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2 urodegenerative disorder characterized by an endolysosomal accumulation of cholesterol and other lipi
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
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
12 is degraded by acidic thiol-proteases in the endolysosomal apparatus and then metabolized, as in mamm
15 ts underscore the importance of misregulated endolysosomal biogenesis in Wnt signaling and cancer.
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
23 here that NAADP-mediated Ca(2+) release from endolysosomal Ca(2+) stores activates inward membrane cu
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
31 colipin TRP (TRPML) proteins are a family of endolysosomal cation channels with genetically establish
33 have identified two-pore channels (TPCs) as endolysosomal channels that are regulated by NAADP; howe
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
40 oparticles are rapidly internalized into the endolysosomal compartment of cancer cells, and exhibit a
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.
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
74 wever, the biological significance of excess endolysosomal Cu accumulation has not been assessed.
76 ecessary for their efficient endocytosis and endolysosomal degradation and present three lines of evi
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
82 al proteases (cathepsins) mitigates the fast endolysosomal degradation of the MOG40-48 core epitope.
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
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
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,
101 st common PD-causing LRRK2 mutation, linking endolysosomal dysfunction to the pathogenesis of LRRK2-m
103 lic consequences of Complex I inhibition and endolysosomal effects of imiquimod might also contribute
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
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
112 y that couples the cell's metabolic state to endolysosomal function and are crucial for physical endu
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
126 ned from these studies that perturbations in endolysosomal, lipid metabolism, and immune response pat
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
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
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
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
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
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
163 rnover of synaptic membrane proteins via the endolysosomal pathway is essential for synaptic function
165 otein-(APP) cleaving enzyme (BACE1) from the endolysosomal pathway to recycling endosomes represents
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
185 data identify Vps34 as a major regulator of endolysosomal pathways in podocytes and underline the fu
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
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
206 e used snapin mutants as tools to assess how endolysosomal sorting and trafficking impact presynaptic
208 : the biogenesis of multivesicular bodies in endolysosomal sorting; the budding of HIV-1 and other vi
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.
219 tive Ca(2+)-permeable cation channels in the endolysosomal system of cells, as candidate targets for
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
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
249 re broadly, our data suggest a role for host endolysosomal trafficking pathways in regulating viral p
253 IRG1, RIN3, and RUFY1 all may be involved in endolysosomal transport-a process known to be important
258 dition to its association with microtubules, endolysosomal tubules follow the plus ends of microtubul
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
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