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1 important roles during the maturation of the phagosome.
2 esulting from an inability to neutralize the phagosome.
3 AP by excluding the p22phox subunit from the phagosome.
4 tant for ubiquitin dynamics on the bacterial phagosome.
5 lated proteins in response to the macrophage phagosome.
6 omotes virulence by detecting the macrophage phagosome.
7  increase in cryptococcal killing within the phagosome.
8 ecruit holotransferrin at the surface of the phagosome.
9 gens within a transient organelle called the phagosome.
10 r production rates and catabolism inside the phagosome.
11 sed by pharmacological neutralization of the phagosome.
12 gocytosis, which sequesters pathogens within phagosomes.
13 ta stp2Delta cells, and occupied more acidic phagosomes.
14  many minutes to engulf these filaments into phagosomes.
15 mation, RVs persisted around bead-containing phagosomes.
16 osis, entrapping them into organelles called phagosomes.
17 I molecules enhances peptide accumulation in phagosomes.
18 ribution and accumulation of cleaved TLR9 to phagosomes.
19 ing Rac2 that maintains a near neutral pH of phagosomes.
20 -, A. fumigatus-, and C. albicans-containing phagosomes.
21 receptor 9 (TLR9)-mediated sensing of DNA in phagosomes.
22 sure chloride levels in phagocytes and their phagosomes.
23 nd localized to the site of partially formed phagosomes.
24 rless strain of Yersinia remains confined to phagosomes.
25 3,4,5)P3, and it persists on PI(3)P-enriched phagosomes.
26 hat ensure efficient killing of pathogens in phagosomes.
27 s of spores, macrophages fail to form mature phagosomes.
28 uired for the recruitment of mitochondria to phagosomes.
29 ly and specifically recruited to early-stage phagosomes.
30 DCs by ensuring optimal TIRAP recruitment to phagosomes.
31 s of synapses containing autophagic vacuoles/phagosomes.
32 sed rate and does not attain maximally sized phagosomes.
33 ote scission of endocytic vesicles, and seal phagosomes.
34 inosa to gauge their exposure to HOCl inside phagosomes.
35 6 was observed to be associated with nascent phagosomes.
36 in maintaining HOCl production in neutrophil phagosomes.
37 sed inhibition of T3S function, allowing for phagosome acidification and bacterial killing.
38 r et al. discover an intriguing link between phagosome acidification and lipid signposts on their out
39 oli and M. smegmatis Polyphosphate inhibited phagosome acidification and lysosome activity in D. disc
40                        Indeed, T3S prevented phagosome acidification and resisted killing inside thes
41 ernalization, identifying a critical role of phagosome acidification to facilitate microbial digestio
42 the MRSA USA300 clone, the USA300-containing phagosome acidified rapidly and acquired the late endoso
43 cells and organelles (e.g., residual bodies, phagosomes) across the seminiferous epithelium.
44  represent a general mechanism for restoring phagosome activity in conditions, where it is lost or im
45 s, including the popular SIINFEKL, can enter phagosomes also via a second unknown energy-dependent me
46                      ELMO1 is present in the phagosome and enhances bacterial clearance by differenti
47  calcium sequestration by melanin inside the phagosome and induction of glycolysis required for effic
48 on, both at an early stage in the macrophage phagosome and later within the necrotic granuloma.
49          Bafilomycin-A, an inhibitor of auto-phagosome and lysosome fusion, inhibited poly I:C-induce
50  by releasing reactive oxygen species in the phagosome and release neutrophil extracellular traps (NE
51 ession programs to survive the nutrient poor phagosome and remodeled the cell wall.
52 nslocation of the autophagy machinery to the phagosome and ultimately LC3 conjugation.
53 h defects in the transport of spermatids and phagosomes and a disruption of cell adhesion most notabl
54 ycobacterium tuberculosis (Mtb) lives within phagosomes and also disrupts these organelles to access
55 ration in Npc1(nmf164) mice, accumulation of phagosomes and autofluorescent material in microglia at
56 nd are crucial for mycobacterial escape from phagosomes and cytosolic translocation.
57 utophagy pathway to facilitate maturation of phagosomes and digestion of their contents.
58 ins play critical roles in the maturation of phagosomes and endosomes following microbial recognition
59 ogenes is able to avoid the NOX2 activity in phagosomes and escape to the cytosol.
60 rotease MarP for Mtb to survive in acidified phagosomes and establish and maintain infection in mice.
61 ive intracellular pathogen that escapes from phagosomes and grows in the cytosol of infected host cel
62 he spatiotemporal dynamics of Mtb-containing phagosomes and identified an interferon-gamma-stimulated
63 in the delivery of lysosomal hydrolases into phagosomes and in digestion of the cargo.
64 rsistent MPs, prevent fusion between damaged phagosomes and intact lysosomes and thereby preserve end
65 ophils and macrophages, engulf microbes into phagosomes and launch chemical attacks to kill and degra
66 r one round of phagocytosis and suggest that phagosomes and lysosomes are capable of bi-directional s
67 somal trafficking, prevent the maturation of phagosomes and modify many signaling pathways inside of
68 ctivity as well as the levels of PA found on phagosomes and phagocytic sites as shown with the PA pro
69 ent macrophage mitochondria are recruited to phagosomes and produce mitochondrially derived reactive
70 nhibits the maturation of R. equi-containing phagosomes and promotes intracellular bacterial survival
71 , hence altering the centripetal movement of phagosomes and their maturation.
72  Moreover, given the localization of IqgC to phagosomes and, most prominently, to macropinosomes, we
73 ated with an inability to evade the maturing phagosome) and were significantly attenuated in murine a
74 cules from the endoplasmic reticulum (ER) to phagosomes, and increases the levels of peptide-empty MH
75 or the cleavage of clathrin-coated vesicles, phagosomes, and mitochondria.
76     However, because pure and tightly sealed phagosomes are difficult to obtain, direct evidence for
77 internal contents visible, while accumulated phagosomes are frequently docked to cathepsin D-positive
78 he mechanisms underlying TLR localization to phagosomes are poorly characterized.
79 by phagocytosis and lysosomes that fuse with phagosomes are traditionally regarded as to a source of
80 e resistant to Mycobacterium marinum-induced phagosome arrest, associated with increased maturation o
81 at PtdIns(3)P behaves similarly in canonical phagosomes as well as endosomes.
82 uld correlate well with phagocytosis because phagosomes become acidified and the average fluorescence
83                                          The phagosome becomes a dynamic hub receiving traffic from m
84 t of Golgi-derived secretory vesicles during phagosome biogenesis, which was important for uptake of
85 nt generation occurs within an intracellular phagosome, but diffusible species can react with the neu
86 s into a membrane bound compartment called a phagosome, but what happens when engulfed pathogens star
87 se with non-matured mycobacterium-containing phagosomes, but fusion events with mycobacterium-contain
88 uent in high zinc conditions, e.g. inside of phagosomes, but that it can be replaced by S18-2 when zi
89 ts confirm that TAP can import peptides into phagosomes, but they suggest that some peptides, includi
90 this study, we monitored peptide import into phagosomes by flow cytometry using two types of fluoresc
91 ciation with p85 results in encapsulation of phagosomes by lipidated LC3 in multi-membrane organelles
92 ive proteasomes within cross-presenting cell phagosomes can generate these peptides.
93 rbation that pathogens encounter within host phagosomes, carbon source deprivation, which leads to tr
94         These pools are rapidly mobilized to phagosomes carrying microbial antigens, and in a signal-
95 l pigment epithelium (RPE) uncovered reduced phagosome clearance and increased mitochondrial number a
96 howed normal particle engulfment but delayed phagosome clearance and reversed diurnal profiles of lev
97  which we identify as a further regulator of phagosome compaction.
98 HO(2) (*)); pK(a) = 4.8], to T. cruzi at the phagosome compartment.
99 tion, nuclear translocation of TFEB requires phagosome completion and fails to occur in cells silence
100 X2) produces reactive oxygen species to kill phagosome-confined bacteria.
101 icles and that its PX domain enables vesicle-phagosome contact by binding to PI(3)P in the phagosomal
102 ify GOP-1 as essential for the maturation of phagosomes containing apoptotic cells, through recruitme
103 r of IFN genes (STING), as well as fusion of phagosomes containing bacilli with lysosomal compartment
104 al acidification blocks TLR9 accumulation on phagosomes containing beta-1,3 glucan beads.
105  LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dyin
106                                              Phagosomes containing live C. albicans cells became tran
107                               However, fewer phagosomes containing live USA300 bacteria than those co
108 ike phagosomes containing wild-type bacilli, phagosomes containing the DeltacpsA mutant recruited NAD
109                                       Unlike phagosomes containing wild-type bacilli, phagosomes cont
110 racterized by frequent phagocytic cups, high phagosome content and CD68 upregulation.
111                            The maturation of phagosomes, defined by the presence of late endocytic ma
112                           The degradation of phagosomes, derived from the ingestion of photoreceptor
113 the cell surface (and then ultimately to the phagosome during phagocytosis) in response to G-protein
114                                              Phagosome-early endosome fusion required PI(3)P, yet did
115 ith SCHU S4 DeltapurMCD, a mutant capable of phagosome escape but of only limited cytosolic replicati
116 red for intracellular replication even after phagosome escape into the cell cytosol.
117 pathogenicity island, required for bacterial phagosome escape, intracellular replication, and virulen
118 ge death, as evidenced by the failure of the phagosome escape-deficient mutant SCHU S4 DeltafevR to i
119 ty in vitro In the absence of MAP7, isolated phagosomes exhibit approximately equal fractions of plus
120 ts influence on the maturation of macrophage phagosomes following the engulfment of C. albicans cells
121 cquisition, intracellular chloride supply to phagosomes for oxidant production, and methods to measur
122        Mitochondria need to be juxtaposed to phagosomes for the synergistic production of ample react
123                                              Phagosomes form during engulfment of large particles and
124 HB2, to encompass bacteria both during early phagosome formation and after L. monocytogenes escaped t
125 p regulating the actin cytoskeletal network, phagosome formation and closure, and phagosome maturatio
126 atidylinositol 4-phosphate (PtdIns4P) during phagosome formation and maturation.
127 calcium sequestration, and calcium-dependent phagosome formation around secondarily encountered ACs i
128 gene expression from disease onset involving phagosome formation as well as natural killer cell and I
129 3-H1 and Dynamin are corecruited at sites of phagosome formation in F-actin-rich cups.
130 tein expression, cell-to-cell differences in phagosome formation, and number of bacterium engulfed.
131 e early stages of microbial phagocytosis and phagosome formation.
132 osome, the events related to endolysosome-to-phagosome fusion do not significantly differ between the
133 ive intracellular pathogen that escapes from phagosomes, grows in the host cytosol, and avoids autoph
134                             Among the Muller phagosomes, >90% matured into phagolysosomes.
135 , direct evidence for peptide transport into phagosomes has remained limited.
136 ms that regulate PtdIns(3)P removal from the phagosome have remained unclear.
137 lbicans infection but is dysregulated on the phagosome in the presence of the invasive hyphal form, w
138 xamined the fate of the S. aureus-containing phagosome in THP-1 macrophages by evaluating bacterial i
139 e or heat-killed Candida albicans-containing phagosomes in a Dectin-1-dependent manner in GM-CSF-deri
140 tide with high TAP affinity is imported into phagosomes in a TAP- and ATP-dependent manner, as expect
141 maturing lipopolysaccharide (LPS)-containing phagosomes in an adaptor protein-3 (AP-3)-dependent mann
142      Toll-like receptor (TLR) recruitment to phagosomes in dendritic cells (DCs) and downstream TLR s
143 cating that extended PtdIns(3)P signaling on phagosomes in the Mtmr4-knockdown cells permitted traffi
144 asma membrane of Candida albicans-containing phagosomes independent of phagocytic ability.
145 hagy marker LC3 localized to single-membrane phagosomes independently of the ULK complex, which is re
146 TLR signaling adaptors TRAM and MyD88 to the phagosome, indicating that the TLR-MyD88 signaling compl
147 d with increased maturation of mycobacterial phagosomes, indicating that extended PtdIns(3)P signalin
148 ecreases the association of LAMP-3 with bead phagosomes, indicating that P27 itself blocks phagosome-
149 and phagocytosis, supported by evidence that phagosomes induced in Cln3(Deltaex1) (-) (6)-derived mou
150  of receptors and their signal cross-talk on phagosomes inside living cells.
151 macrophages, and is required to preserve Mtb phagosome integrity and control Mtb replication.
152 echanisms that contribute to maintaining Mtb phagosome integrity have not been investigated.
153 ng depends on the shrinkage and packaging of phagosomes into a unique cellular compartment, the gastr
154  a pivotal role in the maturation of nascent phagosomes into microbicidal phagolysosomes.
155 s inhibited, indicating that Rab39a converts phagosomes into peptide-loading compartments.
156 acteria they enclose them in small vesicles (phagosomes) into which superoxide is released by activat
157 at signals the transition from early to late phagosomes is accompanied by resurgence of PtdIns4P, whi
158 orting of luminal and membrane proteins into phagosomes is critical for the immune function of this o
159 osphoinositides (PIPs) have been detected on phagosomes, it remained unclear which PIPs actually gove
160  mitochondrial trafficking and mitochondrion-phagosome juxtaposition.
161 ptidoglycan in macrophage and dendritic cell phagosomes leads to activation of the NLRP3 inflammasome
162      However, fungal germination in the late phagosome led to macrophage necrosis.
163 ome speed, but run length was decreased, and phagosome localization and degradation were impaired.
164 s to characterize the third band as the cone phagosomes located in the top of the RPE.
165               At the acidic pH values of the phagosome lumen (pH 5.3 +/- 0.1), high steady-state conc
166 cesses, thus enabling the bacterium to evade phagosome-lysosome fusion and establish an endoplasmic r
167 hagosomes, indicating that P27 itself blocks phagosome-lysosome fusion by modulating the traffic mach
168 LF-exposed Mtb had reduced control and fewer phagosome-lysosome fusion events, which was reversed whe
169    Additionally, PIKfyve inactivation blocks phagosome-lysosome fusion in a manner that can be rescue
170 licates in macrophages in part by inhibiting phagosome-lysosome fusion, until interferon-gamma (IFNga
171 es that generate these PIPs, as mediators of phagosome-lysosome fusion.
172 antibodies revealing C9ORF72 localization to phagosomes/lysosomes.
173 nalized POS vesicles were colocalized with a phagosome marker, suggesting that ABCF1-mediated engulfm
174 esting that lysosomal Ca(2+) released during phagosome maturation activates TFEB.
175 ting lysosomal protein that are required for phagosome maturation and fusion with lysosomes.
176 osomal recycling machinery, to contribute to phagosome maturation and intracellular processing of bor
177 utophagy machinery in turn were required for phagosome maturation and intracellular replication.
178 IFN-gamma signaling via Mal was required for phagosome maturation and killing of intracellular Mycoba
179 the proneurotrophin receptor sortilin during phagosome maturation and mycobacterial killing.
180 and receptor-mediated endocytosis as well as phagosome maturation are unaffected by loss of UCH-L1 in
181                          The role of SapM in phagosome maturation arrest in host macrophages suggests
182                       Thus, PI(3)P regulates phagosome maturation at early and late stages, whereas P
183           Therefore, Rab14 activity promotes phagosome maturation during C. albicans infection but is
184 how for the first time that M. bovis arrests phagosome maturation in a process that depends on P27.
185 sxG (TB9.8) and EsxH (TB10.4), which impairs phagosome maturation in macrophages and is essential for
186             Rab-GTPase mutants that restrain phagosome maturation increase proteasome recruitment and
187                 In the Mreg(-/-) mouse where phagosome maturation is delayed, there was a temporal sh
188 etwork, phagosome formation and closure, and phagosome maturation leading to degradation of the engul
189 epletion delayed the acquisition of the late phagosome maturation markers LAMP1 and lysosomal catheps
190                                              Phagosome maturation requires sequential fusion of the p
191 d propose a model in which PIKfyve modulates phagosome maturation through phosphatidylinositol-3,5-bi
192 h reporter peptides is shortened by enhanced phagosome maturation triggered by TLR signaling.
193 s in wild-type mice and mice with defects in phagosome maturation using a mouse RPE explant model.
194 nd lysosomal compartments, a process called 'phagosome maturation', which leads to the degradation of
195 inked to the biological functions autophagy, phagosome maturation, and lytic vacuole/lysosome, and co
196 mplicated pathways in sarcoidosis, including phagosome maturation, clathrin-mediated endocytic signal
197 erculosis lipoproteins and lipoglycans block phagosome maturation, inhibit class II MHC Ag presentati
198 te that corpses persist because of defective phagosome maturation, rather than recognition defects.
199    Tubular lysosomes have been implicated in phagosome maturation, retention of fluid phase, and anti
200       This subset includes genes involved in phagosome maturation, superoxide production, response to
201 d cellular activation affect many aspects of phagosome maturation.
202 ed in the protein ubiquitination pathway and phagosome maturation.
203 brane recycling, and, in macrophages, blocks phagosome maturation.
204 oplasmic reticulum (calreticulin)-associated phagosome maturation.
205 yelinase (ASMase) and required for efficient phagosome maturation.
206 uggests that TORC1 regulates Draper-mediated phagosome maturation.
207 ing as an extracellular signal that inhibits phagosome maturation.
208  remained unclear which PIPs actually govern phagosome maturation.
209 y viral protein (Vpr) was crucial to perturb phagosome maturation.
210 r efficient clearance of apoptotic cells and phagosome maturation.
211 eins), which is essential for engulfment and phagosome maturation.
212  fusing with lysosomes, in a process termed "phagosome maturation." In this issue, Yin et al. identif
213 , thereby filling in a missing link into how phagosomes mature into cross-presenting vesicles.
214                                              Phagosomes mature into phagolysosomes by sequential fusi
215 urvature and thus local PI(3)P enrichment at phagosomes, may be one of the driving elements underlyin
216 rt of cytosolic peptides into dendritic cell phagosomes, mediated by TAP transporters recruited from
217 at ATP7A-dependent copper transport into the phagosome mediates host defense against S Typhimurium, w
218 with M.tb DK9897 being unable to disrupt the phagosome membrane and make contact to the cytosol.
219 rotein 1A/1B-light chain 3) is conjugated to phagosome membranes using a portion of the canonical aut
220  MAP7 causes a pronounced shift in motility; phagosomes move toward the plus-end ~80% of the time, an
221            Live-cell imaging showed that the phagosomes moved bidirectionally along microtubules in R
222                            Within neutrophil phagosomes, myeloperoxidase uses superoxide generated by
223  both S. aureus isolates survived within hAM phagosomes, neither strain replicated efficiently in the
224                            In the macrophage phagosome, NRAMP1 removes Mn and other essential metals
225 is (Mtb) survives the normally bacteriocidal phagosome of macrophages.
226  was induced at pH 4.5, mimicking the acidic phagosome of macrophages.
227 ability of this bacterium to escape from the phagosome of the host cells via the action of the pore-f
228 t of the TAK1/MKK7/JNK signalling complex to phagosomes of IL-4-activated macrophages.
229 agocytosis, and was dynamically recruited to phagosomes of macrophages during phagocytosis.
230 ceptor (TLR)2, to opposite sides on a single phagosome or bring them into nanoscale proximity without
231 ot be explained through acidification of the phagosome or calcium limitation.
232 rupts ROS-induced interaction of Mst1/2 with phagosomes or mitochondria, and thereby diminishes the M
233  phagocytic internalization, and translocate phagosomes or other cargo to appropriate cellular locati
234                        Although some remodel phagosomes, others rapidly escape into the cytosol of in
235 age inflicted by proteopathic tau and during phagosome parasitism by Mycobacterium tuberculosis.
236  interleukin signalling, endocytosis, the ER-phagosome pathway and antigen-presentation.
237 immunity, the complement system and lysosome/phagosome pathways.
238  included the complement system and lysosome/phagosome pathways.
239 ease in this model is primarily a failure of phagosome physiology with a secondary mitochondrial dysf
240 cassette A4 transporter results in defective phagosome processing and accumulation of lipid debris.
241 the overall uptake of fungal cells, or early phagosome processing.
242 hat C. albicans-driven neutralization of the phagosome promotes hyphal morphogenesis, sufficient for
243 Ibeta-impairs TIRAP and TLR4 localization to phagosomes, reduces proinflammatory cytokine secretion,
244 w chloride is intracellularly transported to phagosomes remain largely unknown.
245 ermining peptide uptake by, and survival in, phagosomes remain little characterized.
246 king of TLR9 to A. fumigatus and C. albicans phagosomes requires Dectin-1 recognition.
247  of PtdIns(4)P impaired SKIP recruitment and phagosome resolution.
248 ed the amount of active Arf6 associated with phagosomes, revealed by the MT2-GFP probe that specifica
249 ium tuberculosis, plays an essential role in phagosome rupture and bacterial cytosolic translocation
250 losis, EsxA and EsxB not only play a role in phagosome rupture and M. tuberculosis cytosolic transloc
251 culosis (Mtb) and plays an essential role in phagosome rupture and translocation to the cytosol of ma
252                               Soon after the phagosome seals, PtdIns4P levels drop precipitously due
253                 Lack of KLC1 did not inhibit phagosome speed, but run length was decreased, and phago
254 of phagocytic cups as well as to the nascent phagosomes that harbor Gal/GalNAc lectin and actin.
255 hosphatidylinositol 3-monophosphate-positive phagosomes that mature into phagolysosomes using a pathw
256                         After formation of a phagosome, the events related to endolysosome-to-phagoso
257 lso appear "colocalized" on the membranes of phagosomes, the intracellular compartments for pathogen
258                                              Phagosomes then fuse with lysosomes and granules to kill
259                                              Phagosomes then fuse with lysosomes to mature into phago
260 zed to participate in cross-presentation, on phagosomes, thereby filling in a missing link into how p
261 AMP1)-positive and LysoTracker-positive late phagosomes; these characteristics were similar in both n
262 ages of infection after bacteria escape from phagosomes, through bacterial replication and the death
263 isms were degraded readily within neutrophil phagosomes, thus indicating that survival in the neutrop
264 n up into MSC endosomes colocalized with Mtb phagosomes, thus suggesting that the latter were fusion
265 mr4-knockdown cells permitted trafficking of phagosomes to acidic late endosomal and lysosomal compar
266  generates sufficient HOCl within neutrophil phagosomes to kill ingested bacteria.
267         (2020) show that lysosomes fuse with phagosomes to maintain phagosomal membrane integrity as
268         Motile endolysosomes contact nascent phagosomes to promote phagocytosis, whereas endo-lysosom
269 g RILP, which were shown earlier to displace phagosomes toward perinuclear lysosomes.
270  critical regulator of endoplasmic reticulum-phagosome traffic required for cross-presentation.
271 ocyte mobility, intercellular tethering, and phagosome transfer.
272                                 However, how phagosomes transmit signals to recruit mitochondria has
273    These results elucidate mechanisms of POS phagosome transport in relation to degradation, and demo
274 KD testes displayed defects in spermatid and phagosome transport, and also spermatid polarity due to
275 RVs fused with lysosomes, whereas associated phagosomes typically did not.
276                                              Phagosomes undergo fusion and fission events with endoso
277 ates of individual mycobacteria delivered to phagosomes versus phagolysosomes and discovered that bac
278 eptor is acquired by mycobacteria-containing phagosomes via interactions with the adaptor proteins AP
279 I molecules rather than SIINFEKL import into phagosomes via TAP.
280       Despite localization to acidified late phagosomes, viable G. bethesdensis cells were recovered
281           The duration of Rab14 retention on phagosomes was prolonged for hyphal cargo and was direct
282 n biochemical activities within the lumen of phagosomes, we have also shown that GH alters physiologi
283 P. stomatis, 52% of the bacterium-containing phagosomes were enriched for the specific granule marker
284                                    Here, POS phagosomes were observed to associate with myosin-7a, an
285 take of the NPs; ii) nanoparticle-containing phagosomes were rapidly processed into phagolysosomes, w
286 N expression increases inside the neutrophil phagosome, where MPO is located, compared with outside t
287  the autophagy-related protein LC3-II to the phagosome, whereas enhancing HIF-1alpha reduced phagosom
288 acrophages, facilitating its escape from the phagosome, which can result in host cell lysis.
289 s internalization of the microorganisms into phagosomes, which are then delivered to endolysosomes fo
290 R9 trafficking to beta-1,3 glucan-containing phagosomes, which may be critical in coordinating innate
291 t microbial intruders by engulfing them into phagosomes, which subsequently mature into microbicidal
292 o promote translation during starvation in a phagosome while repressing it during growth in the cytos
293 maturation requires sequential fusion of the phagosome with early endosomes, late endosomes, and lyso
294 de synthase (NOS2) which instantly fills the phagosome with nitric oxide (NO) to clear the pathogen.
295 might be caused by a defect in the fusion of phagosomes with lysosomes, while this process occurs rap
296 nalyzed the involvement of PIPs in fusion of phagosomes with various endocytic compartments and ident
297                                              Phagosome-with-lysosome fusion (PLF) results in the deli
298 y invades host macrophages, where it escapes phagosomes within a few hours and replicates in the cyto
299  homolog) complex to both macropinosomes and phagosomes within a minute of internalization.
300 ion, although noncanonical autophagy targets phagosomes, xenophagy was required to restrict the growt

 
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