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1 icating that it is predominantly passive and paracellular.
2 iated intercellular barrier and facilitating paracellular absorption of BoNT/A.
3 reased podocyte permeability to albumin in a paracellular albumin influx assay, shRNA-mediated knockd
4               Brain endothelial cells form a paracellular and transcellular barrier to many blood-bor
5 ncreased mortality, yet the contributions of paracellular and transcellular mechanisms to this proces
6                             Advances in both paracellular and transcellular neutrophil migration thro
7 es revealed that molecules permeate via both paracellular and transcellular pathways in the presence
8 ormal tissues and in solid tumors, including paracellular and transcellular pathways that enable pass
9 rease in the water filtration coefficient of paracellular and transcellular pathways, and a decrease
10 idney have different abilities to facilitate paracellular and transcellular transport of water and so
11 lity with emphasis on the cross-talk between paracellular and transcellular transport pathways.
12  utilizes a nanoscale pipet to differentiate paracellular and transcellular transport processes at hi
13 e migration across endothelial cell borders (paracellular) and through endothelial cells (transcellul
14 ng a biophysical model based on parametrized paracellular, aqueous boundary layer, and transcellular
15 ght junction strands and constitute both the paracellular barrier and the pore.
16                                  There was a paracellular barrier defect in rat epidermal keratinocyt
17 face carbohydrates, and HA2-HA3, involved in paracellular barrier disruption by E-cadherin binding.
18 s provide new insight into the mechanisms of paracellular barrier formation by demonstrating that def
19 nd is required for junction organization and paracellular barrier function, but not for apical-basal
20                                   Epithelial paracellular barrier function, determined primarily by t
21                              Claudins have a paracellular barrier function.
22 markedly disrupted, resulting in the loss of paracellular barrier function.
23 important BBB property is the formation of a paracellular barrier made by tight junctions (TJs) betwe
24 wise impairment of transcellular followed by paracellular barrier mechanisms accounts for the BBB def
25 ls have reduced vessel density but increased paracellular barrier permeability.
26          CPE-mediated damage was enhanced if paracellular barrier was impaired by Ca2+ depletion, pro
27                   Their presence generates a paracellular barrier, analogous to animal tight junction
28 r mutant epithelia fail to form an effective paracellular barrier.
29 roteins that are essential components of the paracellular barrier.
30 ogenous mechanism controlling the intestinal paracellular barrier.
31   This limits the molecular understanding of paracellular barriers and strategies for drug delivery a
32  specific claudin subtypes related either to paracellular barriers that impede drug delivery or to tu
33 ve degradation of tight junction proteins or paracellular BBB leakage.
34 c cell lines, supporting the hypothesis that paracellular bile leakage through deficient TJs is invol
35 permeability and liver injuries secondary to paracellular bile regurgitation.
36 gnaling pathway in the kidney that underlies paracellular Ca(++) reabsorption through the tight junct
37 udin14 (Cldn14), an inhibitory factor of the paracellular Ca(2+) transport in the TAL, was significan
38 naling directly and indirectly regulates the paracellular Ca(2+) transport pathway by modulating Cldn
39 reasing the lumen-positive driving force for paracellular Ca(2+) transport.
40 on of NHE3 (including its role in regulating paracellular Ca2+ flux), NHE8, as well as about the comp
41  physical interaction, claudin-14 blocks the paracellular cation channel made of claudin-16 and -19,
42 hat HDAC inhibitors transiently increase the paracellular cation conductance in the thick ascending l
43 -13-dependent claudin-2 expression increases paracellular cation flux in vitro and in vivo without al
44 vates transepithelial resistance by reducing paracellular cation flux.
45 pression, claudin-2 synthesis, and increased paracellular cation flux.
46 lation of Claudin14, a negative regulator of paracellular cation permeability in the thick ascending
47 lation of Claudin16, a positive regulator of paracellular cation permeability.
48 nctions, both claudin-2 and claudin-10b form paracellular cation-selective pores by the interaction o
49 bryonic than the postnatal stages, acts as a paracellular channel for small cations, such as Na(+), s
50 tes renal Ca(++) handling through changes in paracellular channel permeability in the thick ascending
51  passage of small and larger solutes by both paracellular channel-based and some additional mechanism
52                        Claudin-2 forms gated paracellular channels and allows sodium ions and other s
53       We conclude that claudin-2 forms gated paracellular channels and speculate that modulation of t
54    In addition, certain claudins function as paracellular channels for small ions and/or solutes by f
55  of at least two spatially distinct types of paracellular channels in TAL: a cldn10b-based channel fo
56 cells migrated into the lumen moving through paracellular channels within the epithelium.
57 he claudin-8 interaction with claudin-4, the paracellular chloride channel, and delocalization of cla
58 pletion of claudin-8 resulted in the loss of paracellular chloride conductance, through a mechanism i
59  knockdown of KLHL3 profoundly increased the paracellular chloride permeability.
60 ver, the molecular mechanisms underlying the paracellular chloride reabsorption in the collecting duc
61                                          The paracellular claudin channel of the thick ascending limb
62 tant endothelial cells precociously form the paracellular component of the barrier.
63 t has been hypothesized that VECs facilitate paracellular diapedesis by opening their cell-cell junct
64 unctional gaps in the endothelial monolayer (paracellular diapedesis).
65 he sequence of mechanical events involved in paracellular diapedesis.
66  cells and are responsible for regulation of paracellular diffusion and maintenance of cellular polar
67 ateral cell surface domains that serves as a paracellular diffusion barrier, enabling epithelial cell
68 cell junction that functions to prevent free paracellular diffusion between epithelial cells.
69 relation was observed between G, an index of paracellular diffusion of ions, and mannitol permeabilit
70 ity to intact 33-mer or p31-49 did not favor paracellular diffusion of the peptides.
71                       These barriers inhibit paracellular diffusion, thereby protecting the CNS from
72           Although TJs are known to regulate paracellular diffusion, this barrier function has not be
73 tilization in the kidney may be supported by paracellular epithelial transport, a form of passive dif
74 rming that junctional disruption resulted in paracellular exchange between the blood stream and the b
75 ined by tight junction proteins that control paracellular fluid flux.
76 ated knockout of TOCA-1 results in increased paracellular flux and delayed recovery in a calcium swit
77 fected or changed in the opposite direction; paracellular flux and myosin localization were also diff
78 elial electrical resistance and also reduced paracellular flux of fluorescein isothiocyanate-dextran
79 asure transepithelial electrical resistance, paracellular flux of fluorescein isothiocyanate-dextran
80 pores in the tight junction that control the paracellular flux of inorganic ions and small molecules.
81                                TNF increased paracellular flux of large molecules in occludin-suffici
82 nt collecting duct cells displayed increased paracellular flux of sodium, chloride, and urea.
83 ons are cell-cell contacts that regulate the paracellular flux of solutes and prevent pathogen entry
84 to disrupt tight junctions, and this permits paracellular flux of toxin.
85           In vivo, MLCK activation increases paracellular flux of uncharged macromolecules and also t
86 ctivation alters size selectivity to enhance paracellular flux of uncharged macromolecules without af
87 ed to effector caspase activation, increased paracellular flux, and redistribution of zonula occluden
88 is of transepithelial electrical resistance, paracellular flux, mRNA expression, Western blotting, an
89 in stress fibers, cellular contractions, and paracellular gap formation.
90                    Similar enhanced rates of paracellular glucose flux were also observed across exci
91 lial monolayers to PIMs results in increased paracellular glucose flux, as well as apical GLUT-mediat
92  shift from paracellular sodium transport to paracellular hyperabsorption of calcium and magnesium.
93                                         Such paracellular ice penetration occurred in the majority of
94 s used to quantify the rate constants of the paracellular ice penetration process, the penetration-as
95                                              Paracellular ice penetration was generally not observed
96               Magnesium absorption is mainly paracellular in the proximal tubule and in the thick asc
97 lities of all pathways (apical, basolateral, paracellular) in human nasal epithelia cultures using ex
98  role in asthma pathogenesis by enabling the paracellular influx of allergens, toxins, and microbes t
99 monstrated that SPAK significantly increased paracellular intestinal permeability to FITC-dextran.
100 -junction transmembrane proteins that act as paracellular ion channels in epithelial cells.
101 junctions (TJs) play a key role in mediating paracellular ion reabsorption in the kidney.
102  that pathogenic CLDN10 mutations affect TAL paracellular ion transport and cause a novel tight junct
103 ent specific selectivity and permeability of paracellular ion transport.
104 e to water in Ildr1 knockout animals whereas paracellular ionic permeabilities in the Ildr1 knockout
105 d lipoprotein receptor (LSR), a component of paracellular junctions at points in which three cell mem
106 ed airway epithelial cell monolayers via the paracellular junctions.
107 n-5 paradoxically accompanies an increase in paracellular leak and rearrangement of alveolar tight ju
108 ripheral tolerance, and antigen delivered by paracellular leak initiates immune responses in the mese
109 , absorptive oxalate flux occurs through the paracellular "leak" pathway, and net absorption of dieta
110     We investigated whether transcytosis and paracellular leakage are co-regulated.
111                   Importantly, inhibition of paracellular leakage by sphingosine-1-phosphate, which a
112 g transcytosis by dynamin blockade increased paracellular leakage concomitantly with the loss of cort
113  of transcytosis induced a rapid increase in paracellular leakage that was not explained by decreases
114 tinct transport pathways have been proposed: paracellular leakage through epithelial tight junctions
115 dies implicate occludin in the regulation of paracellular macromolecular flux at steady state and in
116 udin interactions are essential for limiting paracellular macromolecular flux.
117 NV2) infection and inflammatory mediators on paracellular macromolecule permeability over time.
118 t junction protein Claudin-10, show enhanced paracellular magnesium and calcium permeability and redu
119 l phosphate absorption occurs through both a paracellular mechanism involving tight junctions and an
120 bsorbed in the proximal tubule, primarily by paracellular mechanisms that are not sensitive to calciu
121  same molecules and mechanisms that regulate paracellular migration also control transcellular migrat
122 xtracellular form that uses transcellular or paracellular migration, or by infecting a host cell that
123 ni CCS treatment of BAT2 cells also enhanced paracellular migration.
124 ion procedure incorporating a dual-pore size paracellular model.
125 as a static structure providing a barrier to paracellular movement and restricting proteins to the ap
126 ulated a rapid and transient increase in the paracellular Na(+) conductance, with a smaller increase
127  ascending limb (TAL) of Henle's loop drives paracellular Na(+), Ca(2+), and Mg(2+) reabsorption via
128                   Leakage can occur between (paracellular) or through (transcytosis) endothelial cell
129 revent flux of most hydrophilic solutes, the paracellular, or shunt, pathway between cells must also
130 tion of dietary oxalate results from passive paracellular oxalate absorption as modified by oxalate b
131                   Claudin-21 also allows the paracellular passage of larger solutes.
132 ased intestinal permeability, which involves paracellular passage regulated through tight junctions (
133 se results suggest that ion flow through the paracellular pathway can be acutely regulated.
134 e claudin-14/16/19 proteins form a regulated paracellular pathway for calcium reabsorption, approache
135 t function as both pores and barriers in the paracellular pathway in epithelial cells.
136                                          The paracellular pathway in the collecting duct of the kidne
137 ociation is required for the anion-selective paracellular pathway in the collecting duct, suggesting
138 ed solute transport, the dynamic role of the paracellular pathway in transepithelial-fluid transport
139 ndings have attested to the concept that the paracellular pathway is physiologically regulated throug
140 at these features are mostly originated from paracellular pathway modifications due to host-parasite
141 Here we applied cysteine scanning to map the paracellular pathway of ion permeation across claudin-2-
142 nhibitors increased calcium reabsorption and paracellular pathway permeability but did not change NaC
143 rmeabilities of the basolateral membrane and paracellular pathway remain largely unknown.
144 rovascular endothelia (HMVEC-Ls) to open the paracellular pathway through Src family kinase (SFK) act
145  the flux of [(3)H]mannitol, a marker of the paracellular pathway, across intestine from wild-type an
146                           To investigate the paracellular pathway, we used primary cultures of differ
147  and ICAM-2 and occurred exclusively via the paracellular pathway.
148 rt depends strongly on the properties of the paracellular pathway.
149 sport in the TAL via the permeability of the paracellular pathway.
150 cell monolayers by transiently affecting the paracellular pathway.
151 rptive mechanisms as well as the role of the paracellular pathway.
152 rane proteins that are key regulators of the paracellular pathway.
153 of claudin-14, the negative regulator of the paracellular pathway.
154 epithelial transport across transcellular or paracellular pathways promises to advance the present un
155 iratory epithelia involves both cellular and paracellular pathways.
156 bly of adherens junctions and opening of the paracellular pathways.
157 ular hyperpermeability via transcellular and paracellular pathways.
158          Although the maximum temperature of paracellular penetration was similar for all four cell s
159                                              Paracellular permeabilities conferred by claudin-2 are c
160 ng PrP(c) knockdown; the cells had increased paracellular permeability (1.5-fold over 48 hours; P < .
161 l adhesion kinase mediates TGF-beta1-induced paracellular permeability and actin cytoskeleton dynamic
162             TGF-beta1 induces an increase in paracellular permeability and actin stress fiber formati
163                     RalA reduction increased paracellular permeability and decreased incorporation of
164 s into TJs, whereas RalB reduction decreased paracellular permeability and increased incorporation of
165 d by Claudin-1 absence, leading to increased paracellular permeability and liver injuries secondary t
166                                  To test for paracellular permeability and size exclusion, FITC-label
167                                         Both paracellular permeability and the localization of TJ pro
168 mutation within ECs prevented VEGF-initiated paracellular permeability and tumor cell transmigration
169  Our findings indicate that transcytosis and paracellular permeability are co-regulated through a sig
170 determined by reduced electrical resistance, paracellular permeability assays, and cell surface E-cad
171 s, occludin S408 dephosphorylation regulates paracellular permeability by remodeling tight junction p
172            SU6656 reduced TNF-alpha-mediated paracellular permeability changes, restored occludin, p1
173  The PAMPA data were modified to include the paracellular permeability component found in cellular mo
174          We observed significant increase in paracellular permeability following siRNA-mediated suppr
175 resistance (TEER), indicating an increase of paracellular permeability for ions.
176 n-regulation of Sgpp2 attenuated LPS-induced paracellular permeability in cultured cells and enhanced
177        Similarly, we observed an increase of paracellular permeability in NRC cells silenced for clau
178     Defect in claudin-1 expression increases paracellular permeability in polarized hepatic cell line
179 d to study cerebrovascular transcellular and paracellular permeability in vivo.
180 artially able to prevent the increase in BEC paracellular permeability induced by cytokines.
181 lts show that HMTBA prevents the increase in paracellular permeability induced by H2O2 or tumour necr
182                          We show that murine paracellular permeability markedly decreases during post
183                            We speculate that paracellular permeability may have evolved as a general
184  cells, while the endocochlear potential and paracellular permeability of a biotin-based tracer in th
185  miRNA functions contributes to the enhanced paracellular permeability of ANDV-infected ECs and that
186                                          The paracellular permeability of bovine retinal endothelial
187                                          The paracellular permeability of endothelial cells is unique
188 esistance was associated with an increase in paracellular permeability of glucose.
189  cofilin-1 by RNA interference increased the paracellular permeability of human colonic epithelial ce
190 tructural changes may selectively affect the paracellular permeability of ions or small molecules, re
191 ght junction membrane proteins that regulate paracellular permeability of renal epithelia to small io
192              Nutrient starvation reduced the paracellular permeability of small-sized urea but not la
193 ed TAL tubules of claudin-10-deficient mice, paracellular permeability of sodium is decreased, and th
194           This coincided with an increase of paracellular permeability of the BBB to the small tracer
195 tinal epithelium to dynamically regulate its paracellular permeability properties and better define t
196 as been demonstrated to transiently increase paracellular permeability properties to provide an addit
197 cture and function, although the increase of paracellular permeability returned to baseline after 24
198 tine tissues from PrP(c-/-) mice had greater paracellular permeability than from wild-type mice (105.
199 s cell polarity, cytoskeleton integrity, and paracellular permeability through inhibition of the smal
200 cing of Claudin-1 in Can 10 clones increased paracellular permeability to a level similar to that of
201 sepithelial resistance, a marked decrease in paracellular permeability to fluorescence isothiocyanate
202 l TER, these monolayers do exhibit increased paracellular permeability to fluorescent dextrans.
203 ltured epithelial cells demonstrate enhanced paracellular permeability to large molecules, revealing
204 rier-forming Caco-2 monolayers and increases paracellular permeability to macromolecular FITC-dextran
205 aired the development of TEER, and increased paracellular permeability to sodium fluorescein in airwa
206 t junction (TJ) has a key role in regulating paracellular permeability to water and solutes in the ki
207                                              Paracellular permeability was assessed by fluorescein is
208   The role of autophagy in the modulation of paracellular permeability was confirmed by pharmacologic
209 lones, Claudin-1 was localized at the TJ and paracellular permeability was decreased, compared to par
210                                              Paracellular permeability was determined by quantifying
211 fects on ER stress activation and epithelial paracellular permeability were examined in vitro as well
212     Changes in barrier function and abnormal paracellular permeability were found in both interfollic
213 tent with the autophagy-induced reduction in paracellular permeability, a marked decrease in the leve
214 n brain endothelial cells leads to increased paracellular permeability, allowing leukocyte entry into
215 l cells in junction formation, regulation of paracellular permeability, and epithelial morphogenesis.
216 ion of claudins, the primary determinants of paracellular permeability, and measured transepithelial
217 tercellular junctional distance, and induced paracellular permeability, loss of apico-basal polarity
218 luten-sensitized mice, P(HEMA-co-SS) reduced paracellular permeability, normalized anti-gliadin immun
219 ell cultures from a VEGF-induced increase in paracellular permeability, whereas recombinant OCLN expr
220 role in regulating the maintenance of TJ and paracellular permeability, which may explain how various
221 and interferon-gamma significantly increased paracellular permeability, which was blocked by cotreatm
222 ght junctions (TJs), structures that control paracellular permeability.
223 s an important role in regulating epithelial paracellular permeability.
224 human microvascular endothelium and measured paracellular permeability.
225 tion of tight and adherens junctions and BEC paracellular permeability.
226  We studied the role of claudin-1 in hepatic paracellular permeability.
227 ability of junctional proteins and increased paracellular permeability.
228 VE-cadherin pathway responses which increase paracellular permeability.
229 EC adherens junctions, resulting in enhanced paracellular permeability.
230 nction protein internalization and increased paracellular permeability.
231 audin-1) that critically regulate epithelial paracellular permeability.
232 ns at junctions, wound healing dynamics, and paracellular permeability.
233 ntal or mutant E. faecalis strains indicated paracellular permeability.
234 ansepithelial resistance (TER) and decreased paracellular permeability.
235 nce and reduced the ratio of sodium/chloride paracellular permeability.
236                                          The paracellular pore appears to primarily be lined by polar
237 er function by activating claudin-2-mediated paracellular pore pathways.
238  into how ion selectivity is achieved in the paracellular pore.
239                                Claudins form paracellular pores at the tight junction in epithelial c
240  extracellular loop (ECL1) of claudins forms paracellular pores in the tight junction that determine
241 and reversible, characteristic of a passive, paracellular process, and blocked by reduced temperature
242  Fc domain, consistent with FcRn-independent paracellular, rather than transcellular, transport of an
243 uring inflammatory TJ complex remodeling and paracellular route formation in brain endothelial cells.
244  and Cl-secretory pathways together with the paracellular route in health and disease will help devel
245 of apparent permeability coefficient suggest paracellular route of transport of investigated compound
246  internalization via macropinocytosis during paracellular route opening.
247 ellular route directly through the cell or a paracellular route through cellular junctions.
248 lectric resistance (TEER) and opening of the paracellular route to 4kDa fluorescent dextran but not 7
249  non-toxic manner but transiently opened the paracellular route to both 4 and 70kDa fluorescent dextr
250 mechanisms in parallel to the well-described paracellular route to modulate solute transport from the
251 e predominantly (but not exclusively) by the paracellular route, (ii) the aqueous boundary layer thic
252 y <50% were predominantly transported by the paracellular route, surprisingly with several of the com
253                                   As for the paracellular route, this appears to be enhanced by gliad
254 uman IEC, which occurred predominately via a paracellular route, was significantly associated with cl
255 er also flow into the intestinal lumen via a paracellular route.
256 sepithelial translocation, potentially via a paracellular route.
257 nsulin suggested its uptake occurred via the paracellular route.
258  sodium reabsorption takes transcellular and paracellular routes.
259  to actin may allow for accommodation of the paracellular seal to physiological or pathological alter
260 is necessary for tight junction assembly and paracellular sealing in trophectoderm epithelium.
261 tive apical ion transport is balanced out by paracellular shunting of acid/base.
262           We show that claudin-10 determines paracellular sodium permeability, and that its loss lead
263 ubule (PT) of the kidney, claudin-2 mediates paracellular sodium reabsorption.
264 oltage is increased, leading to a shift from paracellular sodium transport to paracellular hyperabsor
265  tricellular tight junctions (tTJs) seal the paracellular space between epithelial cells.
266 a1 tightened the monolayer by decreasing the paracellular space between migrating epithelial cells.
267 lls that restricts solutes from crossing the paracellular space, creating a microenvironment within s
268 nd nutrients would be dissipated through the paracellular space.
269 nnect adjacent epithelial cells and seal the paracellular space.
270 selectively permeable barriers that seal the paracellular space.
271 menon: penetration of extracellular ice into paracellular spaces at the cell-cell interface.
272 ns (TJs), down-regulation of which may widen paracellular spaces between cells, allowing greater flui
273 ing perturbations in the permeability of the paracellular spaces between epithelial barriers.
274  therefore, actively plays a role in opening paracellular spaces to promote transmucosal fluid effux
275 pport an increased movement of cells through paracellular spaces.
276 -mediated vesicular transport, and the other paracellular, through interendothelial junctions.
277 ith IFN-gamma induced endothelial leakage of paracellular tracers.
278 scle, intravascular adherence and subsequent paracellular transmigration of neutrophils elicited by t
279  or PAF-elicited intravascular adherence and paracellular transmigration of neutrophils.
280                                              Paracellular transmigration predominates (>/=90% of even
281 il preference for the transcellular over the paracellular transmigration route.
282 E-cadherin cleavage, loss of cell adherence, paracellular transmigration, and basolateral invasion.
283                  Similar to their effects on paracellular transmigration, antibodies against PECAM or
284 otes ICAM-1-mediated neutrophil crawling and paracellular transmigration.
285 , and the mechanisms by which CaSR regulates paracellular transport in the kidney remain unknown.
286                    Our results indicate that paracellular transport in the PT is required for efficie
287 lial and endothelial cells that regulate the paracellular transport of ions, solutes, and immune cell
288 eptors, integrins, play a role in regulating paracellular transport of renal proximal tubule cells.
289 zed iron oxide nanoparticles, activating the paracellular transport pathway and facilitating the loca
290 portance of transcellular (vesicular) versus paracellular transport pathways by LECs and how mechanic
291  of tight and adherens junctions that define paracellular transport properties of terminally differen
292  maintaining epithelial polarity, regulating paracellular transport, and providing barrier function.
293 roximal tubule allows both transcellular and paracellular transport, while the collecting duct primar
294 uctural and functional components regulating paracellular transport.
295 ude wider than what is normally reported for paracellular transport.
296 ited to small molecules, as expected for the paracellular water and Na(+) channel formed by claudin-2
297                   Vasopressin cannot correct paracellular water loss in Ildr1 knockout animals despit
298 xpression of Ildr1 significantly reduces the paracellular water permeability.
299  tricellular tight junction is important for paracellular water permeation and that Ig-like domain co
300 -2 is a tight junction protein that mediates paracellular water transport in intestinal epithelia, re

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