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1 ic reduction in presynaptic neurotransmitter release.
2 itochondrial BAX clustering and cytochrome c release.
3 ions with each cell type, alongside cytokine release.
4 lyte has been used to quantify intracellular release.
5 increases sFlt-1 and soluble endoglin (sEng) release.
6 promotes ATP hydrolysis and rapid phosphate release.
7 of inefficient clearance following synaptic release.
8 the mechanism responsible for conductive ATP release.
9 tin loops by protecting cohesin against loop release.
10 and the SNAREs in membrane fusion to trigger release.
11 rolled chemoattractant and therapeutic agent release.
12 lization inhibitor, that might afford better release.
13 ise spatial and temporal control over the CO release.
14 e uptake, phagolysosomal escape, and epitope release.
15 ction site, as well as the lack of prolonged release.
16 as not been previously investigated in HSV-1 release.
17 ntain SV pool size and thus neurotransmitter release.
18 K(+) (K(ATP) ) channels to increase insulin release.
19 TRPV4 contributed to 50% stretch-induced ATP release.
20 yed growth benefits to at least 1 month post release.
26 essfully harnessed this novel radical strain-release amination as part of a multicomponent cascade co
27 sis infers the interaction between astrocyte-released amyloid precursor protein (APP) and death recep
30 Swabbing led to a smaller change in cortisol release and behaviour on the first day of analysis compa
31 chael addition, are not specific to O-glycan release and can also eliminate phosphoryl substitutions.
32 stration enhanced neurotrophic growth factor release and decreased the astroglial and microglial acti
34 ances L-DOPA uptake, leading to increased DA release and GSIS reduction in an autocrine/paracrine man
37 volve cleavage with cathepsin B or papain to release and measure the antibody-conjugated drug (acDrug
40 ses substantially increased neurotransmitter release and shortened sleep duration, and these effects
41 sing Cdk9 and either PP4 or PP1 govern pause release and the elongation-termination transition, respe
42 CM) to explore the kinetics of allograft sEV release and the extent to which donor sEVs might induce
43 -iron diets or Gpx4 depletion promotes 8-OHG release and thus activates the TMEM173/STING-dependent D
44 s well but also facilitates spontaneous GABA release and triggers an increase in the density of inhib
47 vating cell signaling, SOS autoinhibition is released and is followed by accelerative allosteric feed
48 nsitize cardiomyocytes to spontaneous Ca(2+)-releases and arrhythmogenic afterdepolarizations, partic
49 rable after enzyme opening and pyrophosphate release, and it appears to limit the rate of processive
52 t drug-loading capacity and inefficient drug release, and require complex modification processes.
53 c-acid rich glycocalyx also induced protease release, and this was partially abrogated by sialidase p
54 y, the reversible pH-responsive and non-drug release antibacterial resin adhesives ingeniously overco
55 alterations in spontaneous neurotransmitter release are a key factor to account for disease heteroge
57 orded 10, which was a full agonist in Ca(2+)-release assays; its potency and binding affinity for Ins
63 eter crater into a continental glacier could release between 8.7 x 10(13) to 5.0 x 10(15) kg of H(2)O
64 aves high-molecular-weight kininogen (HK) to release bradykinin with a catalytic efficiency ~1500-fol
66 cells, we found that inhibition of glutamate release by a submaximal concentration of enkephalin was
67 compound (simvastatin) blocked ATP and IL-33 release by lowering the expression of VDAC-1 in the plas
72 ted, but have an expansion block that can be released by impairing regulatory T cell associated signa
73 both of its subunits, and this inhibition is released by interaction with H2A-H2B, allowing FACT-H2A-
74 in vivo from which transcription factors are released by mitogen-activated protein kinase (MAPK)-stim
76 ceptors [Ins(1,4,5)P(3)R] and the ability to release Ca(2+) from intracellular stores via type 1 Ins(
77 usters of type-2 ryanodine receptors (RyR2s) release Ca(2+) from the sarcoplasmic reticulum (SR) via
78 ar imaging measures of dopamine synthesis or release capacities, dopamine D(2/3) receptor (D2/3R) or
80 is related to the mitochondria's ability to release cytochrome c into the cytosol, which triggers th
82 the conclusion that polarized cholangiocytes release distinct sEV pools to mediate communication via
85 ials contain various additives, which can be released during the entire lifespan of plastics and pose
88 All modern standards exhibit rapid growth releases every circa 30 years, most likely caused by reg
91 g the stress-sensitive peptide corticotropin-releasing factor (CRF), which has been identified in cri
93 rom the CyNCh (Cysteamine Bitartrate Delayed-Release for the Treatment of NAFLD in Children) clinical
94 ecreted phospholipase A(2) (sPLA(2)) enzymes release free fatty acids, including arachidonic acid, an
98 ulates gonadotropin-releasing hormone (GnRH) release from GnRH neurons to control the reproductive ax
99 em uses a consistent mechanism involving ATP release from ISCs and activation of P2RY1 autoreceptors
101 We report a new approach to monitor drug release from nanocarriers via a paclitaxel-methylene blu
102 Ca(2+) transients in ICC-SS occurred by release from stores most probably via inositol trisphosp
103 amined 2013 9-10 year olds in the first data release from the Adolescent Brain Cognitive Development
104 picture of the factors influencing the AITC release from the particles is proposed, which describes
105 nds present as soluble forms were completely released from all breads' matrix already at the oral pha
106 account for the rapid transport of sediment released from behind incinerated vegetation, which can f
108 dogenous neuropeptide cholecystokinin (CCK), released from dentate CCK interneurons, in regulating ne
109 : each night the symbionts catabolize chitin released from hemocytes (phagocytic immune cells) that t
110 ochrome c, a proapoptotic peroxidase that is released from mitochondria during sustained oxidative st
111 e heat shock response, RNA Pol II is rapidly released from pausing at heat shock-induced genes, while
112 on infectious virions of ZIKV when they are released from specific cell types, and enhances virus at
113 0(14) and 2.5 x 10(15) g of black carbon was released from the target and ejected into the atmosphere
114 icant proportion of the total U (20-57%) was released from these three shales after reaction with fra
115 tionally, scaling the relative abundances of released glycan ligands according to their relative abun
116 VH through spinal PAR-2 activation and CGRP release, goats received an injection of 2,4,6-trinitro-b
117 s a pivotal role in such adaptation, and its release has been causally associated with the activity o
121 of kisspeptin, which modulates gonadotropin-releasing hormone (GnRH) release from GnRH neurons to co
124 n signaling increases allergen-induced IL-33 release, ILC2 cytokine production, and airway inflammati
131 e spatial and temporal profiles of NT and NM release in the brain using genetically encoded sensors f
132 estingly, VAChTcKO mice had reduced dopamine release in the dorsomedial striatum but not in the dorso
133 ernalization into endolysosomes, Tat must be released in order for it to activate the HIV-1 LTR promo
134 to be taken up by the target cells and then released in the appropriate cellular compartment to func
135 es to potential large-scale seafloor methane releases in ways that provide insight for future modelli
136 investigate the effect of intra-uterine slow-release insemination (SRI) on pregnancy rates in women w
139 ario, pro-inflammatory factors are intensely released into the bloodstream, causing the so-called "cy
140 age product from this fragmentation event is released into the conditioned medium of cells expressing
141 s show that both substrate translocation and release involve movements of the bulky transport domain
142 Using 3D cell culture, it is shown that drug release is commensurate with cell density, revealing mor
143 gether our data support the model that TFIIB release is important for Pol II to successfully escape t
145 he carotenoid does not act as a spring that, releasing its internal strain, induces the dissociation,
150 Thus, the betaAR-mediated modulation of the release machinery and the subsequent increase in the siz
151 ling is under the tight control of glutamate release machinery mediated through vesicular glutamate t
152 ENT G-protein-coupled receptors modulate the release machinery, causing long-lasting changes in synap
155 sulation formulation with a microbiota-based release mechanism and show that it facilitates oral deli
160 Ultimately, the combination of controlled release microspheres with a thermoresponsive hydrogel pr
162 ites and gene bodies suggests that Pol II is released more efficiently into the bodies of beta genes
163 irically-based estimate of on-board and post-release mortality of bycaught marine turtles that has un
164 ating covalent chemistry-mediated EV capture/release, multimarker antibody cocktails, nanostructured
165 mission, when large amounts of glutamate are released, Na(+) accumulated in the terminals, activated
166 hich calls for the development of controlled-release nanoparticle (NP) technologies to further improv
170 e protection against alpha-toxin through the release of ADAM10 on exosomes-extracellular vesicles of
171 e skin could be independently tuned to allow release of adjuvants and antigen from days up to two wee
172 rotein, EZH2, results in cleavage of B2 RNA, release of B2 RNA from chromatin, and activation of ther
174 BIK1, which is essential for the subsequent release of BIK1 from the FLS2-BAK1 complex and activatio
175 classic oncogenes in tumor development, the release of bioactive amines, and indolent growth of the
178 eading to concurrent delivery and sequential release of dual cargos toward combinatorial therapy.
180 ters with calcium transients stimulating the release of gliotransmitters that regulate synaptic and n
182 un fiber (EF) composite to provide sustained-release of GRFT, and to examine its safety and efficacy
183 n immune defence which includes a process of release of histones and DNA as neutrophil extracellular
188 rature diagrams, which was attributed to the release of internal pressure in bulk samples that disint
190 egulatory factors that ultimately affect the release of kisspeptin, which modulates gonadotropin-rele
191 ding the drop in myocardial NADH levels, the release of lipofuscin-like pigments, and the increase in
193 ing this approach, we detected a significant release of MNPs after 3.5 minutes incubation using just
194 rbent assay to measure levels of spontaneous release of molecules from mast cells in colonic mucosa f
197 s been thought to be in part mediated by the release of myokines, skeletal muscle-specific cytokines,
198 ly characterized together with the potential release of Na(+) and Ca(2+) cations, revealing suitable
199 ag polyproteins orchestrate the assembly and release of nascent virus particles from the plasma membr
202 generates chromosomal abnormalities and the release of nuclear DNA into the cytoplasm, activating th
203 the gene therapy efficacy by prolonging the release of nucleic acid drug payload for sustained, long
205 e the ultra-high loading and high-efficiency release of pH indicators, the ALISA exhibitssatisfactory
208 IgE to these autoallergens, which provoke a release of proinflammatory mediators from skin mast cell
209 gation inhibitors to purportedly inhibit the release of puromycin-labeled nascent peptides from ribos
211 circumstances of the undeclared 2017 nuclear release of ruthenium that led to widespread detections o
213 The sequential dissolution and autonomous release of the chemoattractant and killing agents result
214 in the circulation time of the conjugate and release of the drug for full activity at the target site
215 sphorylating the adaptor ACT1 leading to the release of the essential ubiquitin ligase TRAF6 from the
217 ion is followed by subsequent dithiothreitol release of the isolated EVs for downstream functional an
220 ylate derivatives, initiating the downstream release of the small molecule drug by a retro DA reactio
222 gastrointestinal passage and controlling the release of these therapeutic cells across the intestinal
223 ine glioblastoma models and thus enhance the release of tumor-specific biomarkers into the bloodstrea
224 lled chemical or electrochemical capture and release of UO(2)(2+) in monophasic (organic) or biphasic
229 a terminalis AT1aR neurons induced glutamate release onto magnocellular neurons and was sufficient to
232 During herbivory, marine diatom species release oxylipins that impair grazer reproduction and se
233 eceptor availability (P = 0.02) and dopamine release (P = 0.05) also predicted improvements in clinic
239 This is accompanied by an increase in OSN release probability and a reduction in GABA(B) receptor
240 LbL composition and architecture, component release profiles in the skin could be independently tune
244 on profiles of several commercial controlled-release proton pump inhibitors in simulated stomach and
247 om this family are able to undergo click-and-release reactions, finding interesting applications in c
248 are responsible for the pathological calcium release, regarding the tissue origin of the arrhythmic b
251 apillary cells control pollen germination by releasing resources only to compatible pollen thereby al
252 ement and survivorship immediately following release, retained survivorship benefits during 1 and 6 m
254 oading as a function of the level of vesicle release.SIGNIFICANCE STATEMENT Auditory information is e
256 eurotransmitter receptors facing presynaptic release sites is a fundamental determinant of their coac
259 GSH-triggered MnO degradation simultaneously released smaller Au NPs as numerous cavitation nucleatio
260 w that apoptotic lymphocytes and macrophages release specific metabolites, while retaining their memb
263 We conclude that, as in model A, the Pi release step is before the first tension-generating step
265 sufficient to induce intracellular protease release, suggesting altered membrane integrity after the
266 -potential-independent spontaneous glutamate release, suggesting plumes are a consequence of ineffici
267 spontaneous release without altering evoked release, suggesting that aberrant spontaneous release is
269 ase, a recently identified mediator of HSV-1 release, syndecan-1 has not been previously investigated
274 Syt1/Syt7 double mutants displayed more release than Syt1 mutants alone, indicating SYT7 does no
275 ll-cycle transition and profiles of cytokine release that resembled those of normal memory T cells.
276 slocations above a critical strain energy to release the accumulated strain energy as the film thickn
277 n their metastable Z isomer liquid phase and release the energy by optically triggered crystallizatio
278 RARRES1, which is proteolytically cleaved to release the extracellular domain, was endocytosed by pod
280 ly photosensitive RGCs (ipRGCs) in mice that release the inhibitory neurotransmitter gamma-aminobutyr
282 ete maturation of VI, and is responsible for releasing the lytic protein from the hexon cavity during
283 structural integrity, and eventually burst, releasing their contents into the extracellular matrix.
284 hrough the primary interface and that Ca(2+) releases this interaction, inducing PIP(2)/membrane bind
285 activation antagonizes CRF-mediated hormone release, this storage/resurfacing mechanism may allow fo
286 t, and this is mediated in part by astrocyte-released thrombospondins (TSPs) and activation of their
290 n for modulators of hypotonicity-induced ATP release using HEK-293 cells and murine cerebellar granul
291 and the cellular process of neurotransmitter release via exocytosis and provide a better physical fra
292 n surface, where the duration of transmitter release was quantified and correlated to the vesicle siz
294 n bursts has been associated to neuropeptide release, we hypothesized that I(h) would be important fo
295 cancer cell invasion, and vesicular content release, we sought to elucidate the signaling pathway do
296 apid micellar breakdown and concomitant drug release, when in breast cancer cells with increased leve
297 d levels were increased 2 weeks after tendon release, when the levels of high-energy phosphates and g
298 ion diminishes sarcoplasmic reticulum Ca(2+) release, which, in turn, reduces diastolic cytosolic Ca(
300 a single mutation that augments spontaneous release without altering evoked release, suggesting that