戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ated protein aggregates, lipofuscinosis, and endolysosomal abnormalities.
2 urodegenerative disorder characterized by an endolysosomal accumulation of cholesterol and other lipi
3                                              Endolysosomal acidification and the endosomal transporte
4 betaA3/A1-crystallin is essential for normal endolysosomal acidification, and thereby, normal activat
5 ocytes restored V-ATPase activity and normal endolysosomal acidification, thereby increasing the leve
6                                The resulting endolysosomal alkalization impedes macrophage antigen pr
7 ing brain homeostasis, as dysfunction of the endolysosomal and autophagic pathways has been associate
8 gnized early neuropathologic features in the endolysosomal and autophagy systems of neurons, includin
9 associated defects in RAB7L1 or LRRK2 led to endolysosomal and Golgi apparatus sorting defects and de
10 d in pigment cells, localizes exclusively to endolysosomal and melanosomal membranes unlike most G pr
11 resentation on MHC-II involve both classical endolysosomal and nonclassical cytosolic pathways.
12 is degraded by acidic thiol-proteases in the endolysosomal apparatus and then metabolized, as in mamm
13                         Here, we identify an endolysosomal ATP-sensitive Na(+) channel (lysoNa(ATP)).
14 n mutations in the ATP13A2 gene encoding the endolysosomal ATPase ATP13A2.
15 ts underscore the importance of misregulated endolysosomal biogenesis in Wnt signaling and cancer.
16 us to examine the relationship between MITF, endolysosomal biogenesis, and Wnt signaling.
17 nal delivery, microvillus morphogenesis, and endolysosomal biogenesis.
18 -1-induced Ca(2+) response is abolished upon endolysosomal but not Golgi disruption.
19 omal membrane fusion involving P2X4-mediated endolysosomal Ca(2+) release and subsequent CaM activati
20  However, the molecular mechanisms for intra-endolysosomal Ca(2+) release and the downstream Ca(2+) t
21                                        Intra-endolysosomal Ca(2+) release is required for endolysosom
22              We propose that NAADP regulates endolysosomal Ca(2+) storage and release via TPCs and co
23 here that NAADP-mediated Ca(2+) release from endolysosomal Ca(2+) stores activates inward membrane cu
24 in A1, indicating Ca(2+) release from acidic endolysosomal Ca(2+) stores.
25 ly releases Ca(2+) from acidic intracellular endolysosomal Ca(2+) stores.
26 cellular sphingosine and subsequently caused endolysosomal calcium accumulation, which in turn led to
27 ilic drugs (CADs), this mechanism led to the endolysosomal calcium as a critical target for developme
28 s and lysosomes and were proposed to mediate endolysosomal calcium release triggered by the second me
29 radation of Ags is performed by pH-dependent endolysosomal cathepsins.
30 protein (TbMLP) orthologous to the mammalian endolysosomal cation channel Mucolipin 1.
31 colipin TRP (TRPML) proteins are a family of endolysosomal cation channels with genetically establish
32                 Two-pore channels (TPCs) are endolysosomal cation channels.
33  have identified two-pore channels (TPCs) as endolysosomal channels that are regulated by NAADP; howe
34                         We conclude that the endolysosomal channels TPC1 and TPC2 are essential for a
35 es, lysosomal dysfunction due to loss of the endolysosomal Cl(-) transporter ClC-b/CLCN7 delayed degr
36 hat HSP70 release involves transit though an endolysosomal compartment and is inhibited by lysosomotr
37                   Trafficking of TLR3 to the endolysosomal compartment arising from fusion of late en
38 ion and exocytosis, as well as regulation of endolysosomal compartment identity.
39                                     The host endolysosomal compartment is often manipulated by intrac
40 oparticles are rapidly internalized into the endolysosomal compartment of cancer cells, and exhibit a
41 artment that fuses with lysosome to form the endolysosomal compartment.
42 embrane and associated components within the endolysosomal compartment.
43 s to the Toll-like Receptor (TLR) containing endolysosomal compartment.
44 c acids by TLR9 requires its cleavage in the endolysosomal compartment.
45 MP3) and LAMP1 indicating enhancement of the endolysosomal compartment.
46 rafficking from the endoplasmic reticulum to endolysosomal compartments and its subsequent proteolyti
47  strategy to restrict receptor activation to endolysosomal compartments and prevent TLRs from respond
48 ospholipase C inhibition and alkalization of endolysosomal compartments blocked its activation by TNF
49 imiting membrane and, to a lesser extent, to endolysosomal compartments by confocal fluorescence and
50 which then prevents the acidification of the endolysosomal compartments by inhibiting vacuolar ATPase
51 ion or block the fusion of autophagosomes to endolysosomal compartments caused an increase in C99 lev
52 ring proteolytic cleavage and trafficking to endolysosomal compartments for ligand-induced signaling.
53                                 Membranes of endolysosomal compartments in macrophages are often dama
54 ath), that localizes to the cell surface and endolysosomal compartments in neurons.
55                         Traffic through late endolysosomal compartments is regulated by sequential si
56 Dietary fat accumulates in lipid droplets or endolysosomal compartments that undergo selective expans
57 a molecular connection between the Golgi and endolysosomal compartments to enhance proliferative mTOR
58 nd monocytes, but not basophils, traffics to endolysosomal compartments under steady-state conditions
59 9 traffics from the endoplasmic reticulum to endolysosomal compartments where it is cleaved by reside
60 dly traffic these soluble peptides into late endolysosomal compartments where they are subject to deg
61 y, thereby compromising acidification of the endolysosomal compartments, leading to reduced gamma-sec
62 ke receptors (TLRs) detect and signal within endolysosomal compartments, triggering the induction of
63 ran, a bulk-endocytosis marker, and with the endolysosomal compartments.
64 eceptor 9 (TLR9) recognizes microbial DNA in endolysosomal compartments.
65 ent cells, leading to GLUT1 mis-sorting into endolysosomal compartments.
66 fective exocytosis and impaired integrity of endolysosomal compartments.
67 implement a manual patch-clamp technique for endolysosomal compartments.
68  by increasing the APP/BACE-1 convergence in endolysosomal compartments.
69 rts TLRs from the early endosome to the late endolysosomal compartments.
70 e degradation of APP C-terminal fragments in endolysosomal compartments.
71 heckpoints that restrict their activation to endolysosomal compartments.
72 en 1), indicating a lack of integrity in the endolysosomal compartments.
73 asitophorous vacuole (PV) that acquires host endolysosomal components.
74 wever, the biological significance of excess endolysosomal Cu accumulation has not been assessed.
75                             HIV PIs modified endolysosomal degradation and epitope production of prot
76 ecessary for their efficient endocytosis and endolysosomal degradation and present three lines of evi
77 inding and internalization as well as faster endolysosomal degradation compared with Bet v 1.
78                                              Endolysosomal degradation of Bet v 1 and Mal d 1 resulte
79 rface binding and the kinetics of uptake and endolysosomal degradation of Bet v 1, Api g 1, and Mal d
80 strate a novel mechanism for endocytosis and endolysosomal degradation of class I, which may be appli
81      Beclin 2 is required for ligand-induced endolysosomal degradation of several G protein-coupled r
82 al proteases (cathepsins) mitigates the fast endolysosomal degradation of the MOG40-48 core epitope.
83 lts from enhanced endocytosis and subsequent endolysosomal degradation of the target proteins.
84 aluate the possible relationship between the endolysosomal degradation pathway and autophagy on the p
85 bial virulence factors; however, the role of endolysosomal degradation pathways in these processes is
86 ays, supporting the hypothesis that impaired endolysosomal degradation underlies the pathogenesis of
87                                              Endolysosomal degradation was simulated in vitro by usin
88 ell-activating region, low susceptibility to endolysosomal degradation, and induction of a Bet v 1-in
89 2, interacts with KSHV GPCR, facilitates its endolysosomal degradation, and inhibits vGPCR-driven onc
90                     Resulting from perturbed endolysosomal degradation, Plaa mutant neurons accumulat
91 h Dau c 1 was still detectable after 48 h of endolysosomal degradation.
92 nic effects of KSHV GPCR by facilitating its endolysosomal degradation.
93  of activated cell surface receptors via the endolysosomal degradative pathway.
94 ospholipid vesicles and gastrointestinal and endolysosomal digestions in the presence or absence of l
95 t can be turned on by redox activation after endolysosomal disruption and delivery into the cytosol,
96 nown, however, about the role of DNase II in endolysosomal DNA sensing by TLR9.
97                  To identify genes governing endolysosomal dynamics, we conducted a global fluorescen
98                   Our findings indicate that endolysosomal dysfunction and abnormalities of alpha-syn
99  tools to study aberrant lipid metabolism of endolysosomal dysfunction associated with AD.
100                       To further explore how endolysosomal dysfunction causes PD-related neurodegener
101 st common PD-causing LRRK2 mutation, linking endolysosomal dysfunction to the pathogenesis of LRRK2-m
102 lein-independent neurotoxicity consequent to endolysosomal dysfunction.
103 lic consequences of Complex I inhibition and endolysosomal effects of imiquimod might also contribute
104 ways on" reporter and subcellular imaging of endolysosomal escape by confocal microscopy.
105  for the investigation of new strategies for endolysosomal escape of biomacromolecules to facilitate
106  render targeted in vivo delivery, efficient endolysosomal escape, and dynamic control over activatio
107  capsids before and after pH shift exhibited endolysosomal escape.
108 me that intracellular endothelin-1 activates endolysosomal ET(B) receptors and increase cytosolic Ca(
109 ndothelin-1 acts in an intracrine fashion on endolysosomal ET(B) to induce nitric oxide formation, th
110               Both proteins were digested by endolysosomal extracts of mdDC.
111              All proteins were digested with endolysosomal extracts, and the resulting peptides were
112 y that couples the cell's metabolic state to endolysosomal function and are crucial for physical endu
113 eins involved in translation, secretion, and endolysosomal function.
114 egulator of lysosomes, leading to diminished endolysosomal function.
115 nsient, and after resealing of the membrane, endolysosomal fusion continued.
116                                Secretory and endolysosomal fusion events are driven by SNAREs and cof
117 intracellular Na(+) channels able to control endolysosomal fusion, a key process in autophagic flux.
118 re not synonymous, even in the context of an endolysosomal genetic defect linked to Parkinsonism, and
119 l PI(3)P pool has separable consequences for endolysosomal homeostasis and cortical remodeling.
120 embrane influx, promote efflux, and maintain endolysosomal homeostasis.
121                Similar to TLR11, TLR12 is an endolysosomal innate immune receptor that colocalizes an
122 es and intact lysosomes and thereby preserve endolysosomal integrity.
123                        Moreover, the primary endolysosomal ion is Na(+), not K(+), as had been previo
124 t exhibited rapid release in the presence of endolysosomal lipases.
125           Earlier work demonstrated that the endolysosomal lipid PI(3,5)P2 activates V-ATPases contai
126 ned from these studies that perturbations in endolysosomal, lipid metabolism, and immune response pat
127                                              Endolysosomal localization and cleavage of intracellular
128 the sequential recruitment of early and late endolysosomal markers to the elongating tPCs.
129 l phagocytes, macrophages are susceptible to endolysosomal membrane damage inflicted by the pathogens
130 lly control PI conversion in endocytosis and endolysosomal membrane dynamics during endosome maturati
131 te [PtdIns(3,5)P2] and for the regulation of endolysosomal membrane dynamics in mammals.
132 a thus suggest a new molecular mechanism for endolysosomal membrane fusion involving P2X4-mediated en
133 endolysosomal Ca(2+) release is required for endolysosomal membrane fusion with intracellular organel
134 ignaling through the actin cytoskeleton with endolysosomal membrane trafficking events.
135  by the CUE domain promotes Vps9 function in endolysosomal membrane trafficking via promotion of loca
136  P2X4 and calmodulin (CaM) form a complex at endolysosomal membrane where P2X4 activation recruits Ca
137 , measurement of channel currents across the endolysosomal membrane), including control experiments,
138  this paper, by direct patch-clamping of the endolysosomal membrane, we report that PI(3,5)P(2), an e
139 ciated with impaired activation of mTORC1 at endolysosomal membranes, the accumulation of the mannose
140 cies-mediated rupture of the photosensitised endolysosomal membranes, the spatio-temporal selectivity
141                         Found in vacuolar or endolysosomal membranes, they regulate the conductance o
142 y the long Irgm1 isoforms can be detected on endolysosomal membranes.
143  that maintains or restores the integrity of endolysosomal membranes.
144 ivities at both the plasma membrane (PM) and endolysosomal membranes.
145 T) using a photosensitiser that localises in endolysosomal membranes.
146 o compromised retromer-mediated recycling of endolysosomal membranes.
147 lease from acidic-like Ca(2+) stores via the endolysosomal NAADP-sensitive two-pore channels.
148 on mast cells, a cell type unusually rich in endolysosomal organelles (secretory granules).
149 ught to take place at the cell surface or in endolysosomal organelles.
150 bilizing messenger that releases Ca(2+) from endolysosomal organelles.
151 l activities and characteristics in isolated endolysosomal organelles.
152 t lysosomal trafficking regulator Lyst links endolysosomal organization to the selective control of t
153 verexpression of P2X4, as well as increasing endolysosomal P2X4 activity by alkalinization of endolys
154             Previously, we demonstrated that endolysosomal P2X4 forms channels activated by luminal a
155 from WT and polymorphic variant carriers for endolysosomal patch-clamp experimentation to confirm key
156 In contrast to the alternatively used planar endolysosomal patch-clamp technique, this method is a vi
157                           The development of endolysosomal patch-clamp techniques has made it possibl
158 olyubiquitination leads to degradation by an endolysosomal pathway and demonstrate a novel mechanism
159 mmals has been considered to function in the endolysosomal pathway and in the biosynthetic pathway on
160 lar NTHI avoids, escapes, or neutralizes the endolysosomal pathway and persists within human respirat
161 Chlamydial inclusions are uncoupled from the endolysosomal pathway and undergo fusion with cellular o
162 ae that regulate membrane trafficking in the endolysosomal pathway by activating Rab5 GTPases.
163 rnover of synaptic membrane proteins via the endolysosomal pathway is essential for synaptic function
164              Maturation of organelles in the endolysosomal pathway requires exchange of the early end
165 otein-(APP) cleaving enzyme (BACE1) from the endolysosomal pathway to recycling endosomes represents
166 nscriptional level by trafficking within the endolysosomal pathway where MARCH1 is proteolyzed.
167 e membrane remodeling, interactions with the endolysosomal pathway, actin rearrangements and microtub
168 t manner, is subsequently trafficked via the endolysosomal pathway, and is killed in lysosomes after
169 hila phagosome exists completely outside the endolysosomal pathway, and the M. tuberculosis phagosome
170 n a trafficking defect of two cargoes of the endolysosomal pathway, influenza A virus (IAV) and epide
171 its of the retromer, Rh1 is processed in the endolysosomal pathway, leading to a dramatic increase in
172 d that pffs are rapidly trafficked along the endolysosomal pathway, where most of the material remain
173 TrCP ubiquitin E3 ligase and occurred via an endolysosomal pathway.
174 pool size by enhancing SV trafficking to the endolysosomal pathway.
175 in targeted HIV-1 Gag for degradation by the endolysosomal pathway.
176 radation by lysosomes and trafficking in the endolysosomal pathway.
177  the degradation of endocytic cargoes by the endolysosomal pathway.
178 in-modified cargoes are sequestered into the endolysosomal pathway.
179 quired for trafficking and tubulation in the endolysosomal pathway.
180  digestive PVs that fully mature through the endolysosomal pathway.
181  that regulates membrane transport along the endolysosomal pathway.
182  (MHC-I) from the trans-Golgi network to the endolysosomal pathway.
183 regulate postinternalization steps along the endolysosomal pathway.
184 gned to localize within organelles along the endolysosomal pathway.
185  data identify Vps34 as a major regulator of endolysosomal pathways in podocytes and underline the fu
186 ellular protein complex implicated in TGN to endolysosomal pathways.
187 mport through transmembrane transporters and endolysosomal pathways.
188  fundamental question: are SVs sorted toward endolysosomal pathways?
189                            Here we show that endolysosomal pH is critical for receptor sorting and tu
190 lls a carbohydrate epitope is generated upon endolysosomal processing of group B streptococcal type I
191 RNase-L also regulated the expression of the endolysosomal protease, cathepsin-E, and endosome-associ
192 It was also shown that altered expression of endolysosomal proteases (cathepsins) mitigates the fast
193          Here, we identify the cathepsin L/B endolysosomal proteases functioning in a direct and rate
194                   Dau c 1 was incubated with endolysosomal proteases, and the resulting fragments wer
195 binding cassette transporter 2 (ABCA2) is an endolysosomal protein most highly expressed in the centr
196   These findings demonstrate that sorting of endolysosomal proteins begins at an earlier stage and in
197 r a different mechanism in which two sets of endolysosomal proteins undergo early segregation to dist
198  human two-pore channels (TPC1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium sign
199  fusion and protein transport) interact with endolysosomal Rabs to coordinate their signaling activit
200  impeding binding of the C-loop of NPC1, the endolysosomal receptor for EBOV.
201 2) ubiquitination, which leads to Galpha(i2) endolysosomal sequestration and destruction.
202 ected against proteolytic degradation by the endolysosomal serine protease cathepsin G.
203        This protection requires the vacuolar/endolysosomal signaling lipid PI3,5P2 We show that Pho85
204 eutrophil extracellular trap production, and endolysosomal signaling.
205                         Endocytosis, but not endolysosomal size, contributes to cortical remodeling b
206 e used snapin mutants as tools to assess how endolysosomal sorting and trafficking impact presynaptic
207 containing protein 1 (UBXD1) cofactor during endolysosomal sorting of caveolin-1.
208 : the biogenesis of multivesicular bodies in endolysosomal sorting; the budding of HIV-1 and other vi
209 sensitive, presumably arising from different endolysosomal sources.
210 common pathogenic mechanisms associated with endolysosomal storage disorders.
211 sion has dramatic and contrasting effects on endolysosomal structures and dynamics, implicating a rol
212 PC2, but not TPC1, caused a proliferation of endolysosomal structures, dysregulating intracellular tr
213 significantly enriched for components of the endolysosomal system (>60%, P < 0.001) and included many
214 fied the two-pore channels (TPCs) within the endolysosomal system as NAADP-regulated Ca(2+) channels
215 t work has further dissected the role of the endolysosomal system in both bone formation by osteoblas
216 oles of PIs in different compartments of the endolysosomal system in mammalian cells and discuss the
217 g of plasma membrane-derived MAG through the endolysosomal system in primary cells and brain tissue.
218    In addition, Notch trafficking across the endolysosomal system is critical in its regulation.
219 tive Ca(2+)-permeable cation channels in the endolysosomal system of cells, as candidate targets for
220                          Transport along the endolysosomal system requires multiple fusion events at
221                              The compromised endolysosomal system resulting from AMPK or Tfeb inactiv
222                            Organelles of the endolysosomal system undergo multiple fission and fusion
223 cretory compartments, catabolic steps of the endolysosomal system, and intracellular trafficking.
224 jor mechanism for mobilizing Ca(2+) from the endolysosomal system, resulting in localized Ca(2+) sign
225 hich are required for their targeting to the endolysosomal system.
226 cytes had defects in the organization of the endolysosomal system.
227 tive phenotypes of mutations that affect the endolysosomal system.
228  intracellular ion channels expressed in the endolysosomal system.
229 ficiency of downstream sorting events in the endolysosomal system.
230 +)-permeable ion channels present within the endolysosomal system.
231 release channels, which are localized on the endolysosomal system.
232 cuole is rendered nonfusogenic with the host endolysosomal system.
233 kaging into coated vesicles destined for the endolysosomal system.
234 cal roles as Ca(2+) -release channels of the endolysosomal system.
235 ce between pathogenic infection and the host endolysosomal system.
236  membrane fusion events in the secretory and endolysosomal systems, and all SNARE-mediated fusion pro
237      Here, we report a novel function of the endolysosomal T. gondii sortilin-like receptor (TgSORTLR
238 e, a class III lipid kinase, is required for endolysosomal TLR-induced expression of type I IFN in mo
239 evoked Ca(2+) release or genetic ablation of endolysosomal TPC1 or TPC2 channels attenuates glucose-
240  activity in a manner that is independent of endolysosomal trafficking and parallel to the Scribble m
241 artite regulation of presynaptic activity by endolysosomal trafficking and sorting: LE transport regu
242 tablish the importance of ubiquitin-mediated endolysosomal trafficking at the synapse.
243               Our data suggest that impaired endolysosomal trafficking in both motor neurons and Schw
244                     Moreover, Fig4-regulated endolysosomal trafficking in Schwann cells is essential
245                                     Although endolysosomal trafficking is well defined, how it is reg
246           Pyk2 depletion resulted in altered endolysosomal trafficking of HPV16 and accelerated unfol
247 ate photoreceptor homeostasis by influencing endolysosomal trafficking of Rhodopsin and TRP.
248 role of Cul3 in regulating late steps in the endolysosomal trafficking pathway.
249 re broadly, our data suggest a role for host endolysosomal trafficking pathways in regulating viral p
250 rsity of Beclin family members in autophagy, endolysosomal trafficking, and metabolism.
251 5-bisphosphate, and plays a critical role in endolysosomal trafficking.
252 olae-mediated pathway, bypassing degradative endolysosomal trafficking.
253 IRG1, RIN3, and RUFY1 all may be involved in endolysosomal transport-a process known to be important
254 dule mutants show intact internalization and endolysosomal transport.
255 yzed and shown to have distinct functions in endolysosomal transport.
256 HC molecules themselves is not necessary for endolysosomal tubule formation.
257                                              Endolysosomal tubules can be stained with acidotropic dy
258 dition to its association with microtubules, endolysosomal tubules follow the plus ends of microtubul
259                                              Endolysosomal tubules in DCs exhibit dynamic and saltato
260 he cell surface via long tubular structures (endolysosomal tubules).
261              DCs lacking MyD88 can also form endolysosomal tubules, demonstrating that MyD88-dependen
262    Indeed, nocodazole causes the collapse of endolysosomal tubules.
263                                          The endolysosomal two-pore channels (TPCs), TPC1 and TPC2, h
264 lumenal pH (approximately 5) and fusion with endolysosomal vesicles, the PV is considered phagolysoso
265 internalized class I chains are delivered to endolysosomal vesicles, where they undergo degradation.
266 gs, TRPM2 expression in DCs is restricted to endolysosomal vesicles, whereas in neutrophils, the chan
267 omplex and/or localization of the complex to endolysosomal vesicles.

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top