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Готові списки джерел за темами / Membrane destabilization / Статті в журналах

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Статті в журналах з теми "Membrane destabilization"

Автор: Grafiati

Опубліковано: 10 березня 2023

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1

Sun, Jan, Elena E. Pohl, Oxana O. Krylova, Eberhard Krause, Igor I. Agapov, Alexander G. Tonevitsky, and Peter Pohl. "Membrane destabilization by ricin." European Biophysics Journal 33, no. 7 (March 26, 2004): 572–79. http://dx.doi.org/10.1007/s00249-004-0400-9.

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2

Storm, G., and E. Wagner. "Membrane destabilization for improved cystolic delivery." Advanced Drug Delivery Reviews 38, no. 3 (August 1999): 195. http://dx.doi.org/10.1016/s0169-409x(99)00028-9.

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3

Schutzbach, John S., and John W. Jensen. "Bilayer membrane destabilization induced by dolichylphosphate." Chemistry and Physics of Lipids 51, no. 3-4 (November 1989): 213–18. http://dx.doi.org/10.1016/0009-3084(89)90008-x.

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4

Luján, H. D., and D. H. Bronia. "Intermembrane lipid transfer duringTrypanosoma cruzi-induced erythrocyte membrane destabilization." Parasitology 108, no. 3 (April 1994): 323–34. http://dx.doi.org/10.1017/s0031182000076162.

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SUMMARYThe ability ofTrypanosoma cruzito induce erythrocyte membrane destabilizationin vitrowas studied. Epimastigote forms adhered to human erythrocytes and caused fusion or lysis of the red cells, depending on the conditions of the interaction. Red cells were fused in the presence of calcium, while haemolysis was induced in the absence of the cation. Dextran 60 C facilitated fusion but delayed lysis. Optimum pH and temperature for fusion were 7·4 and 37 °C, respectively. Lipid alterations were produced in the plasma membrane of the red cell during the interaction with the parasite. A Ca2+-independent increase of lysophospholipids and free fatty acids was common to both the lysis and fusion processes. A relative increase of 1, 2-diacylglycerides was unique to the fusion process and these changes were dependent on Ca2+. The transfer of free fatty acids and lysophospholipids fromT. cruzito erythrocyte membranes was demonstrated using parasites pre-labelled with radioactive phospholipids. Pre-treatment of parasites with exogenous phospholipase A2abolished the fusogenicity, while lysis was increased. Neither fusion nor haemolysis occurred when the parasites were pre-treated with fatty acid free albumin, phospholipase A2inhibitors or when these compounds were present in the medium during the parasite-erythrocyte interaction. Our results suggest thatT. cruziinduces erythrocyte membrane destabilizationin vitroby transfer of lipid material in a calcium independent manner and that this ion is necessary for other membrane alterations that lead to erythrocyte fusion.

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5

Steponkus, Peter. "Membrane destabilization resulting from freeze-induced dehydration." Cryobiology 24, no. 6 (December 1987): 555. http://dx.doi.org/10.1016/0011-2240(87)90096-4.

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6

Morales, Joselyn, та Suren A. Tatulian. "Membrane Destabilization by Alzheimer's Amyloid β Peptide". Biophysical Journal 104, № 2 (січень 2013): 239a—240a. http://dx.doi.org/10.1016/j.bpj.2012.11.1351.

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7

Jin, Seok Min, Michael Lazarou, Chunxin Wang, Lesley A. Kane, Derek P. Narendra, and Richard J. Youle. "Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL." Journal of Cell Biology 191, no. 5 (November 29, 2010): 933–42. http://dx.doi.org/10.1083/jcb.201008084.

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PINK1 is a mitochondrial kinase mutated in some familial cases of Parkinson’s disease. It has been found to work in the same pathway as the E3 ligase Parkin in the maintenance of flight muscles and dopaminergic neurons in Drosophila melanogaster and to recruit cytosolic Parkin to mitochondria to mediate mitophagy in mammalian cells. Although PINK1 has a predicted mitochondrial import sequence, its cellular and submitochondrial localization remains unclear in part because it is rapidly degraded. In this study, we report that the mitochondrial inner membrane rhomboid protease presenilin-associated rhomboid-like protein (PARL) mediates cleavage of PINK1 dependent on mitochondrial membrane potential. In the absence of PARL, the constitutive degradation of PINK1 is inhibited, stabilizing a 60-kD form inside mitochondria. When mitochondrial membrane potential is dissipated, PINK1 accumulates as a 63-kD full-length form on the outer mitochondrial membrane, where it can recruit Parkin to impaired mitochondria. Thus, differential localization to the inner and outer mitochondrial membranes appears to regulate PINK1 stability and function.

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8

Harper, Sandra L., Sira Sriswasdi, Hsin-Yao Tang, Massimiliano Gaetani, Patrick G. Gallagher та David W. Speicher. "The common hereditary elliptocytosis-associated α-spectrin L260P mutation perturbs erythrocyte membranes by stabilizing spectrin in the closed dimer conformation". Blood 122, № 17 (24 жовтня 2013): 3045–53. http://dx.doi.org/10.1182/blood-2013-02-487702.

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Key Points The common HE mutation αL260P reduces spectrin tetramer links between junctional complexes in red cell membranes by favoring closed dimers. Favoring closed spectrin dimer formation is a new mechanism of red cell membrane destabilization by hereditary anemia mutations.

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9

Lau, Wai Leung, David S. Ege, James D. Lear, Daniel A. Hammer, and William F. DeGrado. "Oligomerization of Fusogenic Peptides Promotes Membrane Fusion by Enhancing Membrane Destabilization." Biophysical Journal 86, no. 1 (January 2004): 272–84. http://dx.doi.org/10.1016/s0006-3495(04)74103-x.

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10

Brasseur, Robert. "Tilted peptides: a motif for membrane destabilization (Hypothesis)." Molecular Membrane Biology 17, no. 1 (January 2000): 31–40. http://dx.doi.org/10.1080/096876800294461.

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11

Muga, Arturo, Henry H. Mantsch, and Witold K. Surewicz. "Membrane binding induces destabilization of cytochrome c structure." Biochemistry 30, no. 29 (July 23, 1991): 7219–24. http://dx.doi.org/10.1021/bi00243a025.

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12

Lonez, Caroline, Marc F. Lensink, Bouna-Moussa Tandia, Michel Vandenbranden, and Jean-Marie Ruysschaert. "Cationic Lipids: from Membrane Destabilization to Cell Signaling." Biophysical Journal 98, no. 3 (January 2010): 435a. http://dx.doi.org/10.1016/j.bpj.2009.12.2362.

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13

PRACHAYASITTIKUL, Virapong, Chartchalerm ISARANKURA-NA-AYUDHYA, Tanawut TANTIMONGCOLWAT, Chanin NANTASENAMAT, and Hans-Joachim GALLA. "EDTA-induced Membrane Fluidization and Destabilization: Biophysical Studies on Artificial Lipid Membranes." Acta Biochimica et Biophysica Sinica 39, no. 11 (November 2007): 901–13. http://dx.doi.org/10.1111/j.1745-7270.2007.00350.x.

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14

Voisine, Richard, Claude Willemot, and Louis Vézina. "MICROSOMAL MEMBRANE CHANGES IN IRRADIATED CAULIFLOWER DURING STORAGE." HortScience 25, no. 9 (September 1990): 1086d—1086. http://dx.doi.org/10.21273/hortsci.25.9.1086d.

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Cauliflowers (Brassica oleracea) were irradiated at 0, 2, and 4 kGy and stored 8 days at 13°C. Development of yellow color and browning of the in florescence, increase in membrane electrolyte leakage and reduction of protein recovery in microsomal membranes were observed over the storage period. Changes in membrane free fatty acids, lipid phosphorus content, peroxydation level, and fatty acid composition of polar lipids also occurred. These results indicate an important modification of cellular membranes. The direct effect of gamma rays on membrane lipids via free radical production and subsequent destabilization of the lipid bilayer during storage could be responsable for earlier onset of senescence.

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15

Lee, S., N. Jang, and Y. Watanabe. "Effect of residual ozone on membrane fouling reduction in ozone resisting microfiltration (MF) membrane system." Water Science and Technology 50, no. 12 (December 1, 2004): 287–92. http://dx.doi.org/10.2166/wst.2004.0725.

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The effect of residual ozone on reducing the membrane fouling was investigated using ozone resisting microfiltration membrane. It was found out that the fouling was reduced effectively by maintaining residual ozone in the membrane module. To clarify the reason why the residual ozone reduces the membrane fouling, research was focused on the molecular degradation reaction and particle destabilization reaction induced by residual ozone. The major reason of membrane fouling reduction was attributed to the reduction of reversible resistance induced by the cake layer. The reversible resistance was reduced due to degradation of organic substances in the cake layer. In addition to degradation reaction, the increase of fouling particle size due to residual ozone in the cake layer is another important process for fouling reduction. This effect has been referred to as ozone-induced destabilization reaction. The calcium present in the raw water influenced this reaction. The increase of fouling particles size improves the filterability through the cake layer and backwashing efficiency.

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16

Pascual, Roberto, Miguel R. Moreno, and José Villalaín. "A Peptide Pertaining to the Loop Segment of Human Immunodeficiency Virus gp41 Binds and Interacts with Model Biomembranes: Implications for the Fusion Mechanism." Journal of Virology 79, no. 8 (April 15, 2005): 5142–52. http://dx.doi.org/10.1128/jvi.79.8.5142-5152.2005.

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ABSTRACT The human immunodeficiency virus gp41 envelope protein mediates the entry of the virus into the target cell by promoting membrane fusion. In order to gain new insights into the viral fusion mechanism, we studied a 35-residue peptide pertaining to the loop domain of gp41, both in solution and membrane bound, by using infrared and fluorescence spectroscopy. We show here that the peptide, which has a membrane-interacting surface, binds and interacts with phospholipid model membranes and tends to aggregate in the presence of a membranous medium and induce the leakage of vesicle contents. The results reported in this work, i.e., the destabilization and fusion of negatively charged model membranes, suggest an essential role of the loop domain in the membrane fusion process induced by gp41.

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17

Chang, Rupert, Shlomo Nir, and Francis R. Poulain. "Analysis of binding and membrane destabilization of phospholipid membranes by surfactant apoprotein B." Biochimica et Biophysica Acta (BBA) - Biomembranes 1371, no. 2 (May 1998): 254–64. http://dx.doi.org/10.1016/s0005-2736(98)00031-5.

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18

Tian, P., J. M. Ball, C. Q. Zeng, and M. K. Estes. "The rotavirus nonstructural glycoprotein NSP4 possesses membrane destabilization activity." Journal of virology 70, no. 10 (1996): 6973–81. http://dx.doi.org/10.1128/jvi.70.10.6973-6981.1996.

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19

Silberstein, Anatoli, Tajib Mirzabekov, W. French Anderson, and Yanina Rozenberg. "Membrane destabilization assay based on potassium release from liposomes." Biochimica et Biophysica Acta (BBA) - Biomembranes 1461, no. 1 (November 1999): 103–12. http://dx.doi.org/10.1016/s0005-2736(99)00152-2.

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20

Malekkhaiat Häffner, S., E. Parra-Ortiz, M. W. A. Skoda, T. Saerbeck, K. L. Browning, and M. Malmsten. "Composition effects on photooxidative membrane destabilization by TiO2 nanoparticles." Journal of Colloid and Interface Science 584 (February 2021): 19–33. http://dx.doi.org/10.1016/j.jcis.2020.09.046.

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21

Hazlett, Karsten R. O., David L. Cox, Marc Decaffmeyer, Michael P. Bennett, Daniel C. Desrosiers, Carson J. La Vake, Morgan E. La Vake, et al. "TP0453, a Concealed Outer Membrane Protein of Treponema pallidum, Enhances Membrane Permeability." Journal of Bacteriology 187, no. 18 (September 15, 2005): 6499–508. http://dx.doi.org/10.1128/jb.187.18.6499-6508.2005.

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ABSTRACT The outer membrane of Treponema pallidum, the noncultivable agent of venereal syphilis, contains a paucity of protein(s) which has yet to be definitively identified. In contrast, the outer membranes of gram-negative bacteria contain abundant immunogenic membrane-spanning β-barrel proteins mainly involved in nutrient transport. The absence of orthologs of gram-negative porins and outer membrane nutrient-specific transporters in the T. pallidum genome predicts that nutrient transport across the outer membrane must differ fundamentally in T. pallidum and gram-negative bacteria. Here we describe a T. pallidum outer membrane protein (TP0453) that, in contrast to all integral outer membrane proteins of known structure, lacks extensive β-sheet structure and does not traverse the outer membrane to become surface exposed. TP0453 is a lipoprotein with an amphiphilic polypeptide containing multiple membrane-inserting, amphipathic α-helices. Insertion of the recombinant, nonlipidated protein into artificial membranes results in bilayer destabilization and enhanced permeability. Our findings lead us to hypothesize that TP0453 is a novel type of bacterial outer membrane protein which may render the T. pallidum outer membrane permeable to nutrients while remaining inaccessible to antibody.

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22

Boya, Patricia, Karine Andreau, Delphine Poncet, Naoufal Zamzami, Jean-Luc Perfettini, Didier Metivier, David M. Ojcius, Marja Jäättelä, and Guido Kroemer. "Lysosomal Membrane Permeabilization Induces Cell Death in a Mitochondrion-dependent Fashion." Journal of Experimental Medicine 197, no. 10 (May 19, 2003): 1323–34. http://dx.doi.org/10.1084/jem.20021952.

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A number of diseases are due to lysosomal destabilization, which results in damaging cell loss. To investigate the mechanisms of lysosomal cell death, we characterized the cytotoxic action of two widely used quinolone antibiotics: ciprofloxacin (CPX) or norfloxacin (NFX). CPX or NFX plus UV light (NFX*) induce lysosomal membrane permeabilization (LMP), as detected by the release of cathepsins from lysosomes. Inhibition of the lysosomal accumulation of CPX or NFX suppresses their capacity to induce LMP and to kill cells. CPX- or NFX-triggered LMP results in caspase-independent cell death, with hallmarks of apoptosis such as chromatin condensation and phosphatidylserine exposure on the plasma membrane. LMP triggers mitochondrial membrane permeabilization (MMP), as detected by the release of cytochrome c. Both CPX and NFX* cause Bax and Bak to adopt their apoptotic conformation and to insert into mitochondrial membranes. Bax−/− Bak−/− double knockout cells fail to undergo MMP and cell death in response to CPX- or NFX-induced LMP. The single knockout of Bax or Bak (but not Bid) or the transfection-enforced expression of mitochondrion-targeted (but not endoplasmic reticulum–targeted) Bcl-2 conferred protection against CPX (but not NFX*)-induced MMP and death. Altogether, our data indicate that mitochondria are indispensable for cell death initiated by lysosomal destabilization.

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23

Haikou, Maria N., Paraskevi Zagana, Panayiotis V. Ioannou, and Sophia G. Antimisiaris. "Arsonoliposome Interaction with Thiols: Effect of Pegylation and Arsonolipid Content of Arsonoliposomes on Their Integrity During Incubation in Glutathione." Journal of Nanoscience and Nanotechnology 6, no. 9 (September 1, 2006): 2974–78. http://dx.doi.org/10.1166/jnn.2006.422.

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Increased toxicity of arsonoliposomes towards cancer cells may be attributed to interaction between arsonolipids and cellular thiols which, would result in reduction of As(V) to the more toxic As(III). Cancer cells with high thiol contents may thus be more sensitive to arsonoliposomes, providing that the arsonolipid molecules that are incorporated in the liposome membrane can interact with thiol-containing compounds. For examination of this possibility we investigate the effect of incubating various compositions of arsonoliposomes with glutathione, on their integrity. If glutathione does interact with the As(V) of the arsonolipid headgroup, this should result in an alteration of the arsonoliposome membrane stability. We followed arsonoliposome integrity by measuring the release of vesicle-encapsulated calcein from arsonoliposomes with different lipid compositions, during incubation in glutathione. The results of this study show that the effect of glutathione on arsonoliposome integrity is higher (arsonoliposomes are less stable) when the arsonolipid content of their membranes increases. This indicates that arsonolipid molecules interact with glutathione, and in some cases, depending on the rigidity of their membranes; this interaction leads to a (higher or lower) destabilization of arsonoliposomes. The destabilizing effect of glutathione was higher for arsonoliposomes that were previously found to be less stable during incubation in serum proteins or, in other words, have lower membrane rigidity. In the case of pegylated-arsonoliposomes membrane destabilization was minimal and this may be related to the high stability demonstrated previously for these specific arsonoliposomes, or, it may indicate that pegylation results in prevention (total or partial) of arsonolipid–As interaction with thiols (perhaps because of steric repulsion).

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24

Sánchez-Villalba, Esther, María Elena Arias, Fabiola Zambrano, Pía Loren, and Ricardo Felmer. "Improved exogenous DNA uptake in bovine spermatozoa and gene expression in embryos using membrane destabilizing agents in ICSI-SMGT." Zygote 26, no. 1 (January 15, 2018): 104–9. http://dx.doi.org/10.1017/s0967199417000727.

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SummarySperm-mediated gene transfer (SMGT) is a simple, fast, and economical biotechnological tool for producing transgenic animals. However, transgene expression with this technique in bovine embryos is still inefficient due to low uptake and binding of exogenous DNA in spermatozoa. The present study evaluated the effects of sperm membrane destabilization on the binding capacity, location and quantity of bound exogenous DNA in cryopreserved bovine spermatozoa using Triton X-100 (TX-100), lysolecithin (LL) and sodium hydroxide (NaOH). Effects of these treatments were also evaluated by intracytoplasmic sperm injection (ICSI)-SMGT. Results showed that all treatments bound exogenous DNA to spermatozoa including the control. Spermatozoa treated with different membrane destabilizing agents bound the exogenous DNA throughout the head and tail of spermatozoa, compared with the control, in which binding occurred mainly in the post-acrosomal region and tail. The amount of exogenous DNA bound to spermatozoa was much higher for the different sperm treatments than the control (P < 0.05), most likely due to the damage induced by these treatments to the plasma and acrosomal membranes. Exogenous gene expression in embryos was also improved by these treatments. These results demonstrated that sperm membrane destabilization could be a novel strategy in bovine SMGT protocols for the generation of transgenic embryos by ICSI.

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25

Mason, A. James, Arnaud Marquette, and Burkhard Bechinger. "Zwitterionic Phospholipids and Sterols Modulate Antimicrobial Peptide-Induced Membrane Destabilization." Biophysical Journal 93, no. 12 (December 2007): 4289–99. http://dx.doi.org/10.1529/biophysj.107.116681.

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26

Lobo, ReemaOrison, BK Chandrasekhar Sagar, and ChandrakalaK Shenoy. "Bio-tea prevents membrane destabilization during Isoproterenol-induced myocardial injury." Journal of Microscopy and Ultrastructure 5, no. 3 (2017): 146. http://dx.doi.org/10.1016/j.jmau.2016.09.001.

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27

Düzgüneş, Nejat, and Sergei A. Shavnin. "Membrane destabilization by N-terminal peptides of viral envelope proteins." Journal of Membrane Biology 128, no. 1 (May 1992): 71–80. http://dx.doi.org/10.1007/bf00231872.

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28

Tkeshelashvili, L. K., O. V. Khuiusauri, and K. D. Tsakadze. "On the mechanism of erythrocyte membrane destabilization by copper ions." Journal of Inorganic Biochemistry 36, no. 3-4 (August 1989): 349. http://dx.doi.org/10.1016/0162-0134(89)84590-8.

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29

Louise, Chopinet, Dague Etienne, and Rols Marie-Pierre. "AFM sensing cortical actin cytoskeleton destabilization during plasma membrane electropermeabilization." Cytoskeleton 71, no. 10 (October 2014): 587–94. http://dx.doi.org/10.1002/cm.21194.

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30

Chen, Siyuan, Shiqi Wang, Michal Kopytynski, Marie Bachelet, and Rongjun Chen. "Membrane-Anchoring, Comb-Like Pseudopeptides for Efficient, pH-Mediated Membrane Destabilization and Intracellular Delivery." ACS Applied Materials & Interfaces 9, no. 9 (February 22, 2017): 8021–29. http://dx.doi.org/10.1021/acsami.7b00498.

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31

An, Xiuli, Marcela Salomao, Xinhua Guo, Walter Gratzer, and Narla Mohandas. "Tropomyosin modulates erythrocyte membrane stability." Blood 109, no. 3 (September 28, 2006): 1284–88. http://dx.doi.org/10.1182/blood-2006-07-036954.

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Abstract The ternary complex of spectrin, actin, and 4.1R (human erythrocyte protein 4.1) defines the nodes of the erythrocyte membrane skeletal network and is inseparable from membrane stability under mechanical stress. These junctions also contain tropomyosin (TM) and the other actin-binding proteins, adducin, protein 4.9, tropomodulin, and a small proportion of capZ, the functions of which are poorly defined. Here, we have examined the consequences of selective elimination of TM from the membrane. We have shown that the mechanical stability of the membranes of resealed ghosts devoid of TM is grossly, but reversibly, impaired. That the decreased membrane stability of TM-depleted membranes is the result of destabilization of the ternary complex of the network junctions is demonstrated by the strongly facilitated entry into the junctions in situ of a β-spectrin peptide, containing the actin- and 4.1R-binding sites, after extraction of the TM. The stabilizing effect of TM is highly specific, in that it is only the endogenous isotype, and not the slightly longer muscle TM that can bind to the depleted membranes and restore their mechanical stability. These findings have enabled us identify a function for TM in elevating the mechanical stability of erythrocyte membranes by stabilizing the spectrin-actin-4.1R junctional complex.

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32

Gaussier, Hélène, Thierry Lefèvre, and Muriel Subirade. "Binding of Pediocin PA-1 with Anionic Lipid Induces Model Membrane Destabilization." Applied and Environmental Microbiology 69, no. 11 (November 2003): 6777–84. http://dx.doi.org/10.1128/aem.69.11.6777-6784.2003.

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ABSTRACT To obtain molecular insights into the action mode of antimicrobial activity of pediocin PA-1, the interactions between this bacteriocin and dimyristoylphosphatidylcholine (DMPC) or dimyristoylphosphatidylglycerol (DMPG) model membranes have been investigated in D2O at pD 6 by Fourier transform infrared spectroscopy. The interactions were monitored with respect to alteration of the secondary structure of pediocin, as registered by the amide I′ band, and phospholipid conformation, as revealed by the methylene νs(CH2) and carbonyl ν(C═;O) stretching vibrations. The results show that no interaction between pediocin and DMPC occurs. By contrast, pediocin undergoes a structural reorganization in the presence of DMPG. Upon heating, pediocin self-aggregates, which is not observed for this pD in aqueous solution. The gel-to-crystalline phase transition of DMPG shifts to higher temperatures with a concomitant dehydration of the interfacial region. Our results indicate that pediocin is an extrinsic peptide and that its action mechanism may lie in a destabilization of the cell membrane.

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33

Monnier, Noadya, Aurélien Furlan, Sébastien Buchoux, Magali Deleu, Manuel Dauchez, Sonia Rippa, and Catherine Sarazin. "Exploring the Dual Interaction of Natural Rhamnolipids with Plant and Fungal Biomimetic Plasma Membranes through Biophysical Studies." International Journal of Molecular Sciences 20, no. 5 (February 26, 2019): 1009. http://dx.doi.org/10.3390/ijms20051009.

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Rhamnolipids (RLs) are potential biocontrol agents for crop culture protection. Their mode of action has been proposed as dual, combining plant protection activation and antifungal activities. The present work focuses on the interaction of natural RLs with plant and fungi membrane models at the molecular scale. Representative models were constructed and the interaction with RLs was studied by Fourier transform infrared (FTIR) and deuterium nuclear magnetic resonance (2H NMR) spectroscopic measurements. Molecular dynamic (MD) simulations were performed to investigate RL insertion in lipid bilayers. Our results showed that the RLs fit into the membrane models and were located near the lipid phosphate group of the phospholipid bilayers, nearby phospholipid glycerol backbones. The results obtained with plant plasma membrane models suggest that the insertion of RLs inside the lipid bilayer did not significantly affect lipid dynamics. Oppositely, a clear fluidity increase of fungi membrane models was observed. This effect was related to the presence and the specific structure of ergosterol. The nature of the phytosterols could also influence the RL effect on plant plasma membrane destabilization. Subtle changes in lipid dynamics could then be linked with plant defense induction and the more drastic effects associated with fungal membrane destabilization.

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34

POLYANSKY, ANTON A., PAVEL E. VOLYNSKY, and ROMAN G. EFREMOV. "COMPUTER SIMULATIONS OF MEMBRANE-LYTIC PEPTIDES: PERSPECTIVES IN DRUG DESIGN." Journal of Bioinformatics and Computational Biology 05, no. 02b (April 2007): 611–26. http://dx.doi.org/10.1142/s0219720007002783.

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Structure activity relationships were investigated for membrane-lytic peptides (MLP) Ltc1 and Ltc2a from the latarcin family. The peptides were studied via long-term molecular dynamics (MD) simulations in different membrane environments (detergent micelles, mixed lipid bilayers mimiking eukaryotic and bacterial membranes). The calculated structure of Ltc2a in sodium dodecyl sulfate micelle agrees well with the data obtained by 1H-NMR spectroscopy. This validates the applied modeling approach. The binding mode of MLPs is governed by several factors: (i) the membrane surface curvature; (ii) the conformational plasticity and hydrophobic organization of the peptide, which depend on the arrangement of charged, non-polar and helix-breaking residues in the amino acid sequence. In contrast to Ltc1, insertion of Ltc2a into model membranes induces significant changes in dynamic behavior of lipids in the contact region. Such a prominent membrane destabilization correlates with high membrane-lytic activity of Ltc2a. In all cases the "membrane response" has a local character and is caused by formation of specific peptide-lipid contacts. Results of MD simulations of Ltc2a in model membranes were used to develop a number of its analogs with predefined activity.

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35

Delgado, N. M., M. L. Sánchez-Vázquez, O. Hernández, and R. Reyes. "Correlation Between Sperm Membrane Destabilization by Heparin and Aniline Blue Staining as Membrane Integrity Index." Archives of Andrology 40, no. 2 (January 1998): 147–52. http://dx.doi.org/10.3109/01485019808987937.

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36

Tadros, Wael, Simon A. Houston, Arash Bashirullah, Ramona L. Cooperstock, Jennifer L. Semotok, Bruce H. Reed, and Howard D. Lipshitz. "Regulation of Maternal Transcript Destabilization During Egg Activation in Drosophila." Genetics 164, no. 3 (July 1, 2003): 989–1001. http://dx.doi.org/10.1093/genetics/164.3.989.

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AbstractIn animals, the transfer of developmental control from maternal RNAs and proteins to zygotically derived products occurs at the midblastula transition. This is accompanied by the destabilization of a subset of maternal transcripts. In Drosophila, maternal transcript destabilization occurs in the absence of fertilization and requires specific cis-acting instability elements. We show here that egg activation is necessary and sufficient to trigger transcript destabilization. We have identified 13 maternal-effect lethal loci that, when mutated, result in failure of maternal transcript degradation. All mutants identified are defective in one or more additional processes associated with egg activation. These include vitelline membrane reorganization, cortical microtubule depolymerization, translation of maternal mRNA, completion of meiosis, and chromosome condensation (the S-to-M transition) after meiosis. The least pleiotropic class of transcript destabilization mutants consists of three genes: pan gu, plutonium, and giant nuclei. These three genes regulate the S-to-M transition at the end of meiosis and are thought to be required for the maintenance of cyclin-dependent kinase (CDK) activity during this cell cycle transition. Consistent with a possible functional connection between this S-to-M transition and transcript destabilization, we show that in vitro-activated eggs, which exhibit aberrant postmeiotic chromosome condensation, fail to initiate transcript degradation. Several genetic tests exclude the possibility that reduction of CDK/cyclin complex activity per se is responsible for the failure to trigger transcript destabilization in these mutants. We propose that the trigger for transcript destabilization occurs coincidently with the S-to-M transition at the end of meiosis and that pan gu, plutonium, and giant nuclei regulate maternal transcript destabilization independent of their role in cell cycle regulation.

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37

Mangalanathan, Malathi, Tamiloli Devendhiran, Saraswathi Uthamaramasamy, Keerthika Kumarasamy, K. Mohanraj, Kannagi Devendhiran, T. Suganya, and Mei –. Ching Lin. "Membrane stabilization effect and histological changes in the heart in experimental myocardial rats with Zanthoxulym armatum fruit." South Asian Journal of Engineering and Technology 8, no. 1 (February 8, 2019): 19–26. http://dx.doi.org/10.26524/sajet190805.

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Membrane bound adenosine triphosphatases (ATPases) shed a massive function into the contraction and relaxation of the heart muscle via keeping the normal ion levels within the myocyte. The current study aims to assess the potency of Zanthoxylum armatum (Z. armatum) fruit on membrane bound ATPases and ions in Isoproterenol (ISO) induced myocardial infracted rats. The hydroethanolic extract of Z. armatum fruit was administered at a dose of 200 and 400mg/kg body weight for 30 days to male Wistar albino rats. On 28th and 29th day, ISO (8.5mg/100g body weight) used to be administered to induce myocardial infarction (MI). ISO treated rats confirmed a significant increase in the levels of tissue sodium (Na+) and calcium (Ca2+) ions and membrane bound Ca2+ ATPase then Mg2+ ATPase activity. A significant decrease in tissue potassium (K+), Na +/K+ ATPase was observed which indicates membrane destabilization. Pretreatment with hydroethanolic extract of Z. armatum fruit to ISO induced rats significantly (p<0.05) prevented the altered membrane bound enzymes to near normal status. The findings of the present study indicate the protective effect of Z. armatum fruit on altered ion pumps and destabilization on the cardiac membrane into ISO induced MI rats which might also be due to the presence of phytoconstituents.

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38

Wang, Jie, Klaas Yperman, Peter Grones, Qihang Jiang, Jonathan Dragwidge, Evelien Mylle, Eliana Mor, et al. "Conditional destabilization of the TPLATE complex impairs endocytic internalization." Proceedings of the National Academy of Sciences 118, no. 15 (April 5, 2021): e2023456118. http://dx.doi.org/10.1073/pnas.2023456118.

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In plants, endocytosis is essential for many developmental and physiological processes, including regulation of growth and development, hormone perception, nutrient uptake, and defense against pathogens. Our toolbox to modulate this process is, however, rather limited. Here, we report a conditional tool to impair endocytosis. We generated a partially functional TPLATE allele by substituting the most conserved domain of the TPLATE subunit of the endocytic TPLATE complex (TPC). This substitution destabilizes TPC and dampens the efficiency of endocytosis. Short-term heat treatment increases TPC destabilization and reversibly delocalizes TPLATE from the plasma membrane to aggregates in the cytoplasm. This blocks FM uptake and causes accumulation of various known endocytic cargoes at the plasma membrane. Short-term heat treatment therefore transforms the partially functional TPLATE allele into an effective conditional tool to impair endocytosis. Next to their role in endocytosis, several TPC subunits are also implicated in actin-regulated autophagosomal degradation. Inactivating TPC via the WDX mutation, however, does not impair autophagy, thus enabling specific and reversible modulation of endocytosis in planta.

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39

PINTO, NÍCOLAS C. C., JUCÉLIA B. SILVA, LAURA M. MENEGATI, MARIA CLARA M. R. GUEDES, LUCAS B. MARQUES, THIAGO P. DA SILVA, ROSSANA C. N. DE MELO, et al. "Cytotoxicity and bacterial membrane destabilization induced by Annona squamosa L. extracts." Anais da Academia Brasileira de Ciências 89, no. 3 suppl (August 14, 2017): 2053–73. http://dx.doi.org/10.1590/0001-3765201720150702.

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40

Walters, M. J., A. C. Brown, T. C. Edrington, S. Baranwal, Y. Du, E. T. Lally, and K. Boesze-Battaglia. "Membrane association and destabilization byAggregatibacter actinomycetemcomitansleukotoxin requires changes in secondary structures." Molecular Oral Microbiology 28, no. 5 (May 16, 2013): 342–53. http://dx.doi.org/10.1111/omi.12028.

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41

Dimitrova, Mariana N., and Hideo Matsumura. "Protein-induced leakage and membrane destabilization of phosphatidylcholine and phosphatidylserine liposomes." Colloids and Surfaces B: Biointerfaces 8, no. 6 (May 1997): 287–94. http://dx.doi.org/10.1016/s0927-7765(96)01333-1.

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42

Bazzarelli, Fabio, Teresa Poerio, Rosalinda Mazzei, Napoleone D’Agostino, and Lidietta Giorno. "Study of OMWWs suspended solids destabilization to improve membrane processes performance." Separation and Purification Technology 149 (July 2015): 183–89. http://dx.doi.org/10.1016/j.seppur.2015.05.040.

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43

Steponkus, Peter L., Darryl G. Stout, Joe Wolfe, and Richard V. E. Lovelace. "Possible role of transient electric fields in freezing-induced membrane destabilization." Journal of Membrane Biology 85, no. 3 (October 1985): 191–98. http://dx.doi.org/10.1007/bf01871513.

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44

Bag, Nirmalya, Ashraf Ali, Virander Singh Chauhan, Thorsten Wohland, and Aseem Mishra. "Membrane destabilization by monomeric hIAPP observed by imaging fluorescence correlation spectroscopy." Chemical Communications 49, no. 80 (2013): 9155. http://dx.doi.org/10.1039/c3cc44880k.

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45

Szczepaniak, A., D. Huang, T. W. Keenan, and W. A. Cramer. "Electrostatic destabilization of the cytochrome b6f complex in the thylakoid membrane." EMBO Journal 10, no. 10 (October 1991): 2757–64. http://dx.doi.org/10.1002/j.1460-2075.1991.tb07824.x.

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46

Vahidi, Siavash, Yumin Bi, Stanley D. Dunn та Lars Konermann. "Load-dependent destabilization of the γ-rotor shaft in FOF1 ATP synthase revealed by hydrogen/deuterium-exchange mass spectrometry". Proceedings of the National Academy of Sciences 113, № 9 (16 лютого 2016): 2412–17. http://dx.doi.org/10.1073/pnas.1520464113.

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FoF1 is a membrane-bound molecular motor that uses proton-motive force (PMF) to drive the synthesis of ATP from ADP and Pi. Reverse operation generates PMF via ATP hydrolysis. Catalysis in either direction involves rotation of the γε shaft that connects the α3β3 head and the membrane-anchored cn ring. X-ray crystallography and other techniques have provided insights into the structure and function of FoF1 subcomplexes. However, interrogating the conformational dynamics of intact membrane-bound FoF1 during rotational catalysis has proven to be difficult. Here, we use hydrogen/deuterium exchange mass spectrometry to probe the inner workings of FoF1 in its natural membrane-bound state. A pronounced destabilization of the γ C-terminal helix during hydrolysis-driven rotation was observed. This behavior is attributed to torsional stress in γ, arising from γ⋅⋅⋅α3β3 interactions that cause resistance during γ rotation within the apical bearing. Intriguingly, we find that destabilization of γ occurs only when FoF1 operates against a PMF-induced torque; the effect disappears when PMF is eliminated by an uncoupler. This behavior resembles the properties of automotive engines, where bearings inflict greater forces on the crankshaft when operated under load than during idling.

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47

Carretero, Gustavo Penteado Battesini, Greice Kelle Viegas Saraiva, Magali Aparecida Rodrigues, Sumika Kiyota, Marcelo Porto Bemquerer, Hernan Chaimovich, and Iolanda Midea Cuccovia. "Naphthalimide-Containing BP100 Leads to Higher Model Membranes Interactions and Antimicrobial Activity." Biomolecules 11, no. 4 (April 8, 2021): 542. http://dx.doi.org/10.3390/biom11040542.

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In a large variety of organisms, antimicrobial peptides (AMPs) are primary defenses against pathogens. BP100 (KKLFKKILKYL-NH2), a short, synthetic, cationic AMP, is active against bacteria and displays low toxicity towards eukaryotic cells. BP100 acquires a α-helical conformation upon interaction with membranes and increases membrane permeability. Despite the volume of information available, the action mechanism of BP100, the selectivity of its biological effects, and possible applications are far from consensual. Our group synthesized a fluorescent BP100 analogue containing naphthalimide linked to its N-terminal end, NAPHT-BP100 (Naphthalimide-AAKKLFKKILKYL-NH2). The fluorescence properties of naphthalimides, especially their spectral sensitivity to microenvironment changes, are well established, and their biological activities against transformed cells and bacteria are known. Naphthalimide derived compounds are known to interact with DNA disturbing related processes as replication and transcription, and used as anticancer agents due to this property. A wide variety of techniques were used to demonstrate that NAPHT-BP100 bound to and permeabilized zwitterionic POPC and negatively charged POPC:POPG liposomes and, upon interaction, acquired a α-helical structure. Membrane surface high peptide/lipid ratios triggered complete permeabilization of the liposomes in a detergent-like manner. Membrane disruption was driven by charge neutralization, lipid aggregation, and bilayer destabilization. NAPHT-BP100 also interacted with double-stranded DNA, indicating that this peptide could also affect other cellular processes besides causing membrane destabilization. NAPHT-BP100 showed increased antibacterial and hemolytic activities, compared to BP100, and may constitute an efficient antimicrobial agent for dermatological use. By conjugating BP100 and naphthalimide DNA binding properties, NAPHT-BP100 bound to a large extent to the bacterial membrane and could more efficiently destabilize it. We also speculate that peptide could enter the bacteria cell and interact with its DNA in the cytoplasm.

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48

Johnson, RM, Y. Ravindranath, M. el-Alfy, and G. Jr Goyette. "Oxidant damage to erythrocyte membrane in glucose-6-phosphate dehydrogenase deficiency: correlation with in vivo reduced glutathione concentration and membrane protein oxidation." Blood 83, no. 4 (February 15, 1994): 1117–23. http://dx.doi.org/10.1182/blood.v83.4.1117.1117.

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Abstract Chronic nonspherocytic hemolytic anemia has been observed in a recently described glucose-6-phosphate dehydrogenase (G6PD) variant, G6PDWayne. The mechanical properties of these erythrocytes and other G6PD variants were examined. The deformability of G6PD-deficient erythrocytes was normal, as determined by osmotic scan ektacytometry, and was not significantly affected by hemolytic crisis. In the common varieties of G6PD deficiency, the mechanical stability of the red blood cell (RBC) membrane was greater than normal, but G6PDWayne membranes were abnormally susceptible to shear-induced fragmentation. There was no evidence for a concurrent genetic defect in spectrin, because self- association constants and tryptic digests were normal. The fragility of G6PDWayne membranes appeared to be a consequence of oxidative damage to membrane thiol groups associated with a low glutathione (GSH) level in these RBCs. Associations among GSH level, thiol oxidation, and membrane instability were also found when a larger group of G6PD-deficient RBCs were examined. In normal erythrocytes, 1-chloro-2,4-dinitrobenzene was used to reduce GSH levels by 50%. Membrane thiol oxidation and membrane fragility both increased when these cells were kept at 4 degrees C for 3 to 5 days. Our findings suggest that chronic depletion of GSH leads to the destabilization of membrane skeleton through oxidation of membrane protein thiols.

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49

Johnson, RM, Y. Ravindranath, M. el-Alfy, and G. Jr Goyette. "Oxidant damage to erythrocyte membrane in glucose-6-phosphate dehydrogenase deficiency: correlation with in vivo reduced glutathione concentration and membrane protein oxidation." Blood 83, no. 4 (February 15, 1994): 1117–23. http://dx.doi.org/10.1182/blood.v83.4.1117.bloodjournal8341117.

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Анотація:

Chronic nonspherocytic hemolytic anemia has been observed in a recently described glucose-6-phosphate dehydrogenase (G6PD) variant, G6PDWayne. The mechanical properties of these erythrocytes and other G6PD variants were examined. The deformability of G6PD-deficient erythrocytes was normal, as determined by osmotic scan ektacytometry, and was not significantly affected by hemolytic crisis. In the common varieties of G6PD deficiency, the mechanical stability of the red blood cell (RBC) membrane was greater than normal, but G6PDWayne membranes were abnormally susceptible to shear-induced fragmentation. There was no evidence for a concurrent genetic defect in spectrin, because self- association constants and tryptic digests were normal. The fragility of G6PDWayne membranes appeared to be a consequence of oxidative damage to membrane thiol groups associated with a low glutathione (GSH) level in these RBCs. Associations among GSH level, thiol oxidation, and membrane instability were also found when a larger group of G6PD-deficient RBCs were examined. In normal erythrocytes, 1-chloro-2,4-dinitrobenzene was used to reduce GSH levels by 50%. Membrane thiol oxidation and membrane fragility both increased when these cells were kept at 4 degrees C for 3 to 5 days. Our findings suggest that chronic depletion of GSH leads to the destabilization of membrane skeleton through oxidation of membrane protein thiols.

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50

Harrison, RA. "Capacitation mechanisms, and the role of capacitation as seen in eutherian mammals." Reproduction, Fertility and Development 8, no. 4 (1996): 581. http://dx.doi.org/10.1071/rd9960581.

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Capacitation, the process whereby spermatozoa are rendered capable of interacting with and fertilizing the egg, was discovered more than 40 years ago. However, our understanding of it is still far from satisfactory. Several factors conspire to obfuscate studies of capacitation mechanisms: the inherent functional heterogeneity of sperm populations, the range of functions used as parameters of capacitation (whence the endpoint of the process has become conceptually uncertain), and the several profound differences between model in vitro fertilization (IVF) systems and the situation in vivo in the female reproductive tract. Recent investigations in the author's laboratory have shown that bicarbonate/CO2, an essential component for successful IVF, causes rapid changes in lipid architecture of the sperm plasma membrane and slower changes in surface coating. These changes are accompanied by membrane destabilization and cell death. Evidence suggests that bicarbonate's actions are mediated through cyclic nucleotide signalling. Of particular note is the heterogeneity in rate of response to bicarbonate shown by individual cells in the sperm populations. Taken together with other observations, the findings suggest that capacitation is a series of positive destabilizing events that eventually lead to cell death. The 'capacitated' state would then be a window of destabilization within which spermatozoa can undergo a zona-induced acrosome reaction and display hyperactivated motility. Further along the destabilization pathway, spontaneous acrosome reactions would occur before total membrane degeneration. In vivo, capacitation would be a conflict between destabilization and sperm survival. Concentrations of bicarbonate are maintained low in the cauda epididymidis, where sperm survive for long periods, and one may speculate that hormonal control of local bicarbonate/CO2 in oviducal 'storage' sites in the female tract could allow 'safe' sequestering of live spermatozoa until around the time of ovulation; the environment may then change to produce a 'capacitating' effect, whence, due to the inherent functional heterogeneity of the sequestered population, small numbers of capacitated spermatozoa are released sequentially. In this way, a succession of spermatozoa in the correct physiological state may be provided for the freshly ovulated egg.

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