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1 oncentrations of other macromolecules (e.g., phospholipid).
2 nterfaces and indirectly via an intercalated phospholipid.
3 gulated cell death driven by peroxidation of phospholipids.
4 ed in impaired membrane homeostasis of other phospholipids.
5 did not have externalized negatively-charged phospholipids.
6 oagulation proteins, proteolytic enzymes, or phospholipids.
7 ck (GCB), is presented for the enrichment of phospholipids.
8 or flexibility of MscL when bound to various phospholipids.
9 ath associated with oxidized polyunsaturated phospholipids.
10 ly bound cardiolipin molecules and two other phospholipids.
11 mportant matrix interferences like salts and phospholipids.
12 ed/unsaturated fatty acids, eicosanoids, and phospholipids.
13 of cholesteryl esters, diglyceride and other phospholipids.
14 ess able to incorporate LA into its membrane phospholipids.
15 ipids from cells and bacteria and surfactant phospholipids.
16 ted the antiviral impact of de novo-produced phospholipids.
17 oteins that interact with SNARE proteins and phospholipids.
18 sically disordered protein that binds acidic phospholipids.
19 ithout the addition of exogenous proteins or phospholipids.
20 s to assembly with FVIIIa in the presence of phospholipids.
21 RNAs, peptides, RNA oligomers and primordial phospholipids.
22 A-OmpF to monitor the transport direction of phospholipids.
23 ndowed with stereospecific binding sites for phospholipids.
24 Their main polar DL lipids are phospholipids.
25 nthesis as it was self-assembled from common phospholipids.
27 rther, the 15LO1-PEBP1-generated ferroptotic phospholipid, 15-HpETE-PE, promoted LC3-I lipidation to
30 osphotransferase 1 (CEPT1), is essential for phospholipid activation of transcription factors such as
33 ia coli MlaFEDB in an apo state and bound to phospholipid, ADP or AMP-PNP to a resolution of 3.3-4.1
34 using purified DGKepsilon and detergent-free phospholipid aggregates, which present a more suitable m
35 gnificantly increase Coil stability, whereas phospholipids alone extended the oxidation lag time up t
36 stituted in membranes formed by zwitterionic phospholipids alone, exposure to agonist fails to elicit
37 ase complex indirectly through contaminating phospholipid and also support factor X activation throug
39 lipoprotein (HDL) biogenesis by transferring phospholipid and cholesterol to delipidated apolipoprote
43 unconventional use of peptide discs made by phospholipids and amphipathic 18A peptides to mediate th
45 and gibberellin biosynthesis, degradation of phospholipids and biosynthesis of glycerolipid, downregu
48 , respectively, the flux of fatty acids from phospholipids and galactolipids into triacylglycerol pro
50 surrounded by an outer membrane composed of phospholipids and lipopolysaccharide, which acts as a ba
51 tamin D, calcium, milk fat globule membrane (phospholipids and other bioactives), and other micronutr
52 lipid bilayer that consists of inner leaflet phospholipids and outer leaflet lipopolysaccharides (LPS
53 epends on pulmonary surfactant, a mixture of phospholipids and proteins, secreted by alveolar type II
54 diponectin selectively bound several anionic phospholipids and sphingolipids, including phosphatidyls
56 sides, the roles of oxysterols, fatty acids, phospholipids, and lipid second messengers are also summ
57 taG and DeltaH for deprotonation) of neutral phospholipids are also evaluated computationally and ran
59 y show that the gas-phase acidities of these phospholipids are high but less extreme than their GB va
64 iated inositol phosphate formation, inositol phospholipid assessments, fluorescence recovery after ph
65 work reveals roles for the peroxisome-ether-phospholipid axis in driving susceptibility to and evasi
66 H. portulacoides, a significant increase of phospholipids bearing n-3 fatty acids (most in PC and PE
67 ter membrane lipid asymmetry by transporting phospholipids between the inner and outer membranes.
69 to investigate molecular orientations in the phospholipid bilayer but cannot resolve the actual distr
70 beta-arrestin with both the receptor and the phospholipid bilayer contribute to its functional versat
73 clofenac in the structural properties of the phospholipid bilayer, suggesting that both ionized and n
76 ation of membrane-embedded components within phospholipid bilayers represents a distinct class of pha
77 stic, molecular dynamics (MD) simulations of phospholipid bilayers responding to electric fields.
78 ptides to mediate the formation of supported phospholipid bilayers with two different types of membra
82 nization of cell membranes and reconstituted phospholipid bilayers; however, the mechanisms by which
83 rib does not require palmitoylation or polar phospholipid binding but instead an independent cortical
84 sized that peptide mimetics derived from the phospholipid binding domain of Myristoylated alanine-ric
86 at domain of alpha-Syn, which interfere with phospholipid binding, are ineffective in enhancing CME.
87 terminus that are linked to deafness disrupt phospholipid binding, sensitize the channel to PIP(2) de
88 w that the N-terminal domain of proSP-B is a phospholipid-binding and -transfer protein whose activit
89 ed for virus infection, whereas the inositol phospholipid-binding and F-actin-binding domains were es
92 nature consistent with adipogenesis, and the phospholipid-binding protein annexin A3 (AnxA3), a negat
93 (Syt1) is an integral membrane protein whose phospholipid-binding tandem C2 domains, C2A and C2B, act
94 ecent advances in the field of mitochondrial phospholipid biosynthesis and trafficking, highlighting
97 By inhibiting and activating the de novo phospholipid biosynthesis, we demonstrated the antiviral
99 Phosphatidic acid (PA) is both a central phospholipid biosynthetic intermediate and a multifuncti
100 ude that the preferential binding of aPLs to phospholipid-bound beta(2)GPI arises from the ability of
101 al enzyme that exchanges fatty acids between phospholipids by phospholipid-lysophospholipid transacyl
102 n mosquitoes the antiviral impact of de novo phospholipids by supplementing infectious blood meals wi
105 portedly, SS-31 primarily interacts with the phospholipid cardiolipin in the inner mitochondrial memb
106 mponent of nucleotides in genetic molecules, phospholipid cell membranes, and energy transfer molecul
107 rane binding is a process mostly mediated by phospholipid charge, whereas fatty acid saturation and m
110 on GUVs with endoplasmic reticulum (ER)-like phospholipid composition results in a complete cycle of
113 y of quercetin in Coil was correlated to the phospholipid concentration and reached a maximum value o
114 assessed the impact of fatty acid (FA) type, phospholipid concentration on MM formation and stability
115 The characteristic fragmentation pattern of phospholipids consisting of the neutral loss of the phos
116 that synthesizes phosphatidylserine (PS), a phospholipid constituent of the inner layer of the plasm
117 5 days) showed rapid changes in the ratio of phospholipids containing ethanolamine, or glycerol as ph
118 phosphatidylglycerol, the major chloroplast phospholipid, contains >40% high-melting-point molecular
119 nd describe that Lp(a), through its oxidized phospholipid content, activates arterial endothelial cel
120 correlate cell drug concentrations with cell phospholipid content, cell volume, sphericity, and other
121 g with liposomes containing cobalt-porphyrin-phospholipid (CoPoP) potently enhances the functional an
124 a-hydroxy beta-methylbutyrate (HMB), lutein, phospholipids, DHA and selected micronutrients including
125 nificantly, coexpressing RcLPCAT with castor phospholipid:diacylglycerol acyltransferase increased no
127 ioning between polar (aqueous) and nonpolar (phospholipid) environments in multilamellar lipid vesicl
128 e revealed the need for a complex mixture of phospholipids, especially phosphatidylserine and phospha
129 n cholesterol binding and binding of anionic phospholipids essential for activity could explain some
130 auses an increase in biliary cholesterol and phospholipid excretion whereas biliary bile salt output
131 S. pombe synthesizing the S.-japonicus-type phospholipids exhibits unfolded protein response and dow
133 in FuFA biosynthesis occurs on pre-existing phospholipid fatty acid chains, and we identified pathwa
134 The results indicate that dry weight (DW), phospholipid fatty acids (PLFAs) and extracellular polym
135 ases (CaPLSases) mediate rapid transmembrane phospholipid flip-flop and as such play essential roles
136 Postendocytic recycling of Snc1 requires a phospholipid flippase (Drs2-Cdc50), an F-box protein (Rc
137 hange in Aminophospholipid ATPase3 (ALA3), a phospholipid flippase predicted to function in vesicle f
138 a membrane once the peptide targets specific phospholipids found on the cytosolic side of the plasma
140 ipids from phospholipids, including membrane phospholipids from cells and bacteria and surfactant pho
141 d with exogenous lipids, was used to extract phospholipids from the membrane outer leaflet, while del
142 symmetry, and in particular the exclusion of phospholipids from the outer leaflet, is key to creating
143 release of this specific drug from vesicular phospholipid gel formulations but describe a general sce
145 domains and intact BON1 to bind to different phospholipids has been investigated, and we demonstrated
147 pids containing ethanolamine, or glycerol as phospholipid head group and in the number of cyclopropan
150 elated gene PR-1, glutathione-S-transferase, phospholipid hydroperoxide glutathione peroxidase and pe
151 nteractions between bile salts alone or with phospholipids, i.e. mixed micelles and the aqueous envir
154 erminal helix of CPn0678 mediates binding to phospholipids in both the plasma membrane and synthetic
161 d sphingomyelins (SM) were the most abundant phospholipids in the RBCs outer leaflet with PC 34:1 and
163 Similar to gasdermin, RCD-1 binds acidic phospholipids in vitro, notably, cardiolipin and phospha
164 ed the interaction between PlsX and membrane phospholipids in vivo and in vitro, and observed that me
165 -yielding non-enzymatic synthesis of natural phospholipids in water opens up new routes for lipid syn
166 ic acid, and generate lysophospholipids from phospholipids, including membrane phospholipids from cel
167 n was lower in visceral adipose tissue (VAT) phospholipids, indicating lower unsaturated fatty acid i
168 uses a tripartite mechanism of Ras, Rac, and phospholipid interactions to localize at the protruding
169 rted activity, confirming that contaminating phospholipid is required to support myosin-related proth
171 model system chosen to mimic the protective phospholipid layers of the gastric mucosa and to describ
173 lation, the TRAF2 RING domain interacts with phospholipids, leading to the translocation of the TRAF2
176 ds contained significantly higher amounts of phospholipids, lysophospholipids, diacylglycerols, stero
179 through its C-terminal -RXG- motif, and how phospholipids markedly stimulate cis-PTase activity.
180 ophysical examples: ion permeation through a phospholipid membrane and protein translocation through
182 n in both n-octylglucoside (OG) micelles and phospholipid membranes in the absence of membrane potent
184 d cells from the animals exhibit deregulated phospholipid metabolism and an aberrant induction of pro
185 s that are markers of neuronal viability and phospholipid metabolism and have also been implicated in
186 etogenesis and are required for ER-localized phospholipid metabolism in vegetative and reproductive g
191 increased, allowing for more cholesterol and phospholipid molecules to be excreted per bile salt.
194 re generally, showcases the utility of yeast phospholipid mutants in dissecting the phospholipid requ
197 mapping of several lipid classes, including phospholipids, neutral lipids, cholesterol, ceramides, a
198 he L(beta) structure, the acyl chains of the phospholipids occupy an ordered array that has melted by
202 ork reports the effect of negatively charged phospholipids on DGKepsilon activity and substrate acyl
203 an HDL either by synthetic gamma-ketoalkenal phospholipids or by oxPLs generated during HDL oxidation
206 re, we report that the self-encoded oxidized phospholipid oxPAPC alters the metabolism of macrophages
207 ifferent neutral lipids but presenting equal phospholipid packing densities differentially recruit AH
208 erefore, it is the hydrophobic nature of the phospholipid packing voids that controls the binding lev
209 acity to synthesize macromolecules including phospholipids, particularly cardiolipin (CL) and phospha
210 ted that DENV actively inhibited the de novo phospholipid pathway and instead triggered phospholipid
211 ode of cell death elicited by iron-dependent phospholipid peroxidation, has been implicated in ischem
213 sible for the synthesis of the most abundant phospholipids, phosphatidylcholine and phosphatidylethan
214 bloodstream infections, and synthesis of the phospholipid phosphatidylethanolamine (PE) is required f
215 ane lipids, comprised of glycolipids and the phospholipid phosphatidylglycerol (PG), are essential fo
216 mbrane of neurosecretory cells by binding to phospholipid PI(4,5)P(2) However, unlike synaptrobrevin-
222 d (C=C db) positional isomers of unsaturated phospholipids (PL) in tissue sections by use of refined
223 shed that the structural differences between phospholipids play an important role in lateral membrane
224 s, which are wrapped by encapsulation agent (phospholipid-polyethylene glycol), is demonstrated using
225 Furthermore, our study identified de novo phospholipid precursor as a blood determinant of DENV hu
227 1-palmitoyl, 2-oleyl phosphatidylcholine, a phospholipid present in high proportions in bile, behave
232 ptosis by synthesizing polyunsaturated ether phospholipids (PUFA-ePLs), which act as substrates for l
237 yeast phospholipid mutants in dissecting the phospholipid requirements of ion channel complexes.
238 erved, elevated levels of neutral lipids and phospholipids resemble previously reported effects on li
239 15LO1-PEBP1 complexes and their hydroperoxy-phospholipids reveals a pathobiologic pathway relevant t
240 veness of liposomes elaborated with rapeseed phospholipid (RP) extracted from a residue of oil proces
241 Cholesterol has been found to correlate with phospholipid saturation for reasons that remain unclear.
243 dy shows that TA and EGCG do not inhibit the phospholipid-scrambling or ion conduction activities of
245 and that channel function is regulated by a phospholipid-sensing domain in TMIE with similarity to t
246 method was validated for some representative phospholipids, showing good repeatability and recovery (
248 ectively, as well as accumulation of several phospholipid species in neurons which have not been stud
249 Intriguingly, it is found that two of these phospholipids, sphingomyelin and phosphatidylcholine, ha
251 MSI analysis of tissue sections exposed to phospholipid substrates produced high-resolution maps of
252 ch are enriched in cholesterol and saturated phospholipids such as sphingomyelin (SM), may form.
253 e (PC), a predominant mitochondrial membrane phospholipid, suggesting that the coordinated expression
254 n storage lipids and an increase in membrane phospholipids, suggesting changes in the Kennedy pathway
255 rison between cholesterol poses and resolved phospholipids suggests that not all cholesterol molecule
257 eration, whereas shifting it toward membrane phospholipid synthesis overcomes regeneration failure in
259 ng E. coli to have its cake (acyl chains for phospholipid synthesis) and eat it (degrade acyl chains
260 ted cellular processes (e.g. triacylglycerol/phospholipid synthesis, lipid droplet formation, nuclear
263 o became psychotic had lower levels of ether phospholipids than CHR individuals who did not (p < .01)
264 and interacts with the hydrophilic head of a phospholipid that occupies the extracellular half of the
266 tidylinositol phosphates (PIPs) are membrane phospholipids that play crucial roles in a wide range of
268 The C-terminal BON domain binds anionic phospholipids through an extensive membrane:protein inte
269 erall, we now propose that DENV reconfigures phospholipids through the remodeling cycle to modify the
272 in clot formation due to exposure of anionic phospholipids to plasma, is a plausible pathogenic mecha
273 Phospholipase D (PLD) hydrolyzes membrane phospholipids to produce phosphatidic acid (PA), which h
275 ge in WFT, but a higher proportion of plasma phospholipid total MUFAs was associated with greater dec
277 laFEDB ABC transporter complex, which drives phospholipid trafficking across the bacterial envelope t
278 ort system called Mla has been implicated in phospholipid trafficking and outer membrane integrity, a
279 ations in the tafazzin (TAZ) gene encoding a phospholipid transacylase required for cardiolipin remod
281 esis: LPS transport via the Lpt machine, and phospholipid transport via the Mla pathway and several r
285 While yeast has one gene that encodes the phospholipid transporter VPS13, humans have four vacuola
287 brane damage induced by these proferroptotic phospholipids triggers compensatory prosurvival pathways
291 in vitro, was able to superficially bind to phospholipid vesicles, nevertheless, it loses the insert
292 y suggests that higher proportions of plasma phospholipid VLSFAs in midlife may be associated with le
295 M1 PUFA containing triglycerides (TG) and phospholipids were correlated with CB LysoPC and LysoPE
296 metabolites, as well as decreased levels of phospholipids, were associated with development of ACLF,
298 ract with model lipid membranes that contain phospholipids with phosphatidyl-ethanolamine headgroups.
299 egulated form of cell death that occurs when phospholipids with polyunsaturated fatty acyl tails are
300 lling through an unexpected interaction with phospholipids, with profound consequences for cellular m