Journal articles: 'Lipid signal'

1

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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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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Sanada, Kamon, and Yoshitaka Fukada. "Lipid Modifications of Signal-Transducing Proteins." membrane 21, no. 3 (1996): 184–90. http://dx.doi.org/10.5360/membrane.21.184.

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12

Spiegel, Sarah, David Foster, and Richard Kolesnick. "Signal transduction through lipid second messengers." Current Opinion in Cell Biology 8, no. 2 (April 1996): 159–67. http://dx.doi.org/10.1016/s0955-0674(96)80061-5.

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Rauch, Susanne, and Oliver T. Fackler. "Viruses, lipid rafts and signal transduction." Signal Transduction 7, no. 1 (February 2007): 53–63. http://dx.doi.org/10.1002/sita.200600113.

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Iozefi, Dmitry Ya, Mikhail A. Vinidchenko, Nikolay S. Demchenko, Oleg I. Kit, Yuriy A. Fomenko, and Dmitry S. Petrov. "Morphological and biochemical heterogeneity in the tissue of pancreatic ductal adenocarcinoma (PDAC) according to structural and spectrometric MRI data." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16727-e16727. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16727.

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e16727 Background: Comparing the MRI characteristics of pancreatic tissue in normal, solid adenocarcinomas and chronic pancreatitis in a multiparametric study, the radiologist needs tools that reduce the subjective component in making a diagnostic decision. The study is devoted to the assessment of structural heterogeneity, diffusion coefficient, lipid and lactate concentration according to MR spectroscopy in vivo. PDAС cells are proliferating and surviving within a particularly severe microenvironment characterized by relative hypovascularity, hypoxia, and nutrient deprivation. In this case cells have to show biochemical flexibility (survival phenotype) in order to adapt to unusual conditions. Methods: 20 patients with pancreatic adenocarcinomas (PDAC), 10 patients with chronic pancreatitis and 10 patients with unchanged pancreas were examined MRI using Signa HD 1.5 t General Electric. The results of their multiparametric imaging and NMR spectroscopy were investigated and compared.The heterogeneity coefficients (HC) were measured as ratio standard deviation in small region of interest to signal intensity in T1FS and T2. Lipid concentration was measured by Dixon method as the pancreatic -to-splenic attenuation ratio. Results: In a small sample, we observed a significant increase in HC in chronic pancreatitis, and in solid tissue in adenocarcinomas in comparison with normal tissue, depending on the main source of the MR signal (hydrogen in the macromolecules or hydrogen of water and fat). In adenocarcinomas, an increase in the signal from lipids (lip13a) peak was revealed, with a decrease in the total lipid concentration. A decrease in lipid concentration in the tumor in the presence of diffusion restriction (ADC 0,001-0,0016 мм2/s) and the appearance of a peak of lactate may be a biochemical marker of adenocarcinoma. In chronic pancreatitis, an increase in the mass fraction of lipids was revealed. Conclusions: The results obtained in current and future in-depth studies are promising for creation of a metabolically oriented diagnostic model of pancreatic cancer.

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Barnett, Katherine C., and Jonathan C. Kagan. "Lipids that directly regulate innate immune signal transduction." Innate Immunity 26, no. 1 (June 10, 2019): 4–14. http://dx.doi.org/10.1177/1753425919852695.

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Pattern Recognition Receptors (PRRs) detect evidence of infection and tissue damage. The activation of these receptors and their downstream signal transduction pathways initiate a protective immune response. These signaling pathways are influenced by their spatial context, and precise subcellular positioning of proteins and protein complexes in these pathways is essential for effective immune responses in vivo. This organization is not limited to transmembrane proteins that reside in specific organelles, but also to proteins that engage membrane lipid head groups for proper positioning. In this review, we focus on the role of cell membranes and protein–lipid interactions in innate immune signal transduction and how their mechanisms of localization regulate the immune response. We will discuss how lipids spatially regulate the sensing of damage or infection, mediate effector activity, and serve as messengers of cell death and tissue damage.

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Rao, N. M., and R. Nagaraj. "Interaction of wild-type signal sequences and their charged variants with model and natural membranes." Biochemical Journal 293, no. 1 (July 1, 1993): 43–49. http://dx.doi.org/10.1042/bj2930043.

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The interaction of synthetic peptides corresponding to wild-type signal sequences, and their mutants having charged amino acids in the hydrophobic region, with model and natural membranes has been studied. At high peptide concentrations, i.e. low lipid/peptide ratios, the signal peptides cause release of carboxyfluorescein (CF) from model membranes with lipid compositions corresponding to those of translocation-competent as well as translocation-incompetent membranes. Interestingly, mutant sequences, which were non-functional in vivo, caused considerable release of CF compared with the wild-type sequences. Both wild-type and mutant signal sequences perturb model membranes even at lipid/peptide ratios of 1000:1, as indicated by the activities of phospholipases A2, C and D. These studies indicate that such mutant signals are non-functional not because of their inability to interact with membranes, but due to defective targeting to the membrane. The signal peptides inhibit phospholipase C activity in microsomes, uncouple oxidative phosphorylation in mitochondria and increase K+ efflux from erythrocytes, and one of the mutant sequences is a potent degranulator of the mast cells. Both wild-type and mutant signal sequences have the ability to perturb vesicles of various lipid compositions. With respect to natural membranes, the peptides do not show any bias towards translocation-competent membranes.

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Polit, Agnieszka, Paweł Mystek, and Ewa Błasiak. "Every Detail Matters. That Is, How the Interaction between Gα Proteins and Membrane Affects Their Function." Membranes 11, no. 3 (March 20, 2021): 222. http://dx.doi.org/10.3390/membranes11030222.

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In highly organized multicellular organisms such as humans, the functions of an individual cell are dependent on signal transduction through G protein-coupled receptors (GPCRs) and subsequently heterotrimeric G proteins. As most of the elements belonging to the signal transduction system are bound to lipid membranes, researchers are showing increasing interest in studying the accompanying protein–lipid interactions, which have been demonstrated to not only provide the environment but also regulate proper and efficient signal transduction. The mode of interaction between the cell membrane and G proteins is well known. Despite this, the recognition mechanisms at the molecular level and how the individual G protein-membrane attachment signals are interrelated in the process of the complex control of membrane targeting of G proteins remain unelucidated. This review focuses on the mechanisms by which mammalian Gα subunits of G proteins interact with lipids and the factors responsible for the specificity of membrane association. We summarize recent data on how these signaling proteins are precisely targeted to a specific site in the membrane region by introducing well-defined modifications as well as through the presence of polybasic regions within these proteins and interactions with other components of the heterocomplex.

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Spencer, Cierra, Barbara A. Bensing, Nagendra N. Mishra, and Paul M. Sullam. "Membrane trafficking of the bacterial adhesin GspB and the accessory Sec transport machinery." Journal of Biological Chemistry 294, no. 5 (December 4, 2018): 1502–15. http://dx.doi.org/10.1074/jbc.ra118.005657.

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The serine-rich repeat (SRR) glycoproteins of Gram-positive bacteria are large, cell wall–anchored adhesins that mediate binding to many host cells and proteins and are associated with bacterial virulence. SRR glycoproteins are exported to the cell surface by the accessory Sec (aSec) system comprising SecA2, SecY2, and 3–5 additional proteins (Asp1 to Asp5) that are required for substrate export. These adhesins typically have a 90-amino acid-long signal peptide containing an elongated N-region and a hydrophobic core. Previous studies of GspB (the SRR adhesin ofStreptococcus gordonii) have shown that a glycine-rich motif in its hydrophobic core is essential for selective, aSec-mediated transport. However, the role of this extended N-region in transport is poorly understood. Here, using protein–lipid co-flotation assays and site-directed mutagenesis, we report that the N-region of the GspB signal peptide interacts with anionic lipids through electrostatic forces and that this interaction is necessary for GspB preprotein trafficking to lipid membranes. Moreover, we observed that protein–lipid binding is required for engagement of GspB with SecA2 and for aSec-mediated transport. We further found that SecA2 and Asp1 to Asp3 also localize selectively to liposomes that contain anionic lipids. These findings suggest that the GspB signal peptide electrostatically binds anionic lipids at the cell membrane, where it encounters SecA2. After SecA2 engagement with the signal peptide, Asp1 to Asp3 promote SecA2 engagement with the mature domain, which activates GspB translocation.

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Ohta, Kaoru, Chihiro Sato, Tsukasa Matsuda, Masaru Toriyama, Victor D. Vacquier, Noritaka Hirohashi, William J. Lennarz, and Ken Kitajima. "Lipid raft on gametic cells as a functional domain for sperm–egg interaction coupled with signal transduction." Zygote 8, S1 (December 1999): S63. http://dx.doi.org/10.1017/s0967199400130321.

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It has been shown that lipid raft, a microdomain of plasma membrane, is a hot spot of signal transduction in somatic cells, because it contains several transducer proteins as well as various receptor molecules. The lipid raft is characterised by its low-density detergent-insoluble nature and by enrichment of glycosphingolipids (GSLs). We hypothesised that lipid raft was also on the gamete surface, and might function as a sperm–egg adhesion site as well as in signal transduction during fertilisation. To test this hypothesis, we have initiated studies using sea urchin gametes. Recently we have demonstrated the presence of the lipid raft in sperm of three sea urchin species as the first example in gametic cells (Ohta et al., 1999). Here we show several lines of evidence for the functional importance of the lipid raft in sperm–egg interaction as well as in subsequent signal transduction.In sea urchin sperm, lipid rafts were able to be prepared as a low-density detergent-insoluble membrane (LD-DIM) fraction and were rich in GSLs including gangliosides and sulphatide, containing more than 50% of the total amount of GSL present in sperm. On the other hand, cholesterol and sphingomyelin were not so enriched, which contrasted with the LD-DIM from MDCK cells, where these lipids were reported to be abundant (Brown & Rose, 1992).

20

Silvius, John R. "Lipid Modifications of Intracellular Signal-Transducing Proteins." Journal of Liposome Research 9, no. 1 (January 1999): 1–19. http://dx.doi.org/10.3109/08982109909044489.

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Walton, T. J. "Inositol lipid signal transduction in phytoalexin elicitation." Biochemical Society Transactions 23, no. 4 (November 1, 1995): 862–67. http://dx.doi.org/10.1042/bst0230862.

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QI, Zhi-gang, Yu-xin LI, Yan WANG, Dao-yin GENG, Kun-cheng LI, Tian-zhen SHEN, and Xin-rong CHEN. "Lipid signal in evaluation of intracranial meningiomas." Chinese Medical Journal 121, no. 23 (December 2008): 2415–19. http://dx.doi.org/10.1097/00029330-200812010-00010.

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23

Olenick, Laura L., Hilary M. Chase, Li Fu, Yun Zhang, Alicia C. McGeachy, Merve Dogangun, Stephanie R. Walter, Hong-fei Wang, and Franz M. Geiger. "Single-component supported lipid bilayers probed using broadband nonlinear optics." Physical Chemistry Chemical Physics 20, no. 5 (2018): 3063–72. http://dx.doi.org/10.1039/c7cp02549a.

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Broadband SFG spectroscopy is shown to offer considerable advantages over scanning systems in terms of signal-to-noise ratios when probing well-formed single-component supported lipid bilayers formed from zwitterionic lipids with PC headgroups.

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Liu, Qingtao, Yunxin Xiao, Adrian Hawley, and Ben J. Boyd. "Lipid-based lyotropic liquid crystalline phase transitions as a novel assay platform using birefringence as the visual signal output." Journal of Materials Chemistry B 8, no. 29 (2020): 6277–85. http://dx.doi.org/10.1039/d0tb00355g.

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Batenburg, A. M., and B. de Kruijff. "Modulation of membrane surface curvature by peptide-lipid interactions." Bioscience Reports 8, no. 4 (August 1, 1988): 299–307. http://dx.doi.org/10.1007/bf01115220.

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Recent reports on the interaction of cardiotoxin and melittin with phospholipid model membranes are reviewed and analyzed. These types of peptide toxins are able to modulate lipid surface curvature and polymorphism in a highly lipid-specific way. It is demonstrated that the remarkable variety of effects of melittin on the organization of different membrane phospholipids can be understood in a relatively simple model, based on the shape-structure concept of lipid polymorphism and taking into account the position of the peptide molecule with respect to the lipids. Based on the strong preference of the peptides for negatively charged lipids and the structural consequences thereof, and on preliminary studies of signal peptide-lipid interaction, a role of inverted or concave lipid structures in the process of protein translocation across membranes is suggested.

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Demel, R. A., E. Goormaghtigh, and B. de Kruijff. "Lipid and peptide specificities in signal peptide-lipid interactions in model membranes." Biochimica et Biophysica Acta (BBA) - Biomembranes 1027, no. 2 (August 1990): 155–62. http://dx.doi.org/10.1016/0005-2736(90)90079-4.

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Marks, F., and G. F�rstenberger. "Fourth colloquium on cellular signal transduction. Lipid mediators: signal transduction and transport." Journal of Cancer Research and Clinical Oncology 121, no. 7 (July 1995): 434–38. http://dx.doi.org/10.1007/bf01212952.

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Prommapan, Plengchart, Nermina Brljak, Troy W. Lowry, David Van Winkle, and Steven Lenhert. "Aptamer Functionalized Lipid Multilayer Gratings for Label-Free Analyte Detection." Nanomaterials 10, no. 12 (December 5, 2020): 2433. http://dx.doi.org/10.3390/nano10122433.

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Lipid multilayer gratings are promising optical biosensor elements that are capable of transducing analyte binding events into changes in an optical signal. Unlike solid state transducers, reagents related to molecular recognition and signal amplification can be incorporated into the lipid grating ink volume prior to fabrication. Here we describe a strategy for functionalizing lipid multilayer gratings with a DNA aptamer for the protein thrombin that allows label-free analyte detection. A double cholesterol-tagged, double-stranded DNA linker was used to attach the aptamer to the lipid gratings. This approach was found to be sufficient for binding fluorescently labeled thrombin to lipid multilayers with micrometer-scale thickness. In order to achieve label-free detection with the sub-100 nm-thick lipid multilayer grating lines, the binding affinity was improved by varying the lipid composition. A colorimetric image analysis of the light diffracted from the gratings using a color camera was then used to identify the grating nanostructures that lead to an optimal signal. Lipid composition and multilayer thickness were found to be critical parameters for the signal transduction from the aptamer functionalized lipid multilayer gratings.

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Wu, Danxia, Muhammad Saleem, Tengbing He, and Guandi He. "The Mechanism of Metal Homeostasis in Plants: A New View on the Synergistic Regulation Pathway of Membrane Proteins, Lipids and Metal Ions." Membranes 11, no. 12 (December 15, 2021): 984. http://dx.doi.org/10.3390/membranes11120984.

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Heavy metal stress (HMS) is one of the most destructive abiotic stresses which seriously affects the growth and development of plants. Recent studies have shown significant progress in understanding the molecular mechanisms underlying plant tolerance to HMS. In general, three core signals are involved in plants’ responses to HMS; these are mitogen-activated protein kinase (MAPK), calcium, and hormonal (abscisic acid) signals. In addition to these signal components, other regulatory factors, such as microRNAs and membrane proteins, also play an important role in regulating HMS responses in plants. Membrane proteins interact with the highly complex and heterogeneous lipids in the plant cell environment. The function of membrane proteins is affected by the interactions between lipids and lipid-membrane proteins. Our review findings also indicate the possibility of membrane protein-lipid-metal ion interactions in regulating metal homeostasis in plant cells. In this review, we investigated the role of membrane proteins with specific substrate recognition in regulating cell metal homeostasis. The understanding of the possible interaction networks and upstream and downstream pathways is developed. In addition, possible interactions between membrane proteins, metal ions, and lipids are discussed to provide new ideas for studying metal homeostasis in plant cells.

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Peng, Ying, Zhuoxuan Li, Zhiyang Zhang, Yinglun Chen, Renyuan Wang, Nixi Xu, Yuanwu Cao, Chang Jiang, Zixian Chen, and Haodong Lin. "Bromocriptine protects perilesional spinal cord neurons from lipotoxicity after spinal cord injury." Neural Regeneration Research 19, no. 5 (September 22, 2023): 1142–49. http://dx.doi.org/10.4103/1673-5374.385308.

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Abstract JOURNAL/nrgr/04.03/01300535-202405000-00046/inline-graphic1/v/2023-09-28T063346Z/r/image-tiff Recent studies have revealed that lipid droplets accumulate in neurons after brain injury and evoke lipotoxicity, damaging the neurons. However, how lipids are metabolized by spinal cord neurons after spinal cord injury remains unclear. Herein, we investigated lipid metabolism by spinal cord neurons after spinal cord injury and identified lipid-lowering compounds to treat spinal cord injury. We found that lipid droplets accumulated in perilesional spinal cord neurons after spinal cord injury in mice. Lipid droplet accumulation could be induced by myelin debris in HT22 cells. Myelin debris degradation by phospholipase led to massive free fatty acid production, which increased lipid droplet synthesis, β-oxidation, and oxidative phosphorylation. Excessive oxidative phosphorylation increased reactive oxygen species generation, which led to increased lipid peroxidation and HT22 cell apoptosis. Bromocriptine was identified as a lipid-lowering compound that inhibited phosphorylation of cytosolic phospholipase A2 by reducing the phosphorylation of extracellular signal-regulated kinases 1/2 in the mitogen-activated protein kinase pathway, thereby inhibiting myelin debris degradation by cytosolic phospholipase A2 and alleviating lipid droplet accumulation in myelin debris-treated HT22 cells. Motor function, lipid droplet accumulation in spinal cord neurons and neuronal survival were all improved in bromocriptine-treated mice after spinal cord injury. The results suggest that bromocriptine can protect neurons from lipotoxic damage after spinal cord injury via the extracellular signal-regulated kinases 1/2-cytosolic phospholipase A2 pathway.

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Zhou, Yong, Hong Liang, Travis Rodkey, Nicholas Ariotti, Robert G. Parton, and John F. Hancock. "Signal Integration by Lipid-Mediated Spatial Cross Talk between Ras Nanoclusters." Molecular and Cellular Biology 34, no. 5 (December 23, 2013): 862–76. http://dx.doi.org/10.1128/mcb.01227-13.

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Lipid-anchored Ras GTPases form transient, spatially segregated nanoclusters on the plasma membrane that are essential for high-fidelity signal transmission. The lipid composition of Ras nanoclusters, however, has not previously been investigated. High-resolution spatial mapping shows that different Ras nanoclusters have distinct lipid compositions, indicating that Ras proteins engage in isoform-selective lipid sorting and accounting for different signal outputs from different Ras isoforms. Phosphatidylserine is a common constituent of all Ras nanoclusters but is only an obligate structural component of K-Ras nanoclusters. Segregation of K-Ras and H-Ras into spatially and compositionally distinct lipid assemblies is exquisitely sensitive to plasma membrane phosphatidylserine levels. Phosphatidylserine spatial organization is also modified by Ras nanocluster formation. In consequence, Ras nanoclusters engage in remote lipid-mediated communication, whereby activated H-Ras disrupts the assembly and operation of spatially segregated K-Ras nanoclusters. Computational modeling and experimentation reveal that complex effects of caveolin and cortical actin on Ras nanoclustering are similarly mediated through regulation of phosphatidylserine spatiotemporal dynamics. We conclude that phosphatidylserine maintains the lateral segregation of diverse lipid-based assemblies on the plasma membrane and that lateral connectivity between spatially remote lipid assemblies offers important previously unexplored opportunities for signal integration and signal processing.

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Centonze, Sara, and Gianluca Baldanzi. "Diacylglycerol Kinases in Signal Transduction." International Journal of Molecular Sciences 23, no. 15 (July 29, 2022): 8423. http://dx.doi.org/10.3390/ijms23158423.

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In recent years, the significant research efforts put into the clarification of the PI3K/AKT/mTOR pathway resulted in the approval of the first targeted therapies based on lipid kinase inhibitors [...]

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Béaslas, Olivier, François Torreilles, Pierre Casellas, Dominique Simon, Gérard Fabre, Michel Lacasa, François Delers, Jean Chambaz, Monique Rousset, and Véronique Carrière. "Transcriptome response of enterocytes to dietary lipids: impact on cell architecture, signaling, and metabolism genes." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 5 (November 2008): G942—G952. http://dx.doi.org/10.1152/ajpgi.90237.2008.

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Intestine contributes to lipid homeostasis through the absorption of dietary lipids, which reach the apical pole of enterocytes as micelles. The present study aimed to identify the specific impact of these dietary lipid-containing micelles on gene expression in enterocytes. We analyzed, by microarray, the modulation of gene expression in Caco-2/TC7 cells in response to different lipid supply conditions that reproduced either the permanent presence of albumin-bound lipids at the basal pole of enterocytes or the physiological delivery, at the apical pole, of lipid micelles, which differ in their composition during the interprandial (IPM) or the postprandial (PPM) state. These different conditions led to distinct gene expression profiles. We observed that, contrary to lipids supplied at the basal pole, apical lipid micelles modulated a large number of genes. Moreover, compared with the apical supply of IPM, PPM specifically impacted 46 genes from three major cell function categories: signal transduction, lipid metabolism, and cell adhesion/architecture. Results from this first large-scale analysis underline the importance of the mode and polarity of lipid delivery on enterocyte gene expression. They demonstrate specific and coordinated transcriptional effects of dietary lipid-containing micelles that could impact the structure and polarization of enterocytes and their functions in nutrient transfer.

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Grassi, Sara, Paola Giussani, Laura Mauri, Simona Prioni, Sandro Sonnino, and Alessandro Prinetti. "Lipid rafts and neurodegeneration: structural and functional roles in physiologic aging and neurodegenerative diseases." Journal of Lipid Research 61, no. 5 (December 23, 2019): 636–54. http://dx.doi.org/10.1194/jlr.tr119000427.

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Lipid rafts are small, dynamic membrane areas characterized by the clustering of selected membrane lipids as the result of the spontaneous separation of glycolipids, sphingolipids, and cholesterol in a liquid-ordered phase. The exact dynamics underlying phase separation of membrane lipids in the complex biological membranes are still not fully understood. Nevertheless, alterations in the membrane lipid composition affect the lateral organization of molecules belonging to lipid rafts. Neural lipid rafts are found in brain cells, including neurons, astrocytes, and microglia, and are characterized by a high enrichment of specific lipids depending on the cell type. These lipid rafts seem to organize and determine the function of multiprotein complexes involved in several aspects of signal transduction, thus regulating the homeostasis of the brain. The progressive decline of brain performance along with physiological aging is at least in part associated with alterations in the composition and structure of neural lipid rafts. In addition, neurodegenerative conditions, such as lysosomal storage disorders, multiple sclerosis, and Parkinson’s, Huntington’s, and Alzheimer’s diseases, are frequently characterized by dysregulated lipid metabolism, which in turn affects the structure of lipid rafts. Several events underlying the pathogenesis of these diseases appear to depend on the altered composition of lipid rafts. Thus, the structure and function of lipid rafts play a central role in the pathogenesis of many common neurodegenerative diseases.

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Fielding, C. J., and P. E. Fielding. "Membrane cholesterol and the regulation of signal transduction." Biochemical Society Transactions 32, no. 1 (February 1, 2004): 65–69. http://dx.doi.org/10.1042/bst0320065.

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The plasma membrane of mammalian cells consists of microdomains differing in lipid and protein composition. Two distinct classes of cholesterol/sphingolipid microdomain (caveolae and lipid rafts) are assembly points for transmembrane signalling complexes. Recent evidence suggests that transient changes in cholesterol content may be important in regulating signal transduction.

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Mollinedo, Faustino, and Consuelo Gajate. "Lipid rafts as signaling hubs in cancer cell survival/death and invasion: implications in tumor progression and therapy." Journal of Lipid Research 61, no. 5 (January 27, 2020): 611–35. http://dx.doi.org/10.1194/jlr.tr119000439.

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Cholesterol/sphingolipid-rich membrane domains, known as lipid rafts or membrane rafts, play a critical role in the compartmentalization of signaling pathways. Physical segregation of proteins in lipid rafts may modulate the accessibility of proteins to regulatory or effector molecules. Thus, lipid rafts serve as sorting platforms and hubs for signal transduction proteins. Cancer cells contain higher levels of intracellular cholesterol and lipid rafts than their normal non-tumorigenic counterparts. Many signal transduction processes involved in cancer development (insulin-like growth factor system and phosphatidylinositol 3-kinase-AKT) and metastasis [cluster of differentiation (CD)44] are dependent on or modulated by lipid rafts. Additional proteins playing an important role in several malignant cancers (e.g., transmembrane glycoprotein mucin 1) are also being detected in association with lipid rafts, suggesting a major role of lipid rafts in tumor progression. Conversely, lipid rafts also serve as scaffolds for the recruitment and clustering of Fas/CD95 death receptors and downstream signaling molecules leading to cell death-promoting raft platforms. The partition of death receptors and downstream signaling molecules in aggregated lipid rafts has led to the formation of the so-called cluster of apoptotic signaling molecule-enriched rafts, or CASMER, which leads to apoptosis amplification and can be pharmacologically modulated. These death-promoting rafts can be viewed as a linchpin from which apoptotic signals are launched. In this review, we discuss the involvement of lipid rafts in major signaling processes in cancer cells, including cell survival, cell death, and metastasis, and we consider the potential of lipid raft modulation as a promising target in cancer therapy.

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P. Eckert, Gunter. "Manipulation of Lipid Rafts in Neuronal Cells." Open Biology Journal 3, no. 1 (March 19, 2010): 32–38. http://dx.doi.org/10.2174/18741967010030100032.

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Lipid rafts are specialized plasma membrane micro-domains highly enriched in cholesterol, sphingolipids and glycosylphosphatidylinositol (GPI) anchored proteins. Lipid rafts are thought to be located in the exofacial leaflet of plasma membranes. Functionally, lipid rafts are involved in intracellular trafficking of proteins and lipids, secretory and endocytotic pathways, signal transduction, inflammation and in cell-surface proteolysis. There has been substantial interest in lipid rafts in brain, both with respect to normal functioning and with certain neurodegenerative diseases. Based on the impact of lipid rafts on multitude biochemical pathways, modulation of lipid rafts is used to study related disease pathways and probably offers a target for pharmacological intervention. Lipid rafts can be targeted by modulation of its main components, namely cholesterol and sphingolipids. Other approaches include the modulation of membrane dynamics and it has been reported that protein-lipid interactions can vary the occurrence and composition of these membrane micro-domains. The present review summarizes the possibilities to modulate lipid rafts with focus on neuronal cells.

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Maraldi, Nadir M., Nicoletta Zini, Spartaco Santi, Massimo Riccio, Mirella Falconi, Silvano Capitani, and F. A. Manzoli. "Nuclear domains involved in inositol lipid signal transduction✠." Advances in Enzyme Regulation 40, no. 1 (June 2000): 219–53. http://dx.doi.org/10.1016/s0065-2571(99)00032-1.

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Kearns, Daniel B., and Lawrence J. Shimkets. "Lipid chemotaxis and signal transduction in Myxococcus xanthus." Trends in Microbiology 9, no. 3 (March 2001): 126–29. http://dx.doi.org/10.1016/s0966-842x(01)01948-5.

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Hasegawa, Tohru. "Lipid peroxide stimulates the proliferative signal of cell." Free Radical Biology and Medicine 9 (January 1990): 168. http://dx.doi.org/10.1016/0891-5849(90)90766-c.

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Barry R., Ganong. "Roles of Lipid Turnover in Transmembrane Signal Transduction." American Journal of the Medical Sciences 302, no. 5 (November 1991): 304–12. http://dx.doi.org/10.1097/00000441-199111000-00009.

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Manzoli, F. A., S. Capitani, L. Cocco, N. M. Maraldi, G. Mazzotti, and O. Barnabei. "Lipid mediated signal transduction in the cell nucleus." Advances in Enzyme Regulation 27 (January 1988): 57–79. http://dx.doi.org/10.1016/0065-2571(88)90010-6.

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Whatley, Ralph E., Guy A. Zimmerman, Thomas M. McIntyre, and Stephen M. Prescott. "Lipid metabolism and signal transduction in endothelial cells." Progress in Lipid Research 29, no. 1 (January 1990): 45–63. http://dx.doi.org/10.1016/0163-7827(90)90005-6.

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Balla, T. "Inositol-lipid binding motifs: signal integrators through protein-lipid and protein-protein interactions." Journal of Cell Science 118, no. 10 (May 15, 2005): 2093–104. http://dx.doi.org/10.1242/jcs.02387.

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Nordzieke, Daniela, and Iria Medraño-Fernandez. "The Plasma Membrane: A Platform for Intra- and Intercellular Redox Signaling." Antioxidants 7, no. 11 (November 20, 2018): 168. http://dx.doi.org/10.3390/antiox7110168.

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Membranes are of outmost importance to allow for specific signal transduction due to their ability to localize, amplify, and direct signals. However, due to the double-edged nature of reactive oxygen species (ROS)—toxic at high concentrations but essential signal molecules—subcellular localization of ROS-producing systems to the plasma membrane has been traditionally regarded as a protective strategy to defend cells from unwanted side-effects. Nevertheless, specialized regions, such as lipid rafts and caveolae, house and regulate the activated/inhibited states of important ROS-producing systems and concentrate redox targets, demonstrating that plasma membrane functions may go beyond acting as a securing lipid barrier. This is nicely evinced by nicotinamide adenine dinucleotide phosphate (NADPH)-oxidases (NOX), enzymes whose primary function is to generate ROS and which have been shown to reside in specific lipid compartments. In addition, membrane-inserted bidirectional H2O2-transporters modulate their conductance precisely during the passage of the molecules through the lipid bilayer, ensuring time-scaled delivery of the signal. This review aims to summarize current evidence supporting the role of the plasma membrane as an organizing center that serves as a platform for redox signal transmission, particularly NOX-driven, providing specificity at the same time that limits undesirable oxidative damage in case of malfunction. As an example of malfunction, we explore several pathological situations in which an inflammatory component is present, such as inflammatory bowel disease and neurodegenerative disorders, to illustrate how dysregulation of plasma-membrane-localized redox signaling impacts normal cell physiology.

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Shibuya, Kazuko, Jun Shirakawa, Tomie Kameyama, Shin-ichiro Honda, Satoko Tahara-Hanaoka, Akitomo Miyamoto, Masafumi Onodera, et al. "CD226 (DNAM-1) Is Involved in Lymphocyte Function–associated Antigen 1 Costimulatory Signal for Naive T Cell Differentiation and Proliferation." Journal of Experimental Medicine 198, no. 12 (December 15, 2003): 1829–39. http://dx.doi.org/10.1084/jem.20030958.

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Upon antigen recognition by the T cell receptor, lymphocyte function–associated antigen 1 (LFA-1) physically associates with the leukocyte adhesion molecule CD226 (DNAM-1) and the protein tyrosine kinase Fyn. We show that lentiviral vector-mediated mutant (Y-F322) CD226 transferred into naive CD4+ helper T cells (Ths) inhibited interleukin (IL)-12–independent Th1 development initiated by CD3 and LFA-1 ligations. Moreover, proliferation induced by LFA-1 costimulatory signal was suppressed in mutant (Y-F322) CD226-transduced naive CD4+ and CD8+ T cells in the absence of IL-2. These results suggest that CD226 is involved in LFA-1–mediated costimulatory signals for triggering naive T cell differentiation and proliferation. We also demonstrate that although LFA-1, CD226, and Fyn are polarized at the immunological synapse upon stimulation with anti-CD3 in CD4+ and CD8+ T cells, lipid rafts are polarized in CD4+, but not CD8+, T cells. Moreover, proliferation initiated by LFA-1 costimulatory signal is suppressed by lipid raft disruption in CD4+, but not CD8+, T cells, suggesting that the LFA-1 costimulatory signal is independent of lipid rafts in CD8+ T cells.

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Bandorowicz-Pikuła, J. "Lipid-binding proteins as stabilizers of membrane microdomains--possible physiological significance." Acta Biochimica Polonica 47, no. 3 (September 30, 2000): 553–64. http://dx.doi.org/10.18388/abp.2000_3978.

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Below the melting point temperature of lipids, artificial lipid membranes usually exist in the ordered gel phase. Above these temperatures lipid acyl chains become fluid and disordered (liquid-crystalline phase). Depending on the chemical composition of artificial membranes, phase separation may occur, leading to the formation of transient or stable membrane domains. A similar phase separation of lipids into ordered and disordered domains has been observed in natural membranes at physiological temperature range. Moreover, it has been reported that certain proteins prefer certain organization of lipids, as for example glycosylphosphatidylinositol-anchored proteins or Src family of tyrosine kinases. The aim of present review is to discuss the possibility that some lipid microdomains are induced or stabilized by lipid-binding proteins that under certain conditions, for example due to a rise of cytosolic Ca2+ or pH changes, may attach to the membrane surface, inducing clustering of lipid molecules and creation of ordered lipid microdomains. These domains may than attract other cytosolic proteins, either enzymes or regulatory proteins. It is, therefore, postulated that lipid microdomains play important roles within a cell, in signal transduction and enzymatic catalysis, and also in various pathological states, as Alzheimer's disease, anti-phosphatidylserine syndrome, or development of multidrug resistance of cancer cells.

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Blazer-Yost, Bonnie L., Judith C. Vahle, Jason M. Byars, and Robert L. Bacallao. "Real-time three-dimensional imaging of lipid signal transduction: apical membrane insertion of epithelial Na+ channels." American Journal of Physiology-Cell Physiology 287, no. 6 (December 2004): C1569—C1576. http://dx.doi.org/10.1152/ajpcell.00226.2004.

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In the distal tubule, Na+ resorption is mediated by epithelial Na+ channels (ENaC). Hormones such as aldosterone, vasopressin, and insulin modulate ENaC membrane targeting, assembly, and/or kinetic activity, thereby regulating salt and water homeostasis. Insulin binds to a receptor on the basal membrane to initiate a signal transduction cascade that rapidly results in an increase in apical membrane ENaC. Current models of this signaling pathway envision diffusion of signaling intermediates from the basal to the apical membrane. This necessitates diffusion of several high-molecular-weight signaling elements across a three-dimensional space. Transduction of the insulin signal involves the phosphoinositide pathway, but how and where this lipid-based signaling pathway controls ENaC activity is not known. We used tagged channels, biosensor lipid probes, and intravital imaging to investigate the role of lipids in insulin-stimulated Na+ flux. Insulin-stimulated delivery of intracellular ENaC to apical membranes was concurrent with plasma membrane-limited changes in lipid composition. Notably, in response to insulin, phosphatidylinositol 3,4,5-trisphosphate (PIP3) formed in the basolateral membrane, rapidly diffused within the bilayer, and crossed the tight junction to enter the apical membrane. This novel signaling pathway takes advantage of the fact that the lipids of the plasma membrane's inner leaflet are not constrained by the tight junction. Therefore, diffusion of PIP3 as a signal transduction intermediate occurs within a planar surface, thus facilitating swift responses and confining and controlling the signaling pathway.

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Yamazaki, Satoshi, Atsushi Iwama, Shin-ichiro Takayanagi, Koji Eto, Hideo Ema, and Hiromitsu Nakauchi. "TGF-β as a candidate bone marrow niche signal to induce hematopoietic stem cell hibernation." Blood 113, no. 6 (February 5, 2009): 1250–56. http://dx.doi.org/10.1182/blood-2008-04-146480.

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Abstract Hematopoietic stem cells (HSCs) reside in a bone marrow niche in a nondividing state from which they occasionally are aroused to undergo cell division. Yet, the mechanism underlying this unique feature remains largely unknown. We have recently shown that freshly isolated CD34−KSL hematopoietic stem cells (HSCs) in a hibernation state exhibit inhibited lipid raft clustering. Lipid raft clustering induced by cytokines is essential for HSCs to augment cytokine signals to the level enough to re-enter the cell cycle. Here we screened candidate niche signals that inhibit lipid raft clustering, and identified that transforming growth factor-β (TGF-β) efficiently inhibits cytokine-mediated lipid raft clustering and induces HSC hibernation ex vivo. Smad2 and Smad3, the signaling molecules directly downstream from and activated by TGF-β receptors were specifically activated in CD34−KSL HSCs in a hibernation state, but not in cycling CD34+KSL progenitors. These data uncover a critical role for TGF-β as a candidate niche signal in the control of HSC hibernation and provide TGF-β as a novel tool for ex vivo modeling of the HSC niche.

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Prestwich, G. D. "Visualizing signalling by phosphoinositide 3-kinase pathway lipids." Biochemical Society Transactions 32, no. 2 (April 1, 2004): 336–37. http://dx.doi.org/10.1042/bst0320336.

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Cells signal through lipids produced by phospholipid and phosphoinositide metabolism that involves three enzymic processes: (i) ester and phosphodiester hydrolysis by phospholipases; (ii) monophosphate hydrolysis by phosphatases; and (iii) phosphorylation of hydroxy groups by kinases. Unregulated enzyme activity correlates with specific pathologies, which are specific targets for therapeutic intervention. Three categories of reagents developed at the University of Utah and at Echelon Biosciences permit monitoring of in vitro enzyme activity and spatiotemporal changes in intracellular lipid concentrations, and identification of lipid–protein interactions.

Journal articles on the topic 'Lipid signal'

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