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1 anelles, or pathogens for degradation to the lysosome.
2 lex was required for its localization at the lysosome.
3 L2 and the viral genome in the late endosome/lysosome.
4 e-membrane vesicle, which is targeted to the lysosome.
5 th a loss in the degradative function of the lysosome.
6 docytic cargo delivery to and degradation in lysosomes.
7 Galphas in endosomal sorting of receptors to lysosomes.
8 ause a block in the fusion of autophagosomes/lysosomes.
9 onoubiquitinated at K374, and is degraded in lysosomes.
10 ogenesis by controlling the acidification of lysosomes.
11 including secretory granules, endosomes, and lysosomes.
12 ted with LC3, and matured into antibacterial lysosomes.
13 on with early endosomes, late endosomes, and lysosomes.
14  molecule that is predicted to accumulate in lysosomes.
15 riazole, also blocks cholesterol export from lysosomes.
16 inutes and then transported to endosomes and lysosomes.
17 the types of organelle such as endosomes and lysosomes.
18 acellular compartments such as endosomes and lysosomes.
19 ase (V-ATPase), a proton pump that acidifies lysosomes.
20  clustering and fusion of late endosomes and lysosomes.
21 side autophagosomes as cargo for delivery to lysosomes.
22 umin distribution between late endosomes and lysosomes.
23 h build-up of Tau oligomers in enlarged auto-lysosomes.
24  is specifically targeted for degradation by lysosomes.
25 ith Arl8b and its subsequent localization to lysosomes.
26 g the membrane potential and pH stability in lysosomes.
27  target transferrin and sphingomyelin to the lysosomes.
28 rt allows the toxins to evade degradation in lysosomes.
29 aggregate, and the complexes are diverted to lysosomes.
30 ves enclosure within endosomes and secretory lysosomes.
31 f the resistant clones, T-DM1 accumulated in lysosomes.
32 tors and sphingomyelin, are delivered to the lysosomes.
33 entation of ER tubules and their delivery to lysosomes.
34 rects degradation of cytoplasmic material in lysosomes.
35 cles move on microtubule tracks to fuse with lysosomes.
36  which slowed the trafficking of TLR9 toward lysosomes.
37 er to displace phagosomes toward perinuclear lysosomes.
38 es the calcium signalling and homeostasis of lysosomes.
39 nternalized PGPFs before trafficking them to lysosomes.
40 d recycling, which delivers nutrients to the lysosomes.
41 ays: autophagy and rerouting of endosomes to lysosomes.
42 adation of endocytic and autophagic cargo in lysosomes.
43 or signaling in the heart involves NAADP and lysosomes.
44 ccumulation of sequestered substrates within lysosomes.
45 lective degradation of cytosolic proteins in lysosomes.
46 e accumulation of pMHC inside late endosomes/lysosomes.
47 g endosomes and autophagosomes from reaching lysosomes.
48 of MKK4 to lysosomes, activating p38 MAPK at lysosomes.
49 lization, except for greater accumulation in lysosomes.
50 the redirection of the Notch receptor to the lysosome, a novel mechanism.
51 ing mechanisms and disease relevance of such lysosome accumulations are not well understood.
52 pite of the nanofactories being localized in lysosomes, acidic organelles that contain a variety of p
53 endent activation and recruitment of MKK4 to lysosomes, activating p38 MAPK at lysosomes.
54  increase of lysosomal biogenesis induced by lysosome alkalizers or serum starvation.
55               Proper glue degradation within lysosomes also requires the Uvrag-containing Vps34 lipid
56 ction of Stx3 is localized to late endosomes/lysosomes, although how it traffics there and its functi
57 ration and metastasis through stimulation of lysosome-anchored Rab7 activity.
58 the lysosome impacts Ca(2+) release from the lysosome and impedes the activity of specific lysosomal
59 tivator increased LAMP2A localization at the lysosome and increased cell survival.
60 cific adapter Vac17 to attach to the vacuole/lysosome and initiate transport.
61 and mouse, is localized to the late endosome/lysosome and interacts with the lysosomal v-ATPase to ne
62  generated via lysosomal proteolysis to exit lysosomes and activate mTORC1.
63 ceptor, and facilitated the acidification of lysosomes and degradation of CTSDmat.
64 f retinal lipofuscin that accumulates in RPE lysosomes and drives the pathogenesis of Stargardt macul
65 lysosomes and promote contacts between FYCO1 lysosomes and endoplasmic reticulum that contain the Ptd
66 but traffic rapidly from the cell surface to lysosomes and have a half-life of less than two hours.
67 uch defects result in protease deficiency in lysosomes and impaired lysosomal proteolysis, as evidenc
68 hereupon IgG is diverted from degradation in lysosomes and is recycled.
69 d mTOR were co-increased and co-localized to lysosomes and physically interacted in lal(-/-) ECs.
70 y comparing the biomolecular compositions of lysosomes and plasma membranes isolated from wild-type a
71 ent of the PtdIns3P-binding protein FYCO1 to lysosomes and promote contacts between FYCO1 lysosomes a
72  in polarization of CD103 and recruitment of lysosomes and Pxn at the contact zone of T lymphocytes w
73 h retromer rescues Glut4 from degradation in lysosomes and retrieves it to the TGN, where insulin--re
74 suggest a possible Ca(2+) buffering role for lysosomes and shed new light on lysosomal functions duri
75 nous PCSK9-mediated degradation in endosomes/lysosomes and showed reduced LDL internalization and deg
76 ase IRAP, the trafficking of CpG and TLR9 to lysosomes and signaling via TLR9 were enhanced in DCs an
77 fusion between damaged phagosomes and intact lysosomes and thereby preserve endolysosomal integrity.
78 focus in particular on the common roles that lysosomes and tunneling nanotubes play in the formation
79  and thereby triggered degradation of YAP in lysosomes and, consequently, relief of YAP-mediated inhi
80 pH, a reduced LDL delivery to late endosomes/lysosomes, and an increased release in the medium of the
81 on, fusion of autophagosomes/amphisomes with lysosomes, and apoptosis.
82 g probes selectively targeting mitochondria, lysosomes, and F-actin demonstrate low toxicity and enab
83 vesicles (M7Vs) are distinct from endosomes, lysosomes, and other familiar vesicles or organelles.
84  pH that delineates individual endosomes and lysosomes, and the therapeutic intracellular target of t
85 in such situations may be largely unfused to lysosomes, and their formation/accumulation under these
86 mal degradation, promote SAA accumulation in lysosomes, and ultimately damage cellular membranes and
87 e vesicles coalesce/aggregate and markers of lysosomes are decreased.
88                     We present evidence that lysosomes are intimately associated with the sarcoplasmi
89 mulation of lipids and swollen dysfunctional lysosomes are linked to several neurodegenerative diseas
90 rade direction toward the soma, where mature lysosomes are mainly located.
91 m distal axons toward the soma, where mature lysosomes are mainly located.
92                                              Lysosomes are membrane-bound organelles mainly involved
93                                              Lysosomes are organelles responsible for the breakdown a
94 g to formation of endo-lysosome-free or endo-lysosome-associated alphaS aggregates, respectively.
95                                          The lysosome-associated membrane protein (LAMP) family inclu
96 compartment, followed by colocalization with lysosome-associated membrane protein 1 (LAMP1)-positive
97 , including alpha-dystroglycan (alphaDG) and lysosome-associated membrane protein 1 (LAMP1).
98 lved in cholesterol export from LEs, and the lysosome-associated membrane proteins (LAMP) 1 and 2 are
99                           Thus, KICSTOR is a lysosome-associated negative regulator of mTORC1 signall
100 ncreased expression of Rab7, a late endosome/lysosome-associated small GTPase.
101 inetics of accumulation of the polyplexes in lysosomes at a similar rate.
102  first time that neuronal activity positions lysosomes at the dendritic spines to facilitate synaptic
103 in Vamp-7 to promote the local exocytosis of lysosomes at the immune synapse, which is required for e
104             By slowing substrate delivery to lysosomes, autophagosome maturational delay, as further
105                         KICSTOR localizes to lysosomes; binds and recruits GATOR1, but not GATOR2, to
106  that lysosome fission is implicated in both lysosome biogenesis and reformation, our findings sugges
107 ey lysosomal Ca(2+) channel controlling both lysosome biogenesis and reformation.
108 ransport to fulfil its function in promoting lysosome biogenesis in the soma, suggesting a potential
109 iptional program that promotes autophagy and lysosome biogenesis.
110 rface-internalized FN is not degraded by the lysosome but instead undergoes recycling and incorporati
111 autophagosomes located in close proximity to lysosomes but not fused with them.
112 AAA-ATPase, p97, in the clearance of damaged lysosomes by autophagy.
113 rigin: blocking the exit of cholesterol from lysosomes by U18666A or NPC1 siRNA prevents ER cholester
114                                 In addition, lysosomes can expel their contents outside of the cell v
115 nd impaired substrate translocation into the lysosome caused by defective CMA in cystinosis.
116 etion of Protrudin or FYCO1, mTORC1-positive lysosomes cluster perinuclearly, accompanied by reduced
117 c cellular uptake and accumulation of MPO in lysosomes coincides with N-retinylidene-N-retinylethanol
118 argeted preferentially to the late endosomes/lysosomes compared with wild-type Htt.
119 ot colocalized with Zn granules found in the lysosome-containing vesicles or Fe agglomerates in the i
120                     We found that microglial lysosome content is also increased as a result of MD.
121 pond to monocular deprivation with increased lysosome content, but signaling through the fractalkine
122 we show that microglial anatomical features, lysosome content, membrane properties, and transcriptome
123 egradation, the contribution of ELMO1 to the lysosome degradation pathways was evaluated by studying
124 und LKB1 phosphorylates SRA resulting in its lysosome degradation.
125                                              Lysosomes degrade cellular components sequestered by aut
126                                          The lysosome degrades and recycles macromolecules, signals t
127 .1, channels through a protein kinase C- and lysosome-dependent mechanism, reducing abundance at the
128 ative agent of Q fever, establishes a unique lysosome-derived intracellular niche termed the Coxiella
129 t builds an invasive protrusion, an isolated lysosome-derived membrane structure specialized to breac
130 dings illustrate how a general mechanism for lysosome dispersal in nonneuronal cells is adapted to dr
131 -subunit complex previously found to promote lysosome dispersal through coupling to the small GTPase
132 endent of TFEB, TFEB up-regulation corrected lysosome distribution and lysosomal LAMP2A localization
133 ells, we visualized alphaS aggregation, endo-lysosome distribution, and endo-lysosome rupture in real
134 use the pH range of 4-7 in the endosomes and lysosomes does not provide complete cleavage of the drug
135 somes and induces the progressive failure of lysosomes, each of which are directly linked by distinct
136 o intracellular transport and then fuse with lysosomes, endosomes and multivesicular bodies through m
137 gnaling and recruitment of IRF7 and p85 into lysosomes, enhancing their degradation.
138 e that endogenous CSPalpha is present in the lysosome-enriched fractions and co-localizes with lysoso
139 , increased levels of lysosomal proteins and lysosome enzyme activities.
140 tophagy can clear mitochondria, peroxisomes, lysosomes, ER, chloroplasts, and the nucleus.
141                                    Localized lysosome exocytosis fuels generation of large, invasive
142 creted lysosomal enzymes and SNAP23-mediated lysosome exocytosis.
143 te that LDL-derived cholesterol travels from lysosomes first to PM to meet cholesterol needs, and sub
144 y TRPML1, suggesting that TRPML1 may promote lysosome fission by activating CaM.
145                                   Given that lysosome fission is implicated in both lysosome biogenes
146                      Consequently, autophagy-lysosome flux and mitochondrial function are compromised
147 ed in transport of cytosolic proteins to the lysosome for degradation.
148 teins that mediate bacterial delivery to the lysosome for degradation.
149 way that delivers cellular components to the lysosome for degradation.
150 nted organelles or proteins are delivered to lysosomes for degradation through autophagosomes.
151 ion, these endosomes deliver mitochondria to lysosomes for degradation.
152 process delivering cytoplasmic components to lysosomes for degradation.
153 port, which facilitates BACE1 trafficking to lysosomes for degradation.
154 d glial cells by affecting their delivery to lysosomes for degradation.
155 transport, and fusion of autophagosomes with lysosomes for degradation.
156 d process that delivers cellular material to lysosomes for degrading, recycling, and generating molec
157                    Furthermore, we show that lysosomes form close associations with mitochondria (med
158 s, and with sparse multivesicular bodies and lysosomes found in our reconstructions.
159 sosome rupture, leading to formation of endo-lysosome-free or endo-lysosome-associated alphaS aggrega
160 phagosome and endosome maturation and proper lysosome function in Drosophila melanogaster We demonstr
161  and the importance of TFEB to autophagosome-lysosome function in these cells.
162 g of ER-mediated endosomal tubule fission to lysosome function links different classes of HSP protein
163 gether, these data reveal that proper LE and lysosome function positively contributes to liver-stage
164 erged as a master regulator of autophagosome-lysosome function, controlling the expression of several
165  for ER-mediated endosomal tubule fission in lysosome function, similar lysosomal abnormalities were
166                               Phagosome-with-lysosome fusion (PLF) results in the delivery of lysosom
167 syntaxin 17, a SNARE promoting autophagosome-lysosome fusion and cargo degradation.
168 loidogenic function, promoting autophagosome-lysosome fusion and increasing betaCTF degradation.
169          Second, CYCLO impeded autophagosome-lysosome fusion as evidenced by the accumulation of LC3,
170  indicating that P27 itself blocks phagosome-lysosome fusion by modulating the traffic machinery in t
171 osomal Ca(2+) release channel P2X4 regulates lysosome fusion through a calmodulin (CaM)-dependent mec
172 achinery regulates fragment formation during lysosome fusion to control morphology and protein lifeti
173 ed that IBDV infection induced autophagosome-lysosome fusion, but without active degradation of their
174                                Dysfunctional lysosomes give rise to lysosomal storage disorders as we
175 is of autophagosomes subsequently unfused to lysosomes) has not been investigated previously.
176 anism by which cells deliver material to the lysosome, has been associated with resistance to antican
177                 Reducing chloride within the lysosome impacts Ca(2+) release from the lysosome and im
178 owth regulator that becomes activated at the lysosome in response to nutrient cues.
179 tionship on the distribution and motility of lysosomes in dendrites.
180 tions, we investigated the roles of TFEB and lysosomes in intracellular Ca(2+) homeostasis.
181 osomal distribution is linked to the role of lysosomes in many cellular functions, including autophag
182 als (bpAPs) could elicit Ca(2+) release from lysosomes in the dendrites.
183 L-6 infusion stimulates a robust increase in lysosomes in the pancreas that is restricted to the isle
184 iated with membranes in, e.g., endosomes (or lysosomes) in the cytosol.
185 idic and proteolytic, ultimately fusing with lysosomes, in a process termed "phagosome maturation." I
186                                    Activated lysosomes, in turn, promote a metabolic shift that mobil
187 ashion, of many essential amino acids out of lysosomes, including leucine, which mTORC1 senses throug
188                                 We find that lysosome inhibition alters their mobility and also decre
189 ither rapidly degraded or forms amyloid in a lysosome-initiated process.
190 f most essential amino acids, converting the lysosome into a cellular depot for them.
191 , and their degradation and recycling in the lysosome is essential for cellular maintenance.
192                             We find that the lysosome is highly enriched in chloride, and that chlori
193                     Rupture of endosomes and lysosomes is a major cellular stress condition leading t
194                  We also find trafficking of lysosomes is correlated with synaptic alpha-amino-3-hydr
195 30 from the trans-Golgi network (TGN) toward lysosomes is mediated by the sorting receptor sortilin i
196 recruitment of host late endosomes (LEs) and lysosomes is reduced in uis4(-) parasites, which lack a
197          These data indicate the position of lysosomes is regulated by synaptic activity and thus pla
198 esized transmembrane cargos to endosomes and lysosomes is thought to occur at the TGN through recogni
199 lathrin-mediated endocytosis and degraded in lysosomes, leading to attenuation of Wnt/beta-catenin si
200                    Accumulation of defective lysosomes leads to lysosomal membrane permeabilization a
201 2+)-permeable channels on late endosomes and lysosomes (LEL).
202  C. elegans homolog of ATP7A/B, localizes to lysosome-like organelles (gut granules) in the intestine
203 tors of cholesterol transport block steps in lysosomes, limiting our understanding of post-lysosomal
204 otein 3 (IFITM3) is a cellular endosome- and lysosome-localized protein that restricts numerous virus
205 of SOG, and reveal an unexpected function of lysosome-located GATOR2 in suppressing mTORC1 signalling
206 n transporters that are then sorted into the lysosome lumen for degradation.
207 ome-enriched fractions and co-localizes with lysosome markers in soma, neurites and synaptic boutons.
208                                              Lysosome-mediated autophagy is essential for cellular su
209 re it prevents PD-L1 from being targeted for lysosome-mediated degradation.
210 ontrols multiple steps in autophagy, a major lysosome-mediated intracellular degradation pathway.
211 fragment formation during homotypic vacuolar lysosome membrane fusion in Saccharomyces cerevisiae Usi
212 ole protein sorting complex (HOPS) to (phago)lysosome membranes, whereas PI(3)P is required for membr
213       However, rather than being degraded by lysosomes, mitochondrion-containing autophagosomes are r
214 at the TFEB/TMEM55B/JIP4 pathway coordinates lysosome movement in response to a variety of stress con
215                  The mechanisms that control lysosome movement in these domains, however, remain poor
216 storage lipids in selectively late endosomes/lysosomes of NPC1-KO cells.
217 iated cellular uptake and delivery of MPO to lysosomes of retinal pigmented epithelial (RPE) cells ac
218 ouples mTORC1 activation to the release from lysosomes of the essential amino acids needed to drive c
219 r conversion to lipofuscin accumulate in the lysosomes of the retinal pigment epithelium and display
220 ell known to target membrane proteins to the lysosome or vacuole for degradation, can also function a
221 ukaryotic cells are self-digested within the lysosome or vacuole.
222 gene (LYST), resulting in formation of giant lysosomes or lysosome-related organelles in several cell
223 on of autophagosomes subsequently unfused to lysosomes (or accumulation of autophagosomes) directly i
224   However, despite hENT3's prominent role in lysosome pathophysiology, the molecular basis of hENT3-m
225 t the synapse fails to explain the autophagy-lysosome pathway (ALP) dysfunction in cells from AD-ANCL
226 broblasts HSP70, ubiquitin and the autophagy-lysosome pathway proteins Lamp2 and p62 relocalized to t
227 Emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mito
228 as evidence for alterations in the autophagy-lysosome pathway.
229 ll as the ubiquitin-proteasome and autophagy-lysosome pathways, resulting in myotube atrophy.
230 nd organelles (endoplasmic reticulum, Golgi, lysosome, peroxisome, mitochondria and lipid droplet) an
231                            Within the acidic lysosome (pH 4.5) after mitophagy, mt-Keima undergoes a
232 g disorders and emphasize the essential role lysosomes play in myelination.
233                                              Lysosomes play key roles in the cellular response to ami
234                                          The lysosome plays an important role in maintaining cellular
235 strate that amino acid availability controls lysosome positioning through Ragulator-dependent, but mT
236  with SKIP for Arl8b binding, which dictates lysosome positioning.
237                                  In neurons, lysosomes regulate alpha-amino-3-hydroxy-5-methyl-4-isox
238 ity-dependent exocytosis of Cathepsin B from lysosomes regulates the long-term structural plasticity
239         We further show that mutants lacking lysosome-related organelles are defective in the product
240 d or fibrocystin, requires the biogenesis of lysosome-related organelles complex-1 (BLOC-1) for cilia
241                                Biogenesis of lysosome-related organelles complex-1 (BLOC-1) is a prot
242 resulting in formation of giant lysosomes or lysosome-related organelles in several cell types.
243 cyl-CoA synthetase ACS-7, which localizes to lysosome-related organelles, is specifically required fo
244 s suggest a key role for miR-153 in endosome/lysosome-related pathways during amelogenesis.
245 deed, specifically targeting Bax only to the lysosome restores autophagic cell death in Bax/Bak1 null
246                                              Lysosomes robustly accumulate within axonal swellings at
247 ytosis-mediated seeding associated with endo-lysosome rupture and have significantly reduced seeding
248 gation, endo-lysosome distribution, and endo-lysosome rupture in real-time.
249 t not in age-matched controls, suggests endo-lysosome rupture is involved in the formation of alphaS
250 ma membrane or via endocytosis-mediated endo-lysosome rupture, leading to formation of endo-lysosome-
251  we show that p97 helps clear late endosomes/lysosomes ruptured by endocytosed tau fibrils.
252 d that brief pharmacological perturbation of lysosomes shortly after the pff treatment causes aberrat
253 olocalized with p85 and IRF7 within LAMP1(+) lysosomes, suggestive of a role in degradation.
254 Rn-binding affinity was directed less to the lysosomes, suggestive of FcRn-directed albumin salvage f
255           Fourier analysis of immunolabelled lysosomes suggests a sarcomeric pattern (dominant wavele
256 Here we show that a decline in the autophagy-lysosome system contributes to this as evidenced by a de
257 n of the GATOR1 component DEPDC5, and by the lysosome-targeted GATOR2 component WDR59 or lysosome-tar
258                    We propose that WipB is a lysosome-targeted phosphatase that modulates cellular nu
259  lysosome-targeted GATOR2 component WDR59 or lysosome-targeted SESN2.
260 affecting other organelles (early endosomes, lysosomes, the Golgi apparatus, the endoplasmic reticulu
261 ysfunction causes secondary failure of local lysosomes, thereby impairing the turnover of ganglioside
262 soma and thus enhances protease transport to lysosomes, thereby restoring lysosomal proteolytic activ
263 marks of the plasma membrane, endosomes, and lysosomes, these compartments contain other functionally
264                               At the vacuole/lysosome, they are integrated by the homotypic fusion an
265 activity is low, cholesterol is delivered to lysosomes through two membrane trafficking pathways: aut
266                TMEM55B overexpression causes lysosomes to collapse into the cell center, whereas depl
267 ogy or degranulation, but it causes LAMP1(+) lysosomes to engorge.
268 rotein (STAMBP) impedes NALP7 trafficking to lysosomes to increase NALP7 abundance.
269                               The ability of lysosomes to move within the cytoplasm is important for
270 n conjugates from a subpopulation of damaged lysosomes to promote autophagosome formation.
271 nteraction, explaining the redistribution of lysosomes to the juxtanuclear area.
272 s a protein kinase complex that localizes to lysosomes to up-regulate anabolic processes and down-reg
273 face, inducing dynein-dependent transport of lysosomes toward the microtubules minus-end.
274 imaging and electron microscopy to show that lysosomes traffic bidirectionally in dendrites and are p
275                                  Strikingly, lysosomes traffic to dendritic spines in an activity-dep
276 ir apical cytoplasm, rearrange mitochondrial/lysosome trafficking, and generate large secretory granu
277 in coordinating cytoskeleton remodeling with lysosome trafficking, the cellular machinery associated
278 sion of Protrudin and FYCO1, mTORC1-positive lysosomes translocate to the cell periphery, thereby fac
279          We conclude that PtdIns3P-dependent lysosome translocation to the cell periphery promotes mT
280 3 (JIP3) as an important regulator of axonal lysosome transport and maturation.
281 uction is amplified by plaque-induced axonal lysosome transport defects.
282 h the critical role of JIP3-dependent axonal lysosome transport in regulating amyloidogenic amyloid p
283 HHC20 colocalized extensively with IFITM3 at lysosomes unlike ZDHHCs 3, 7, and 15, which showed a def
284  at the BM breach site directs exocytosis of lysosomes using the exocyst and SNARE SNAP-29 to form a
285 sensor CaM is required for the regulation of lysosome/vacuole size by TRPML1, suggesting that TRPML1
286           Moreover, the effects of TRPML1 on lysosome/vacuole size regulation were eliminated by Ca(2
287       In this study, we report that enlarged lysosomes/vacuoles induced by either vacuolin-1 or P2X4
288  TRPML1 facilitated the recovery of enlarged lysosomes/vacuoles.
289                         The acidification of lysosomes was facilitated in cells transfected with PGRN
290 e of the JIP3-dependent regulation of axonal lysosomes was revealed by the worsening of the amyloid p
291 ocalize with the lysosomal marker LAMP2, and lysosomes were redistributed and dramatically reduced in
292 evealed that activated STING traffics to the lysosome, where it triggers membrane permeabilization an
293                               RVs fused with lysosomes, whereas associated phagosomes typically did n
294 by Pho85/CDK5 via signaling from the vacuole/lysosome, which is distinct temporally and spatially fro
295  of B-cells relies on the local secretion of lysosomes, which are recruited to the Ag contact site by
296                                  In neurons, lysosomes, which degrade membrane and cytoplasmic compon
297 nternalized and accumulate in late endosomes/lysosomes, while aminolipid-SPIONs reside at the plasma
298 reduced number and increased translucency of lysosomes, while total glycogen content remained unchang
299  This Ca(2+) release triggered the fusion of lysosomes with the plasma membrane, resulting in the rel
300 out mouse neuron primary cultures accumulate lysosomes within focal axonal swellings that resemble th

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