-interacting proteome for both lipids. Finally, we visualized a sphingosine transport deficiency in patient-derived Niemann−Pick disease type C fibroblasts by fluorescence as well as correlative light and electron microscopy, pointing toward the diagnostic potential of such tools. We envision that this type of probe will become important for analyzing and ultimately understanding lipid signaling events in a comprehensive manner.

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Dowds, C. Marie, Sabin-Christin Kornell, Richard S. Blumberg e Sebastian Zeissig. "Lipid antigens in immunity". Biological Chemistry 395, n.º 1 (1 de janeiro de 2014): 61–81. http://dx.doi.org/10.1515/hsz-2013-0220.

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Abstract Lipids are not only a central part of human metabolism but also play diverse and critical roles in the immune system. As such, they can act as ligands of lipid-activated nuclear receptors, control inflammatory signaling through bioactive lipids such as prostaglandins, leukotrienes, lipoxins, resolvins, and protectins, and modulate immunity as intracellular phospholipid- or sphingolipid-derived signaling mediators. In addition, lipids can serve as antigens and regulate immunity through the activation of lipid-reactive T cells, which is the topic of this review. We will provide an overview of the mechanisms of lipid antigen presentation, the biology of lipid-reactive T cells, and their contribution to immunity.

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Terao, Ryo, e Hiroki Kaneko. "Lipid Signaling in Ocular Neovascularization". International Journal of Molecular Sciences 21, n.º 13 (4 de julho de 2020): 4758. http://dx.doi.org/10.3390/ijms21134758.

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Vasculogenesis and angiogenesis play a crucial role in embryonic development. Pathological neovascularization in ocular tissues can lead to vision-threatening vascular diseases, including proliferative diabetic retinopathy, retinal vein occlusion, retinopathy of prematurity, choroidal neovascularization, and corneal neovascularization. Neovascularization involves various cellular processes and signaling pathways and is regulated by angiogenic factors such as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF). Modulating these circuits may represent a promising strategy to treat ocular neovascular diseases. Lipid mediators derived from membrane lipids are abundantly present in most tissues and exert a wide range of biological functions by regulating various signaling pathways. In particular, glycerophospholipids, sphingolipids, and polyunsaturated fatty acids exert potent pro-angiogenic or anti-angiogenic effects, according to the findings of numerous preclinical and clinical studies. In this review, we summarize the current knowledge regarding the regulation of ocular neovascularization by lipid mediators and their metabolites. A better understanding of the effects of lipid signaling in neovascularization may provide novel therapeutic strategies to treat ocular neovascular diseases and other human disorders.

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Huwiler, Andrea, e Josef Pfeilschifter. "Hypoxia and lipid signaling". Biological Chemistry 387, n.º 10/11 (1 de outubro de 2006): 1321–28. http://dx.doi.org/10.1515/bc.2006.165.

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AbstractSufficient oxygen supply is crucial for the development and physiology of mammalian cells and tissues. When simple diffusion of oxygen becomes inadequate to provide the necessary flow of substrate, evolution has provided cells with tools to detect and respond to hypoxia by upregulating the expression of specific genes, which allows an adaptation to hypoxia-induced stress conditions. The modulation of cell signaling by hypoxia is an emerging area of research that provides insight into the orchestration of cell adaptation to a changing environment. Cell signaling and adaptation processes are often accompanied by rapid and/or chronic remodeling of membrane lipids by activated lipases. This review highlights the bi-directional relation between hypoxia and lipid signaling mechanisms.

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Teses / dissertações sobre o assunto "Signaling lipid"

Benarab, Ammar. "Harnessing endothelial lipid signaling for ischemic stroke protection". Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5197.

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Justification : La fonction cérébrovasculaire est essentielle à la santé du cerveau, et les voies de protection vasculaire endogènes peuvent fournir des cibles thérapeutiques pour les troubles neurologiques. La signalisation S1P (sphingosine 1-phosphate) coordonne les fonctions vasculaires dans d'autres organes et les modulateurs S1P1 (récepteur S1P-1), y compris le fingolimod, sont prometteurs pour le traitement de l'AVC ischémique et hémorragique. Cependant, S1P1 coordonne également le trafic lymphocytaire, et les lymphocytes sont actuellement considérés comme la principale cible thérapeutique pour la modulation de S1P1 dans les accidents vasculaires cérébraux. Objectif : Aborder les rôles et les mécanismes d'engagement de la cellule endothéliale S1P1 dans le cerveau naïf et ischémique et son potentiel en tant que cible pour la thérapie cérébrovasculaire. Méthodes et résultats : En utilisant la modulation spatiale de la fourniture et de la signalisation S1P, nous démontrons un rôle protecteur vasculaire critique pour S1P1 endothélial dans le cerveau de souris. Avec un journaliste de signalisation S1P1, nous révélons que la polarisation abluminale protège S1P1 des ligands endogènes et synthétiques circulants après maturation de la barrière hémato-neurale, limitant la signalisation homéostatique à un sous-ensemble de cellules endothéliales artériolaires. La signalisation S1P1 maintient les fonctions endothéliales caractéristiques dans le cerveau naïf et se développe pendant l'ischémie par l'engagement de la fourniture S1P autonome des cellules. La perturbation de cette voie par une déficience sélective des cellules endothéliales dans la production, l'exportation ou le récepteur S1P1 de S1P exacerbe considérablement les lésions cérébrales dans les modèles permanents et transitoires d'AVC ischémique. En revanche, la lymphopénie profonde induite par la perte du lymphocyte S1P1 n'offre une protection modeste que dans le cadre d'une reperfusion. Dans le cerveau ischémique, la cellule endothéliale S1P1 soutient la fonction de barrière hémato-encéphalique, la perméabilité microvasculaire et le réacheminement du sang vers le tissu cérébral hypoperfusé par le biais d'anastomoses collatérales. Le renforcement de ces fonctions par un engagement pharmacologique supplémentaire du pool de récepteurs endothéliaux avec une barrière hémato-encéphalique pénétrant un agoniste sélectif de S1P1 peut réduire davantage l'expansion de l'infarctus cortical dans un délai thérapeutiquement pertinent et indépendamment de la reperfusion. Conclusions : Cette étude fournit des preuves génétiques pour soutenir un rôle central de l'endothélium dans le maintien de la perfusion et de la perméabilité microvasculaire dans la pénombre ischémique qui est coordonnée par la signalisation S1P et peut être exploitée pour la neuroprotection avec des agonistes S1P1 pénétrant la barrière hémato-encéphalique
Rationale: Cerebrovascular function is critical for brain health, and endogenous vascular protective pathways may provide therapeutic targets for neurological disorders. S1P (Sphingosine 1-phosphate) signaling coordinates vascular functions in other organs and S1P1 (S1P receptor-1) modulators including fingolimod show promise for the treatment of ischemic and hemorrhagic stroke. However, S1P1 also coordinates lymphocyte trafficking, and lymphocytes are currently viewed as the principal therapeutic target for S1P1 modulation in stroke. Objective: To address roles and mechanisms of engagement of endothelial cell S1P1 in the naive and ischemic brain and its potential as a target for cerebrovascular therapy. Methods and results: Using spatial modulation of S1P provision and signaling, we demonstrate a critical vascular protective role for endothelial S1P1 in the mouse brain. With an S1P1 signaling reporter, we reveal that abluminal polarization shields S1P1 from circulating endogenous and synthetic ligands after maturation of the blood-neural barrier, restricting homeostatic signaling to a subset of arteriolar endothelial cells. S1P1 signaling sustains hallmark endothelial functions in the naive brain and expands during ischemia by engagement of cell-autonomous S1P provision. Disrupting this pathway by an endothelial cell-selective deficiency in S1P production, export, or the S1P1 receptor substantially exacerbates brain injury in permanent and transient models of ischemic stroke. By contrast, profound lymphopenia induced by loss of lymphocyte S1P1 provides modest protection only in the context of reperfusion. In the ischemic brain, endothelial cell S1P1 supports blood-brain barrier function, microvascular patency, and the rerouting of blood to hypoperfused brain tissue through collateral anastomoses. Boosting these functions by supplemental pharmacological engagement of the endothelial receptor pool with a blood-brain barrier penetrating S1P1-selective agonist can further reduce cortical infarct expansion in a therapeutically relevant time frame and independent of reperfusion. Conclusions: This study provides genetic evidence to support a pivotal role for the endothelium in maintaining perfusion and microvascular patency in the ischemic penumbra that is coordinated by S1P signaling and can be harnessed for neuroprotection with blood-brain barrier-penetrating S1P1 agonists

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Cheong, Fei Ying. "Regulation of lipid signaling at the Golgi by the lipid phosphatases hSAC1 and OCRL1". [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:16-opus-71011.

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Herman, Moreno Maria Dolores. "Structural studies of proteins in apoptosis and lipid signaling". Doctoral thesis, Stockholms universitet, Institutionen för biokemi och biofysik, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8212.

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Signaling pathways control the fate of the cell. For example, they promote cell survival or commit the cell to death (apoptosis) in response to cell injury or developmental stimuli, decisions, which are vital for the proper development and functioning of metazoan. Tight control of such pathways is essential; dysregulation of apoptosis can disrupt the delicate balance between cell proliferation and cell death ending up in pathological processes, including cancer, autoimmunity diseases, inflammatory diseases, or degenerative disorders. We have used a structural genomic approach to study the structure and function of key proteins involved in apoptosis and lipid signaling: the antiapoptotic Bcl-2 family member Bfl-1 in complex with a Bim peptide, the BIR domains of the Inhibitor of Apoptosis (IAP) family members, cIAP2 and NAIP and the a lipid kinase YegS. The structural analysis of the apoptosis regulatory proteins has revealed important information on the structural determinants for recognition of interacting proteins, which can now assist in the development of therapeutic drugs for human diseases. The structural and complementing biochemical studies of the lipid kinase YegS have reveled the first detailed information on a lipid kinase and explained important aspects of its structure-function relationship. Finally, one subject of this work aim to solve what is arguably the most challenging problem in structural projects – to obtain a high production level of proteins suitable for structural studies. We have developed a highthroughput protein solubility screening, the colony filtration (CoFi) blot, which allows soluble clones to be identified from large libraries of protein variants and now constitute a powerful tool for solving difficult protein production problems.

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Aivazian, Dikran A. (Dikran Arvid) 1971. "Lipid-protein interactions of immunoreceptor signaling subunit cytoplasmic domains". Thesis, Massachusetts Institute of Technology, 2001. http://hdl.handle.net/1721.1/8583.

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Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Biology, 2001.
Vita.
Includes bibliographical references (leaves 116-131).
Protein-lipid interactions are emerging as key components of cellular processes such as protein and membrane trafficking and cell-cell signaling. Many proteins bind lipid reversibly, including cytoplasmic proteins involved in signal transduction, such as Ras and Src. Membrane binding is vital for the function of these signaling proteins both through co-localization with other signaling proteins as well as effects of lipid on intrinsic activities. In this thesis, protein-lipid interactions of subunits of key antigen recognition receptors of the immune system are investigated. The proteins studied are the cytoplasmic domains of immunoreceptor signaling subunits that mediate transmembrane signal transduction in response to receptor engagement. The cytoplasmic domains derive from the T cell receptor, the B cell receptor, Fe receptors and Natural Killer cell stimulatory receptors. The TCR, CD3, CD3, CD3, ... and DAP12 cytoplasmic domains all bind lipid, whereas those of B cell receptor Iga and Igp do not. While all of these proteins are unstructured in solution, ... and CD3 undergo extensive increases in secondary structure upon lipid binding. Lipid binding of ... is found to inhibit its accessibility to kinase-mediated phosphorylation. Based on these results it is proposed that interactions with lipid may regulate the function of receptor cytoplasmic domains, as with many cytosolic proteins involved in signaling processes.
by Dikran A. Aivazian.
Ph.D.

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Secor, Jordan Douglas. "Phytochemical Antioxidants Induce Membrane Lipid Signaling in Vascular Endothelial Cells". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338391553.

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Cody, West Kime. "Autotaxin-mediated lipid signaling intersects with LIF and BMP signaling to promote the naive pluripotency transcription factor program". Kyoto University, 2018. http://hdl.handle.net/2433/232302.

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Kline, Michelle A. "Membrane cholesterol regulates vascular endothelial cell viability, function, and lipid signaling". Connect to resource, 2008. http://hdl.handle.net/1811/32175.

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Sadhukhan, Sushabhan. "Metabolism & Signaling of 4-Hydroxyacids: Novel Metabolic Pathways and Insight into the Signaling of Lipid Peroxidation Products". Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1339171892.

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Kilaru, Aruna. "Discovery of Anandamide, a Novel Lipid Signaling Molecule in Moss and Its Implications". Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/4771.

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Herrera-Velit, Patricia. "Bacterial lipopolysaccharides signaling pathways in mononuclear phagocytes involve protein and lipid kinases". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0034/NQ27161.pdf.

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Livros sobre o assunto "Signaling lipid"

Banafshé, Larijani, Woscholski Rudiger e Rosser Colin A, eds. Lipid signaling protocols. New York, N.Y: Humana, 2009.

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Larijani, Banafshé, Rudiger Woscholski e Colin A. Rosser, eds. Lipid Signaling Protocols. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-115-8.

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Waugh, Mark G., ed. Lipid Signaling Protocols. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3170-5.

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Murphy, Eric J. Lipid-mediated signaling. Boca Raton, FL: CRC Press/Taylor & Francis, 2010.

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1963-, Murphy Eric J., e Rosenberger Thad A, eds. Lipid-mediated signaling. Boca Raton: CRC Press/Taylor & Francis, 2009.

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Munnik, Teun, e Ingo Heilmann, eds. Plant Lipid Signaling Protocols. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-401-2.

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Capelluto, Daniel G. S., ed. Lipid-mediated Protein Signaling. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6331-9.

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Munnik, Teun, ed. Lipid Signaling in Plants. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03873-0.

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Kihara, Yasuyuki, ed. Druggable Lipid Signaling Pathways. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50621-6.

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service), SpringerLink (Online, ed. Lipid Signaling in Plants. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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Capítulos de livros sobre o assunto "Signaling lipid"

Luna, Elizabeth J., Thomas Nebl, Norio Takizawa e Jessica L. Crowley. "Lipid Raft Membrane Skeletons". In Membrane Microdomain Signaling, 47–69. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-803-x:047.

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Mak, Lok Hang. "Lipid Signaling and Phosphatidylinositols". In Encyclopedia of Biophysics, 1286–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_537.

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Michaelson, Louise V., e Johnathan A. Napier. "Sphingolipid Signaling in Plants". In Lipid Signaling in Plants, 307–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_20.

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Yanagida, Keisuke, e William J. Valentine. "Druggable Lysophospholipid Signaling Pathways". In Druggable Lipid Signaling Pathways, 137–76. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50621-6_7.

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Mattson, Mark P. "Dietary Modulation of Lipid Rafts". In Membrane Microdomain Signaling, 191–201. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-803-x:191.

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Mosblech, Alina, Ivo Feussner e Ingo Heilmann. "Oxylipin Signaling and Plant Growth". In Lipid Signaling in Plants, 277–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_18.

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Kihara, Yasuyuki. "Introduction: Druggable Lipid Signaling Pathways". In Druggable Lipid Signaling Pathways, 1–4. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50621-6_1.

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Gregus, Ann M., e Matthew W. Buczynski. "Druggable Targets in Endocannabinoid Signaling". In Druggable Lipid Signaling Pathways, 177–201. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50621-6_8.

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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.

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Im, Yang Ju, Brian Q. Phillippy e Imara Y. Perera. "InsP3 in Plant Cells". In Lipid Signaling in Plants, 145–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_10.

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Trabalhos de conferências sobre o assunto "Signaling lipid"

Maiti, Sudipta. "Extra-receptor signaling: how the lipid bilayer transduces neurotransmitter signals". In Multiphoton Microscopy in the Biomedical Sciences XXIV, editado por Ammasi Periasamy, Peter T. So e Karsten König. SPIE, 2024. http://dx.doi.org/10.1117/12.3010037.

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Stamm, N., H. Asperger, M. Ludescher, T. Fehm e H. Neubauer. "PGRMC1 alters de novo lipid biosynthesis resulting in enhanced oncogenic signaling". In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1718184.

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Taylor, Graham, Donald Leo e 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.

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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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Rong, Xi, Kenneth M. Pryse, Jordan A. Whisler, Yanfei Jiang, William B. McConnaughey, Artem Melnykov, Guy M. Genin e Elliot L. Elson. "Confidence Intervals for Estimation of the Concentration and Brightness of Multiple Diffusing Species". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80921.

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Lipid nanodomains in cell membranes are believed to play a significant role in replication of enveloped viruses such as bird flu and HIV and signaling mechanisms underlying pathological conditions such as cancer. However, the forces that govern the formation and availability of these “membrane rafts” are uncertain, and even their existence is questioned. The central challenge is that no suitable imaging modalities exist (Elson, et al., 2010). We are developing tools to characterize and visualize dynamics of lipid nanodomains on idealized systems called giant unilamellar vesicles (GUVs) using fluorescence correlation spectroscopy (FCS) (Figure 1).

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Jiang, Yanfei, Guy M. Genin, Srikanth Singamaneni e Elliot L. Elson. "Interfacial Phases on Giant Unilamellar Vesicles". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80942.

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Lipid nanodomains in cell membranes are believed to play a significant role in a number of critical cellular processes (Elson, et al., 2010). These include, for example, replication processes in enveloped viruses such as bird flu and HIV and signaling mechanisms underlying pathological conditions such as cancer. Due to the potential for developing new disease treatments through the control of these membrane rafts, the biophysics underlying their formation has been the subject of intense study, much of this focused on domain formation in giant unilamellar lipid vesicles (GUVs), a simplified model system.

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Wadgaonkar, R., e X. Jiang. "Sphingolipid Dependent Integration of TNF Receptor Signaling in Endothelial Cell Lipid Microdomains." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2478.

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Hawk, Ernest T., David G. Menter, Sherri Patterson, Michael W. Swank e Raymond N. DuBois. "Abstract 3251: Linking prostaglandin E2 signaling, lipid rafts, and DNA protein kinase". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3251.

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Shokat, Kevan M. "Abstract SY19-01: Chemical genetic investigations of protein and lipid kinase signaling." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-sy19-01.

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Bukowski, Michael, Brij Singh, James Roemmich e Kate Larson. "Lipidomic analysis of TRPC1 Ca2+-permeable channel-knock out mouse demonstrates a vital role in placental tissue sphingolipid and triacylglycerol homeostasis under high-fat diet". In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/tjdt4839.

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Placental function including oxygen delivery and nutrient transport are critical determinants of fetal growth, moderating the risks of obesity and metabolic diseases later in life. Previously, we demonstrated in a mouse model that parental diet and exercise play important roles in placental lipid content and inflammation. Transient receptor potential canonical channel 1 (TRPC1) is a Ca2+-permeable integral membrane protein. We have demonstrated that TRPC1 increases total body adiposity in mice by decreasing the efficacy of exercise to limit adipose accumulation under a high fat (HF) diet. Importantly, intracellular calcium may regulate total body adiposity and increased total body adiposity could promote placental lipid accumulation. Similarly, intracellular calcium regulates membrane lipid content via the activation of the protein kinase C. Membrane lipids such as sphingomyelin are key regulators of cell signaling. Maternal HF diets increase placental tissue lipid concentrations resulting in compromised nutrient transport to fetus. However, the specific lipid species that accumulate due to the absence of the placental TRPC1 gene under maternal HF diet feeding is not yet known. We hypothesized that placental tissue response to a maternal HF diet is disrupted in TRPC1 mice fed a maternal HF diet resulting in greater cellular sphingomyelin concentrations. Results showed placentae from TRPC1 KO mice fed high fat diet (45% en, HF) had increased sphingomyelin concentrations compared to control diet (16% en, NF). Placentae from WT mice fed HF diet exhibited diet-dependent increases in ceramide concentration with no concomitant increase in sphingomyelins compared to NF fed WT mice. Additionally, 11 placental triacylglycerol (TAG) species were different based on diet, 16 based on genotype, and 5 were affected by both diet and genotype. These results suggest that during a HF diet, loss of TRPC1 function reduces placental sphingomyelin hydrolysis into ceramide and that placental TAG concentrations respond in diet- and genotype-dependent manner.

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Muddana, Hari S., Ramachandra R. Gullapalli e Peter J. Butler. "Tension Induces Changes in Lipid Lateral Diffusion in Model Fluid-Phase Membranes". In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206867.

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Shear stress due to blood flow on endothelial cells elicits numerous responses including G-protein coupled receptor activation and integrin-mediated signaling. Shear-induced change in membrane fluidity has been suggested to be one of the earliest mechanosensing mechanism involved in these processes [1, 2]. Alternatively, it has been suggested that shear forces are transduced through glycocalyx directly to transmembrane proteins and cytoskeleton [3], with very little shear force sensed by the membrane. It is not yet clear whether physiological tensions can alter membrane fluidity significantly.

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Relatórios de organizações sobre o assunto "Signaling lipid"

Gatley, S. J. Radiotracers For Lipid Signaling Pathways In Biological Systems. Office of Scientific and Technical Information (OSTI), setembro de 2016. http://dx.doi.org/10.2172/1326385.

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Brown Horowitz, Sigal, Eric L. Davis e Axel Elling. Dissecting interactions between root-knot nematode effectors and lipid signaling involved in plant defense. United States Department of Agriculture, janeiro de 2014. http://dx.doi.org/10.32747/2014.7598167.bard.

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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.

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Barg, Rivka, Kendal D. Hirschi, Avner Silber, Gozal Ben-Hayyim, Yechiam Salts e Marla Binzel. Combining Elevated Levels of Membrane Fatty Acid Desaturation and Vacuolar H+ -pyrophosphatase Activity for Improved Drought Tolerance. United States Department of Agriculture, dezembro de 2012. http://dx.doi.org/10.32747/2012.7613877.bard.

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Background to the topic: In previous works we have shown that Arabidopsis and tomato over-expressing H+-pyrophosphatase show increased tolerance to drought imposed by withholding irrigation of young plants in pots (Park et al. 2005). In addition, young tobacco plants over-expressing fatty acid desaturase 3 (OEX-FAD3) also showed increasing tolerance to drought stress (Zhang et al 2005), and similarly OEX-FAD3 young tomato plants (unpublished data from ARO), hence raising the possibility that pyramiding the two could further improve drought tolerance in tomato. Based on these findings the specific objects originally set were: 1. To analyze the impact of pyramiding transgenes for enhanced fatty acid desaturation and for elevated H+-PPase activity on tomato yielding under water deficit stress conditions. 2. To elucidate the biochemical relationship between elevated desaturation of the membrane lipids and the activities of selected vacuolar transporters in the context of drought responses. 3. To explore the S. pennellii introgression lines as alternative genetic sources for drought tolerance related to enhanced fatty acid desaturation and/or H+-PPase activity. 4. Since OEX-FAD3 increases the levels of linolenic acid which is the precursor of various oxylipins including the stress hormone Jasmonate. (JA), study of the effect of this transgene on tolerance to herbivore pests was added as additional goal. The Major conclusions, solutions, and achievements are: (1) The facts that ectopic over-expression of vacuolarH+-PPases (in line OEX-AVP1) does not change the fatty acid profile compared to the parental MoneyMaker (MM) line and that elevated level of FA desaturation (by OEX-FAD3) does not change the activity of either H+-PPase, H+-ATPaseor Ca2+ /H+ antiport, indicate that the observed increased drought tolerance reported before for increase FA desaturation in tobacco plants and increased H+PPase in tomato plants involves different mechanisms. (2) After generating hybrid lines bringing to a common genetic background (i.e. F1 hybrids between line MP-1 and MM) each of the two transgenes separately and the two transgenes together the effect of various drought stress regimes including recovery from a short and longer duration of complete water withhold as well as performance under chronic stresses imposed by reducing water supply to 75-25% of the control irrigation regime could be studied. Under all the tested conditions in Israel, for well established plants grown in 3L pots or larger, none of the transgenic lines exhibited a reproducible significantly better drought tolerance compare to the parental lines. Still, examining the performance of these hybrids under the growth practices followed in the USA is called for. (3) Young seedlings of none of the identified introgression lines including the S. pennellii homologs of two of the H+-PPase genes and one of the FAD7 genes performed better than line M82 upon irrigation withhold. However, differences in the general canopy structures between the IL lines and M82 might mask such differences if existing. (4). Over-expression of FAD3 in the background of line MP-1 was found to confer significant tolerance to three important pest insects in tomato: Bordered Straw (Heliothis peltigera), Egyptian cotton leafworm (Spodoptera littoralis) and Western Flower Thrips (Frankliniella occidentalis). Implications: Although the original hypothesis that pyramiding these two trasgenes could improve drought tolerance was not supported, the unexpected positive impact on herbivore deterring, as well as the changes in dynamics of JA biosynthesis in response to wounding and the profound changes in expression of wound response genes calls for deciphering the exact linolenic acid derived signaling molecule mediating this response. This will further facilitate breeding for herbivore pest and mechanical stress tolerance based on this pathway.

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