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1 r mTORC1 translocation and activation at the lysosome.
2 accumulation of undegraded substrates in the lysosome.
3 e in response to degradative products of the lysosome.
4 of the C. burnetii-containing vacuole to the lysosome.
5 Rheb), which in turn activates mTORC1 at the lysosome.
6 ential localization of the holoenzyme to the lysosome.
7  that delivers cytoplasmic components to the lysosome.
8 e with WLS and the degradation of WLS in the lysosome.
9  and diminished levels of the enzymes at the lysosome.
10 hagosomes deliver cytoplasmic content to the lysosome.
11 ence in response to LD interactions with the lysosome.
12 agic vesicle to the recycling organelle, the lysosome.
13  back to the cell surface or degraded by the lysosome.
14 protein (LDL), which releases cholesterol in lysosomes.
15 lowered chloride (Cl(-)) content in PSEN1 KO lysosomes.
16  result in an accumulation of cholesterol in lysosomes.
17 that PQLC2 transports across the membrane of lysosomes.
18 URF2 knockdown increases receptor sorting to lysosomes.
19  of unwanted proteins and organelles through lysosomes.
20 aracterized by dysfunctional mitochondria or lysosomes.
21 ins associated with the cytosolic surface of lysosomes.
22  availability of cationic amino acids within lysosomes.
23 inant localization within autophagosomes and lysosomes.
24 y-lipoprotein (LDL)-derived cholesterol from lysosomes.
25 anced the trafficking of phagocytic cargo to lysosomes.
26 y proximal tubular cells, and transferred to lysosomes.
27 ce and subsequently degraded in the hub cell lysosomes.
28 zation of DAF-4/BMPRII to late endosomes and lysosomes.
29 of the cysteine importer for melanosomes and lysosomes.
30 QLC2 mediates C9orf72 complex recruitment to lysosomes.
31  that regulates C9orf72 complex abundance on lysosomes.
32 ar ATPase (vATPase) V0a1 subunit delivery to lysosomes.
33 tion of TAK1 thus activating AMPK on damaged lysosomes.
34 to discover that type I IFN (IFN-I) remodels lysosomes.
35  protease activity, and proteomic profile of lysosomes.
36 f surrounding autophagosomes for delivery to lysosomes.
37 ely, HS-5 cells) by trafficking the BTZ into lysosomes.
38 units and is targeted for degradation within lysosomes.
39 m from defective end-step proteolysis inside lysosomes.
40 r are expressed ubiquitously and localize to lysosomes.
41 les that are morphologically compatible with lysosomes.
42  and Tom1 to ensure their trafficking to the lysosomes.
43 oplasmic reticulum (ER) and reroutes them to lysosomes.
44 cellular accumulation of free cholesterol in lysosomes.
45 erived quality control carriers destined for lysosomes.
46  cell death due to excessive phagocytosis of lysosomes.
47  promotes LDLR degradation in late endosomes/lysosomes.
48 ed vesicles (MDVs) to facilitate delivery to lysosomes.
49 disease, whereas loss of ATP13A2 compromises lysosomes(3).
50 ls lacking functional Rag heterodimer on the lysosome accumulate Ub-Rheb, and blockade of its degrada
51 ar ATPase subunit VMA5 expression, impairing lysosome acidification and inhibiting autophagic protein
52  mutation abolished lysosome enlargement and lysosome acidification induced by wild-type TMEM106B ove
53                              IFN-I-dependent lysosome acidification was associated with elevated intr
54 uding IFITM3, SLC15A3, and CNP contribute to lysosome acidification.
55                    Here, we reveal that endo-lysosomes act as platforms for a new phagocytic signalli
56 n response to external and internal stimuli, lysosomes actively adjust their distribution between per
57 sphate inhibited phagosome acidification and lysosome activity in D. discoideum and macrophages and r
58 y cytoplasmic components are degraded within lysosomes, allowing cells to maintain energy homeostasis
59                        Dynamic regulation of lysosomes allows them to play key roles in cell and tiss
60                   It is also unknown whether lysosomes alone might be sufficient to mediate LD turnov
61 idase 1 (NEU1) form a multienzyme complex in lysosomes along with the molecular chaperone, protective
62                                          The lysosome also extensively communicates with other cellul
63 litates the binding of mTORC1 to Rheb on the lysosome and is another crosstalk between the amino acid
64 th-promoting and catabolic activities of the lysosome and undergo a complex interplay that enables ce
65 mal morphology with enlarged electron-lucent lysosomes and an increased lysosomal content, which was
66  with changes in the location and density of lysosomes and autophagosomes along the axon shaft.
67                                           At lysosomes and endosomes, the Fab1 lipid kinase complex a
68  localized to the membranes of endosomes and lysosomes and is not present or functional on the plasma
69 e role of Arl8B, an adaptor molecule between lysosomes and kinesins.
70  to monitor the dynamic interactions between lysosomes and LDs in real-time.
71                   Coupling APEX2 labeling of lysosomes and metabolic labeling of protein, we identify
72 nduces an increase in the number and size of lysosomes and modifies the pH of these organelles from ~
73 positional and functional alterations in NPC lysosomes and nature of aberrant cholesterol-mTORC1 sign
74 eads to abnormalities in the distribution of lysosomes and PLP1.
75 essed ectopically in HeLa cells localizes to lysosomes and raises lysosomal pH, suggesting that in me
76 ds to the decreased sorting of hydrolases to lysosomes and reduces the autophagic degradation.
77 ulated recruitment of the C9orf72 complex to lysosomes and reveal a novel mechanism that allows cells
78 ealizes endogenous beta-gal visualization in lysosomes and shows brighter fluorescence than Hx-Gal in
79 se cathepsin A (CatA) is distributed between lysosomes and the extracellular matrix (ECM).
80                                           In lysosomes and the ruffled border of osteoclasts, CLC-7 r
81 ing the complement system, oxidative stress, lysosomes, and inflammation is prominent in the later ph
82 ological alterations (endoplasmic reticulum, lysosomes, and NFkB) caused by these samples.
83 ganelles such as mitochondria, chloroplasts, lysosomes, and the endoplasmic reticulum.
84                             Mitochondria and lysosomes are critical for cellular homeostasis, and dys
85                             Mitochondria and lysosomes are functionally linked, and their interdepend
86                                              Lysosomes are in the center of the cellular control of c
87 vious study, we showed that acidified amebic lysosomes are required for both amebic trogocytosis and
88 recently to integrate novel functions of the lysosome as a key signaling center, which can steer the
89    Together, these discoveries highlight the lysosome as a regulatory hub for cellular and organismal
90 y-independent processes of cargo delivery to lysosomes as well as nutrient-dependent lysosomal signal
91                                   Studies of lysosome associated protein transmembrane 4B (LAPTM4B) h
92 utophagy sequestration of Mtb, evolving into lysosome-associated autophagosomal Mtb degradation linke
93  propose that MDV trafficking is mediated by lysosome-associated membrane protein 1 (LAMP-1)-positive
94 lized tetherin is sequestered in a CD63- and lysosome-associated membrane protein 1 (LAMP1)-positive
95 idase (APEX) gene to the endogenous locus of lysosome-associated membrane protein 1 (LAMP1).
96  patients identified increased expression of lysosome-associated membrane protein 3 (LAMP3/CD208/DC-L
97 ding synergy is exclusively dependent on the lysosome biogenesis and autophagy transcription factor H
98 LN6 and the EGRESS complex as key players in lysosome biogenesis and shed light on the molecular etio
99 tion requires the induction of autophagy and lysosome biogenesis for the efficient recycling of macro
100 ysosomal compartments and is involved in the lysosome biogenesis in mammalian cells.
101 tyk knockdown inhibits notochord vacuole and lysosome biogenesis through mTORC1-dependent repression
102 increases association between mTORC1 and its lysosome-borne activators, leading to mTORC1 hyperactivi
103 that SKIP is not just a passive connector of lysosome-bound ARL8 to kinesin-1 but is itself subject t
104 ells where PS is low, LDL cholesterol leaves lysosomes but fails to reach the ER, instead accumulatin
105    Several nanomaterials can be entrapped in lysosomes, but the development of functional nanomateria
106  V-ATPase assembly and activity in mammalian lysosomes, but the signaling pathways controlling this e
107 , such as TPP1, which are transported to the lysosome by receptors, such as M6PR and LRP1, are critic
108 beta-Gal negatively regulates NEU1 levels in lysosomes by competitively displacing this labile sialid
109 esponse to nutrients, mTORC1 is activated on lysosomes by Rag and Rheb guanosine triphosphatases (GTP
110 hexosylganglioside (FucGM1) antibodies using lysosome-cleavable valine-citrulline dipeptide linkers v
111 we found that TMEM106B deficiency results in lysosome clustering in the perinuclear region and a decr
112                       Instead, it stimulates lysosome clustering near the nucleus as seen in TMEM106B
113 hly oxidizing reactive oxygen species in the lysosome combined with a cell-protective expression of t
114  to precisely localize sites of mitochondria-lysosome contact and reveal increases in local viscosity
115 roblasts and found both altered mitochondria-lysosome contact dynamics and defective contact-dependen
116 mitochondrial calcium uptake at mitochondria-lysosome contact sites was modulated by the outer and in
117 ch was mediated by tethering of mitochondria-lysosome contact sites.
118 on mitochondria associated with mitochondria-lysosome contact.
119       Thus, our work highlights mitochondria-lysosome contacts as key contributors to interorganelle
120 scopy, we identified a role for mitochondria-lysosome contacts in regulating mitochondrial calcium dy
121                However, whether mitochondria-lysosome contacts serve additional functions by facilita
122 ced trafficking of this mutant Mtb strain to lysosomes correlated with enhanced intracellular bacteri
123 strated that the degradative activity of the lysosome created by proteases, such as TPP1, which are t
124 tic release of beta-coronaviruses results in lysosome deacidification, inactivation of lysosomal degr
125 he mTOR pathway, reduces the number of large lysosomes, decreases apoptosis, and activates autophagy,
126 ny cellular functions, from cell division to lysosome degradation and autophagy.
127 nd is subjected to cytoplasmic autophagosome-lysosome degradation, via the autophagy protein LC3.
128 nction impedes Endoplasmic Reticulum (ER)-to-lysosome delivery of ClC-7.
129 ysosomal polyamine export as a mechanism for lysosome-dependent cell death that may be implicated in
130 g high levels of autophagy, an intracellular lysosome-dependent degradative pathway that clears the c
131 ate oxidative stress and promote autophagy-a lysosome-dependent degradative pathway that disposes of
132                               Autophagy is a lysosome-dependent intracellular degradation system requ
133                         However, we reveal a lysosome-dependent reaction that cleaves the GLUT8 prote
134 al steroidogenesis, suggesting conversion of lysosome-derived cholesterol to pregnenolone.
135 acterial pathogen that replicates inside the lysosome-derived Coxiella-containing vacuole (CCV).
136 lysosomes is instrumental for characterizing lysosome-driven pathways at the molecular level and moni
137 , and occupancy, which report on activity of lysosome-driven pathways.
138 tosis, reflecting its failure to localize to lysosomes due to CDK1-dependent RAPTOR phosphorylation.
139 n of ponatinib uptake and sequestration into lysosomes during the development of acquired drug resist
140  measure pHlys for improved understanding of lysosome dynamics, which is increasingly considered a th
141 endomembrane components including endosomes, lysosomes, endoplasmic reticulum and Golgi.
142 omains 2 (ADAP2), gamma-interferon-inducible lysosome/endosome-localized thiolreductase (GILT), and l
143 , we found that the D252N mutation abolished lysosome enlargement and lysosome acidification induced
144   We show that HPgammaCD treatment increases lysosome-ER association and enhances autophagic activity
145 ling of protein, we identify that individual lysosomes exhibit substantial heterogeneity in protein a
146  in the perinuclear region and a decrease in lysosome exocytosis and cell surface PLP levels.
147 luding direct plasma membrane translocation, lysosome exocytosis, exosome formation, membrane vesicul
148  that modulates secretion routes, increasing lysosome exocytosis.
149 utophagy) targets cytoplasmic cargoes to the lysosome for degradation.
150 s the targeting of cytosolic material to the lysosome for degradation.
151 proteins and organelles are delivered to the lysosome for degradation.
152 gos, which are subsequently delivered to the lysosome for degradation.
153 Tf-independent pathway and trafficked to the lysosome for degradation.
154 h cytoplasmic contents are trafficked to the lysosome for degradation.
155 or surplus mitochondria via targeting to the lysosome for destruction.
156 ntracellular components and delivers them to lysosomes for degradation and recycling.
157 mes transfer cytosolic material to acidified lysosomes for degradation following soluble N-ethylmalei
158 ed signaling receptors and other proteins to lysosomes for degradation, but they also modulate interc
159  which cells deliver cytoplasmic contents to lysosomes for degradation.
160 les and aggregated proteins are delivered to lysosomes for degradation.
161 rting of nephrin from recycling endosomes to lysosomes for degradation.
162 discoveries have transformed the view of the lysosome from a static organelle dedicated to the dispos
163                               Isolated liver lysosomes from mice treated with either of two orally bi
164                       NCs also trafficked to lysosomes from the apical side and, additionally, from t
165 al for ceramide hydrolysis and regulation of lysosome function and cellular homeostasis.
166  We demonstrated that PKR contributes to the lysosome function and regulates misfolded prion protein
167             We propose that IFN-I control of lysosome function broadly impacts host defense against d
168 demonstrate a role for enhanced autophagy or lysosome function in immune evasion by selective targeti
169          We hypothesized that PKR-associated lysosome function is critical for cancer but not normal
170                                              Lysosome function is essential for cellular homeostasis,
171 nduction of the lysosomal genes required for lysosome function.
172                                         Many lysosome functions are determined by a lumenal pH of ~5.
173                             (2020) show that lysosomes fuse with phagosomes to maintain phagosomal me
174 rnover after treatment with an autophagosome-lysosome fusion inhibitor, chloroquine, indicating that
175 omycin-A, an inhibitor of auto-phagosome and lysosome fusion, inhibited poly I:C-induced IDO and HLA-
176 f nanopore-mediated local calcium influx for lysosome fusion, represents a biophysical mechanism for
177 cells because of inhibition of autophagosome-lysosome fusion.
178 xidation, allowing calcium entry to initiate lysosome fusion.
179                                Endosomes and lysosomes harbor Rab5 and Rab7 on their surface as key p
180                         For many decades the lysosome has been recognized as the terminal center of c
181  REporter), which localizes predominantly in lysosomes, has a dynamic range of pH 4.0 to 6.5, and can
182 osomes to promote phagocytosis, whereas endo-lysosome immobilization prevents it.
183 ipid droplets or organelles) to the vacuole (lysosome in mammals) for degradation and recycling.
184 y supplied PA vesicles deliver mTORC1 to the lysosome in the absence of amino acids, Rag GTPases, gro
185 and thereby sustain mTORC1 activation at the lysosome in the absence of amino acids.
186  substrates remains robustly targeted to the lysosome in the absence of several core ATGs, including
187 triggered by loss of cell adhesion activates lysosomes in C. elegans epidermis during developmental r
188  basal mTORC1 activity that drives defective lysosomes in cells and mice, leading to accumulation of
189 ng studies, we found that most endosomes and lysosomes in freshly isolated SMCs from cerebral arterie
190 itochondria, endoplasmic reticulum (ER), and lysosomes in HSC metabolism.
191  monitor the interaction of mitochondria and lysosomes in living cells.
192 in is localized in the ER, Golgi, and in the lysosomes in LMH cells.
193  of the morphology, content, and function of lysosomes in PARK2 KO neurons and reveal an important ne
194 d autophagosome formation and trafficking to lysosomes in primary human monocyte-derived macrophages
195  related beta2-adrenergic agonists reacidify lysosomes in PSEN1 Knock out (KO) cells and fibroblasts
196 e been localized to the mitochondria and the lysosome; including instability of mitochondrial DNA due
197 ated with changes in the complement cascade, lysosomes, innate immune response, and glycosaminoglycan
198                                 Mitochondria-lysosome interactions are essential for maintaining intr
199  dynamic tracking of functional mitochondria-lysosome interactions in living cells.
200 nsity indicates the progress of mitochondria-lysosome interplay during mitophagy.
201    Transport of LDL-derived cholesterol from lysosomes into the cytoplasm requires NPC1 protein; NPC1
202                                          The lysosome is an acidic multi-functional organelle with ro
203                                          The lysosome is an essential catabolic organelle that consum
204               While mTORC1 activation at the lysosome is well characterized, it is not clear how this
205 resolved issue is how ASMase residing within lysosomes is released extracellularly within seconds to
206 sicles can tether with endocytic organelles (lysosomes/late endosomes) by forming membrane contact si
207 the dissociation of mTOR from the surface of lysosomes leading to decreased mTORC1 activation.
208 membrane contacts between the late endosomes/lysosomes (LEL) and the endoplasmic reticulum (ER).
209 lized to the membranes of late endosomes and lysosomes (LELs).
210 phila tissues demonstrate an accumulation of lysosome-like organelles that precedes neurodegeneration
211 r bacterium that replicates within an acidic lysosome-like parasitophorous vacuole (PV) in human macr
212 localization from 6 to 12 months of age with lysosome-like structures observed in the photoreceptors.
213     Here, working in yeast, we show that the lysosome-like vacuole maintains mitochondrial respiratio
214  intracellular pathogen that replicates in a lysosome-like vacuole through activation of a Dot/Icm-ty
215 robial peptides linked to cathepsin B in the lysosomes (MACs) can be applied for the treatment of mul
216 C1) occur on the lysosome surface, increased lysosome mass with aging leads to higher mTORC1 activity
217                                              Lysosomes mediate enzymatic degradation of vesicle cargo
218 ta indicate that one such potential pathway, lysosome-mediated degradation of autophagy cargoes, is c
219 eplete RAS proteins through an autophagosome-lysosome-mediated degradation pathway.
220  estrogen-induced mammary cell death was via lysosome-mediated programmed cell death through upregula
221                                              Lysosome-mediated signalling pathways and transcription
222 llular components through autophagosomes and lysosomes, mediates the downregulation of mammalian SIRT
223 e findings identify a selective mechanism of lysosome membrane turnover that is induced by stress and
224               Here, we describe a peroxisome-lysosome metabolic link that restricts autophagic degrad
225 everal cellular compartments (i.e., nucleus, lysosomes, mitochondria, and cytoplasm) is extremely adv
226 of lysosomes to kinesin-1 and, consequently, lysosome movement toward the cell periphery.
227 WT CASMCs, which was associated with reduced lysosome-multivesicular body (MVB) interaction.
228 ipheral and perinuclear regions and modulate lysosome-nucleus signaling pathways; in turn, the nucleu
229 nal heavy and light chains accumulate in the lysosome of macrophages, leading to histiocytic reaction
230 c material and its subsequent degradation in lysosomes of eukaryotic cells, thereby providing cell-au
231 h partial colocalization in mitochondria and lysosomes of water-soluble thioglycosylated zinc(II) por
232  bacteria did not return to vacuoles such as lysosomes or autophagosomes and macrophages did not die.
233  stress responses that either originate from lysosomes or regulate lysosomal functions.
234 ansported to intra-endothelial compartments (lysosomes) or transcellularly released at the tissue sid
235 imarily accumulate within late endosomes and lysosomes, organelles that participate in the degradatio
236  liposomes also participated in the endosome/lysosome pathway (with high-efficiency BBB crossing obse
237                   Importantly, the autophagy-lysosome pathway contributes to the loss of SIRT1 during
238 dge of how the disease affects the autophagy-lysosome pathway, as activating autophagy when the pathw
239 tatic tumor cells through a macropinocytosis-lysosome pathway, endowing tumor cells with augmented su
240 d mitochondria through the autophagosome and lysosome pathways.
241                                              Lysosome pH (pHlys) is often increased in neurodegenerat
242  (0 < 5.0), allowed us to specifically stain lysosomes (pH ~ 4.5-5.0) in live cells.
243  pathways included the complement system and lysosome/phagosome pathways.
244 d innate immunity, the complement system and lysosome/phagosome pathways.
245       Conversely, Rap1 depletion expands the lysosome population, which markedly increases associatio
246                                              Lysosomes promote cellular homeostasis through macromole
247                           The levels of many lysosome proteins are significantly decreased in the TME
248 and specifically causes EZH2 degradation via lysosomes, reducing the cellular H3K27me3 level.
249  mammals and birds, has been documented as a lysosome-related organelle, the maturation paths of xant
250  a pathway mediating formation of intestinal lysosome-related organelles (LROs) is required for biosy
251 on of SGs might occur in a manner similar to lysosome-related organelles (LROs).
252 ranules and melanosomes, which like WPBs are lysosome-related organelles, we hypothesized that BLOC-2
253 ially entered macrophages and accumulated in lysosomes releasing Isoniazid.
254 ity-control mechanisms that maintain healthy lysosomes remain poorly characterized.
255 r, how the mTORC1 interacts with Rheb on the lysosome remains elusive.
256 owever, the transport function of ATP13A2 in lysosomes remains unclear.
257 between these organelles, the function(s) of lysosomes required to sustain mitochondrial health remai
258           Adequate function of endosomes and lysosomes requires finely tuned luminal ion homeostasis
259 s driven by active AMPK enriched on adjacent lysosomes, revealing previously uncharacterized signalin
260 ing conjugates that bind both a cell-surface lysosome-shuttling receptor and the extracellular domain
261 they remain unable to label mitochondria and lysosomes simultaneously and dynamically track their int
262  a function for LC3 lipidation in regulating lysosome size and activity through microautophagy.
263  machinery, show reduced ability to regulate lysosome size and degradative capacity in response to ac
264 f cystinosis-including cystine accumulation, lysosome size, the autophagy pathway, and apoptosis-and
265 dosis, and its targeting to and stability in lysosomes strictly depend on PPCA.
266 of rapamycin complex 1 (mTORC1) occur on the lysosome surface, increased lysosome mass with aging lea
267                                The autophagy-lysosome system has been identified as a main intersecti
268  and degrees of involvement of the autophagy-lysosome system that have been discovered in ALS/FTD.
269 ear-infrared fluorescent probe Lyso-Gal with lysosome-targeting ability was developed for lysosomal b
270 a similar hemicyanine probe, Hx-Gal, without lysosome-targeting ability, Lyso-Gal realizes endogenous
271 'TLR adaptor interacting with SLC15A4 on the lysosome' (TASL), abrogated responses to endolysosomal T
272 by an intracellular route independent of the lysosome-terminal endocytic pathway.IMPORTANCE Herpes si
273 try of HSV-1 is independent of the canonical lysosome-terminal pathway.
274 is a cysteine protease of late endosomes and lysosomes that can be secreted; it exhibits maximal acti
275 rophages clear pathogens by phagocytosis and lysosomes that fuse with phagosomes are traditionally re
276 the melanosome-the organelle, related to the lysosome, that synthesizes pigment-but have unclear func
277 s that subsequently fuse with the vacuole or lysosome, thereby delivering cargo for degradation.
278 sequestration of unesterified cholesterol in lysosomes, thereby activating the sterol response elemen
279              Finally, HO2 is degraded by the lysosome through chaperone-mediated autophagy, distinct
280 l ion homeostasis and novel pH modulation of lysosomes through beta2-adrenergic regulation of ClC-7,
281 wever, the emerging evidence has brought the lysosome to the center of nutrient sensing as the organe
282 reased autophagosomes and the recruitment of lysosomes to aggresomes following proteasome inhibition.
283 d autophagosomes, which ultimately fuse with lysosomes to enable degradation of their substrates.
284        This interaction inhibits coupling of lysosomes to kinesin-1 and, consequently, lysosome movem
285            However, why cells require acidic lysosomes to proliferate and which nutrients become limi
286 se) ARL8 on the lysosomal membrane to couple lysosomes to the anterograde microtubule motor kinesin-1
287 ude that LDL cholesterol normally moves from lysosomes to the PM.
288 elective autophagy instead reroutes MHC-I to lysosomes, using the ubiquitin-binding receptor NBR1, pr
289                                              Lysosome (vacuole) and mitochondria decline interdepende
290                                  As such the lysosome was attributed a rather passive role in cellula
291           Through proteomic profiling of NPC lysosomes, we find pronounced proteolytic impairment com
292 rorganelle contacts between mitochondria and lysosomes were identified and found to regulate mitochon
293 tarvation, a fraction of p27 is recruited to lysosomes, where it interacts with LAMTOR1, a component
294 lysosomal damage triggers LC3 recruitment on lysosomes, where lipidated LC3 interacts with the lysoso
295 ant phosphoinositide lipids at endosomes and lysosomes, whereas PI 4-phosphates, such as phosphatidyl
296 on of chloride channel-7 (ClC-7) delivery to lysosomes which reverses markedly lowered chloride (Cl(-
297 cific accumulation of AMP-CatB in macrophage lysosomes, which is the key location for bactericidal ac
298 vation in HSCs led to further enlargement of lysosomes while suppressing glucose uptake.
299 ced levels of lysosomal enzymes and enlarged lysosomes with abnormal storage material.
300 abel mitochondria with blue fluorescence and lysosomes with red fluorescence, and the correlation bet

 
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