ライフサイエンスコーパス: endolysosome

1 ally related to PD-associated pathways (i.e. endolysosome).

2 y are located in acid-filled calcium stores (endolysosomes).

3 or ubiquitin-dependent TLR9 targeting to the endolysosome.

4 n of Smad4 and colocalizes with Smad4 at the endolysosome.

5 cluding mitochondria, the autophagosome, and endolysosome.

6 ructural collapse of the nanocarriers in the endolysosome.

7 mbrane undergoes rapid recycling through the endolysosome.

8 TLRs from the endoplasmic reticulum (ER) to endolysosomes.

9 by agonist endocytosis and delivery into the endolysosomes.

10 ivering CpG-oligodeoxynucleotides to TLR9 in endolysosomes.

11 face of the plasma membranes of cells and in endolysosomes.

12 processing within, or in close proximity to, endolysosomes.

13 nsing receptors TLR7 and TLR9 from the ER to endolysosomes.

14 in the periphery for eventual processing in endolysosomes.

15 brane and accumulation of the transporter in endolysosomes.

16 ell surface, further suggesting the role for endolysosomes.

17 that probably depends on the alkalization of endolysosomes.

18 e endosomes and fused with lysosomes to form endolysosomes.

19 xicity is downstream of Fe(2+) released from endolysosomes.

20 upon it is endocytosed and internalized into endolysosomes.

21 om patients and it is primarily localised in endolysosomes.

22 the Fab1 complex that controls signaling at endolysosomes.

23 calized to endolysosomes and 17aE2 acidifies endolysosomes.

24 hat AAMDC, RabGAP1L, and Rab7a colocalize in endolysosomes.

25 ed constitutive perforations in ~5% of their endolysosomes.

26 gmentation due to mistrafficking of cargo to endolysosomes.

27 ded maturation process involving fusion with endolysosomes.

28 order characterized by lipid accumulation in endolysosomes.

29 plasmic reticulum (ER), Golgi apparatus, and endolysosomes.

30 ively regulate the interaction of SNX19 with endolysosomes.

31 duced digestion of extracellular proteins in endolysosomes.

32 r-mediated endocytosis and internalized into endolysosomes.

33 ogenous Tat has to escape the degradation by endolysosomes.

34 ail to uncoat and accumulate within LAMP1(+) endolysosomes.

35 DNase II digests DNA in endolysosomes.

36 fined mechanisms of amino acid transfer into endolysosomes.

37 ease in the concentration of Cu localized to endolysosomes.

38 endent of receptor and ligand trafficking in endolysosomes.

39 nal PrP27-30 core that is stable for days in endolysosomes.

40 (TLRs) from the endoplasmic reticulum to the endolysosomes.

41 s, (2) concentration dependently deacidified endolysosomes, (3) decreased endolysosome Fe(2+) concent

42 ions cause abnormal accumulation of enlarged endolysosomes accompanied by impaired interaction betwee

43 lysosome localization prevents 17aE2-induced endolysosome acidification.

44 els, with the pathway signaling higher glial endolysosome activity for phagocytosis.

45 In contrast to the tubules that emerge from endolysosomes after uptake of soluble ligands and TLR st

46 S) activation of macrophages protected their endolysosomes against damage initiated by the phagocytos

47 Endolysosomes also accumulated acidotropic probes and co

48 oach to reduce APP protein levels and rescue endolysosome and autophagy dysfunction in APP duplicatio

49 presumably by altering their fusion with the endolysosome and delivery of their contents into the cyt

50 TPC2 is an endolysosome and melanosome localized non-selective cati

51 trongly influences its processing within the endolysosome and potentially controls the identity of pe

52 phate (PtdIns(3,5)P2), a master architect of endolysosome and vacuole identity, is thought to be nece

53 CD151 prevents proteins from (1) buildup in endolysosomes and (2) discharge through exosomes, to lim

54 s, estrogen receptor a (ERa) is localized to endolysosomes and 17aE2 acidifies endolysosomes.

55 is composed of acid-hydrolase-active, acidic endolysosomes and acid hydrolase-inactive, non-acidic, t

56 e have also shown that acid-hydrolase-active endolysosomes and acid-hydrolase-inactive, terminal stor

57 structures that are positive for markers of endolysosomes and are filled with aberrant storage mater

58 icles, leading to their impaired delivery to endolysosomes and consequent lysosomal dysfunction.

59 hypothesis that HIV-1 Tat can accumulate in endolysosomes and contribute to the activation of latent

60 , ubiquitination decreases localization with endolysosomes and decreases antiviral activity.

61 al role in the enhancing effects of 17aE2 on endolysosomes and dendritic spines.

62 g-isoform of ZAP (ZAPL/PARP-13.1/zc3hav1) to endolysosomes and enhancing the antiviral activity of th

63 Trafficking to endolysosomes and function of SLC15A4 were dependent on

64 f human V-ATPase a-subunits are localized to endolysosomes and Golgi, respectively.

65 ages show elevated TLR9 in signal-permissive endolysosomes and increased response, while wild types s

66 quine promoted the release of HIV-1 Tat from endolysosomes and induced HIV-1 LTR transactivation.

67 osis concentrates extracellular solutes into endolysosomes and is increased in cells stimulated by gr

68 thway promoting the accumulation of enlarged endolysosomes and lysosome secretion.

69 invasion due to the dual activity of TPC2 in endolysosomes and melanosomes.

70 estrogen receptor subtype ERa is present on endolysosomes and plays a critical role in the enhancing

71 eatment prevents the development of enlarged endolysosomes and reduction in dendritic spines.

72 endolysosomes may enhance Tat degradation in endolysosomes and restrict LTR transactivation.

73 vating TRPML1 channels with ML-SA1 acidified endolysosomes and restricted Tat-mediated HIV-1 LTR tran

74 by a marked reduction in TLR3 transport into endolysosomes and subsequent proteolytic processing.

75 ively modulates the anterograde transport of endolysosomes and that loss of alpha-syn expression resu

76 cleic acid-sensing TLRs and their ligands to endolysosomes and the formation of the LAMP2+VAMP3+ hybr

77 cation, HIV-1 Tat must first escape from the endolysosomes and then enter the nucleus.

78 perinuclear positioning of large (> 800 nm) endolysosomes; and (iii) decreased levels of the tetrasp

79 Endolysosomes are important for neuronal function, and e

80 vacuole, and mitochondria, microtubules, and endolysosomes are recruited to the vacuole perimeter.

81 , in the absence of LRRK2 and Rab8A, damaged endolysosomes are targeted to lysophagy.

82 We found that endolysosomes are the principal organelles in which acid

83 RK2 recruits the Rab GTPase Rab8A to damaged endolysosomes as well as the ESCRT-III component CHMP4B,

84 fication of TAPE (TBK1-associated protein in endolysosomes) as a novel regulator of the RLR pathways.

85 M3/V-ATPase-tetraspanin-VCP/p97 complexes on endolysosome, as a protein quality control and inflammat

86 ent with an almost exclusive localization to endolysosomes at the resting state.

87 These results suggest that acidifying endolysosomes by activating TRPML1 or BK channels may pr

88 senger that mobilizes Ca(2+) from the acidic endolysosomes by activation of the two-pore channels TPC

89 We isolated endolysosomes by independently targeting two lysosomal m

90 We demonstrated that chelating endolysosome calcium with high-affinity rhodamine-dextra

91 compartments, is colocalized with CpG in the endolysosome, can be immunoprecipitated with TLR9, and b

92 Motile endolysosomes contact nascent phagosomes to promote phag

93 Moreover, endolysosomes contain various pattern recognition recept

94 , a noncanonical potassium (K(+)) channel in endolysosomes, contributes to their pH stability and is

95 Cells respond to endolysosome damage by either repairing the damage or ta

96 es for extended periods of time, and induces endolysosome de-acidification as well as enlargement.

97 Because of findings that endolysosome de-acidification with, for example, the wea

98 17aE2 protected against HIV-1 gp120-induced endolysosome deacidification and reductions in dendritic

99 f Fe(2+) are central to iron trafficking and endolysosome deacidification releases Fe(2+) into the cy

100 nistically caused by HERV-K Env endocytosis, endolysosome deacidification, and endolysosome Fe(2+) ef

101 Our findings demonstrate a novel endolysosome-dependent pathway that governs the ERa-medi

102 atidylinositol 4,5-bisphosphate PI(4,5)P2 in endolysosomes, driving local hyper-polymerization of F-a

103 naptic turnover and is selectively sorted to endolysosomes during activity-dependent bulk endocytosis

104 tudies provide evidence for linkages between endolysosome dysfunction and neurodegeneration involving

105 17aE2 protected against HIV-1 gp120-induced endolysosome dysfunction and reductions in dendritic spi

106 en established between neurodegeneration and endolysosome dysfunction over the course of aging, this

107 ria are globally and dynamically targeted by endolysosomes (ELs) during MOMP.

108 ts carrying the R194C mutation show enlarged endolysosomes, enhanced lysosomal Ca(2+) release and hyp

109 olysosome, knockout of SIRT2 did not exhibit endolysosome enlargement for increased EV release.

110 This excludes the time for endolysosome enlargement, which takes between 1 and 48 h

111 dent two-pore channels (TPCs) attenuated Tat endolysosome escape and LTR transactivation.

112 tosolic calcium with BAPTA-AM attenuated Tat endolysosome escape and LTR transactivation.

113 vestigated the involvement of calcium in Tat endolysosome escape and subsequent LTR transactivation.

114 alcium released from TPCs is involved in Tat endolysosome escape and subsequent LTR transactivation.

115 spikes around PDGs--or any organelle of the endolysosome family--are visualized in real time and rev

116 tly deacidified endolysosomes, (3) decreased endolysosome Fe(2+) concentrations, (4) increased cytoso

117 docytosis, endolysosome deacidification, and endolysosome Fe(2+) efflux into the cytoplasm.

118 ine in pancreatic cancer cells to perform an endolysosome-focused CRISPR-Cas9 screen for genes mediat

119 itutively ubiquitinated and recruited to the endolysosome for degradation.

120 ral envelope, trapping viral RNAs inside the endolysosome for enzymatic decomposition.

121 ween Vpu and IRF3 that redirects IRF3 to the endolysosome for proteolytic degradation, thus allowing

122 cence images capturing cargo delivery within endolysosomes for clearance.

123 er repairing the damage or targeting damaged endolysosomes for degradation via lysophagy.

124 into phagosomes, which are then delivered to endolysosomes for enzymatic degradation.

125 s HIV-1 Tat enters endolysosomes, resides in endolysosomes for extended periods of time, and induces

126 ndoplasmic reticulum (ER) after synthesis to endolysosomes for proteolytic cleavage and activation.

127 -neuronal cells, and drive redistribution of endolysosomes from the axon to the soma in hippocampal n

128 By directly recording TPCs in endolysosomes from wild-type and TPC double-knockout mic

129 ll adhesion at cell surface, CD151 maintains endolysosome function by sustaining VCP/p97-mediated pro

130 Taken together, we show that ApoE4 impacts endolysosome function in primary neurons, but that chang

131 rocyte-specific deletion of Bmal1 influences endolysosome function, autophagy, and protein degradatio

132 ve genome-wide screen for genes required for endolysosome function.

133 sphate (PtdIns(3,5)P2) helps control various endolysosome functions including organelle morphology, m

134 n, promoted vacuole enlargement in cells and endolysosome fusion in a cell-free assay.

135 complex with SNAP29 and VAMP7 to mediate MDV-endolysosome fusion in a manner dependent on the homotyp

136 r VAMP8 interaction to promote autophagosome-endolysosome fusion.

137 er virus, was thought to enter cells through endolysosomes harboring its glycoprotein receptor, Niema

138 ol cells exhibit an (i) increased density of endolysosomes; (ii) increased perinuclear positioning of

139 ing of ATP7A from the trans-Golgi network to endolysosomes in macrophages harboring amastigotes.

140 exit the endoplasmic reticulum and travel to endolysosomes in mouse macrophages and dendritic cells.

141 xpected presence of intrinsically perforated endolysosomes in neurons, suggesting involvement in the

142 itro microscopy showed activation within the endolysosomes in target cells.

143 hat RUFY3 and RUFY4 promote concentration of endolysosomes in the juxtanuclear area of non-neuronal c

144 em into the cytosol, highlighting a role for endolysosomes in the uptake of polyamines into cells.

145 derstanding of these secretory events during endolysosome inhibition remains incomplete.

146 nsequently, XIAP E3 ligase activity recruits endolysosomes into mitochondria, resulting in Smac degra

147 the translocation of Ags from phagosomes or endolysosomes into the cytosol, where antigenic peptides

148 ntibody against the CD98 receptor and by the endolysosome iron chelator deferoxamine.

149 Receptor activation in the endolysosome is regulated through a proteolytic mechanis

150 still efficiently form but their fusion with endolysosomes is blocked.

151 localization to and antiviral remodeling of endolysosomes is differentially regulated by S-palmitoyl

152 cargo delivery to and/or accumulation within endolysosomes is instrumental for characterizing lysosom

153 IRT1 increased EV release with enlarged late endolysosome, knockout of SIRT2 did not exhibit endolyso

154 n arrival in Niemann-Pick C1 (NPC1)-positive endolysosomes (LE/Lys), we propose that trafficking to L

155 The small GTPase ARL8 associates with endolysosomes, leading to the recruitment of several eff

156 esulting accumulation of storage material in endolysosomes leads us to propose that AP-5 deficiency r

157 ls of TLR3 and TLR7, but not TLR8, prevented endolysosome leakage and attenuated HIV-1 Tat-mediated H

158 Thus, downregulation of endolysosome levels by Qki loss helps glioma stem cells

159 rotective effects of 17aE2 were mediated via endolysosome localization of ERa.

160 creases in dendritic spine density depend on endolysosome localization of ERa.

161 spines; such protective effects depended on endolysosome localization of ERa.

162 xpressing an ERa mutant that is deficient in endolysosome localization prevents 17aE2-induced endolys

163 ytoplasmic peripheral proteins and regulates endolysosome-localized membrane channel activity.

164 dolysosome-specific PIP, binds and activates endolysosome-localized mucolipin transient receptor pote

165 lysosomal P2X4 activity by alkalinization of endolysosome lumen, promoted vacuole enlargement in cell

166 te HIV-1 LTR, we hypothesize that acidifying endolysosomes may enhance Tat degradation in endolysosom

167 dings suggest that HIV-1 Tat accumulation in endolysosomes may play an important role in controlling

168 esicular pathway of amino acid delivery into endolysosomes, mediated by the actin cytoskeleton.

169 Mechanistically, Qk deletion decreases endolysosome-mediated degradation and enriches receptors

170 equired for transport (ESCRT)-III system for endolysosome membrane repair, but the toxic effects of t

171 At the endolysosome membrane, CD151 links VCP/p97 to (1) IFITM3

172 e ensuing loss of ESCRT function compromises endolysosome membranes, thereby facilitating escape of a

173 ARE-mediated fusion of the autophagosome and endolysosome membranes.

174 y the endosome lumen, and is associated with endolysosome neuropathology, NHE6-mediated mechanisms in

175 a series of quantitative parameters such as endolysosome number, size, shape, position within cells,

176 ligand recognition and TLR engagement in the endolysosome occurred normally.

177 fragments with the gold nanoparticles in the endolysosome of the living cells.

178 inic acid adenine dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treated lymphokine-

179 cation channel ubiquitously expressed in the endolysosomes of mammalian cells and its loss-of-functio

180 ane, endoplasmic reticulum, mitochondria and endolysosomes of T cells and their role in shaping immun

181 ubunit 1 (BLOC1S1) control mitochondrial and endolysosome organelle homeostasis and function.

182 Whole-endolysosome patch clamping presents new opportunities t

183 important to determine HERV-K Env effects on endolysosome pH and whether HERV-K Env-induced neurotoxi

184 tivated potassium (BK) channel in regulating endolysosome pH, as well as Tat-mediated HIV-1 LTR trans

185 al sorting, and (2) V-ATPase, which dictates endolysosome pH, to support functional assembly of V-ATP

186 of Sequestosome 1 (SQSTM1/p62) by RNF26 and endolysosome positioning, participates in the lysosomal

187 demonstrated that fusion events, which form endolysosomes, precede the onset of acid hydrolase activ

188 e SNARE Syntaxin-17 mediates MDV fusion with endolysosomes, promoting the delivery of mitochondrial c

189 milar to LROs from HPS patients, but for all endolysosomes rather than a specialized subset.

190 ly disialogangliosides-function as essential endolysosome receptors that are required for infection b

191 H within intracellular compartments, such as endolysosomes, rely on the activity of chloride/proton t

192 he underlying mechanisms whereby Tat escapes endolysosomes remain unclear.

193 Here, we determined the involvement of endolysosome-resident transient receptor potential mucol

194 SLC15A4 is an endolysosome-resident transporter linked with autoinflam

195 macologically blocking and knocking down the endolysosome-resident two-pore channels (TPCs) attenuate

196 tes we found that exogenous HIV-1 Tat enters endolysosomes, resides in endolysosomes for extended per

197 re, and most seeded cells had no evidence of endolysosome rupture.

198 axonal transport - including autophagosomes, endolysosomes, signalling endosomes, mitochondria and sy

199 mal membrane, we report that PI(3,5)P(2), an endolysosome-specific PIP, binds and activates endolysos

200 Endolysosome stores of Fe(2+) are central to iron traffi

201 When carried to the endolysosome, such compounds can modulate the proteolyti

202 odomains of TLR9 and TLR7 are cleaved in the endolysosome, such that no full-length protein is detect

203 small, fluorescent fluid-phase solutes into endolysosomes sufficiently fast to explain growth factor

204 The endolysosome system plays central roles in both autophag

205 rine organ functions by interacting with the endolysosome system, yet shows multiple features not ful

206 trafficking and organelle tubulation in the endolysosome system.

207 (TPCs) were identified as a novel family of endolysosome-targeted calcium release channels gated by

208 ing endocytosis and its internalization into endolysosomes, Tat must be released in order for it to a

209 e new model, ebolavirus enters cells through endolysosomes that contain both NPC1 and TPC2.

210 controlling the motility and positioning of endolysosomes that involves tethering to the ER by a sor

211 we identify a function for mammalian SKP1 in endolysosomes that is independent of its established rol

212 stable "cleaved/associated" TLR3 present in endolysosomes that recognizes dsRNA and signals.

213 ition of ARF6 impaired TLR9 trafficking into endolysosomes, thereby inhibiting proceed functional cle

214 endolysosomal chloride currents and enlarges endolysosomes through a Ca(2+)/calmodulin-dependent way.

215 ilization enable efficient repair of damaged endolysosomes, through both ESCRT (endosomal sorting com

216 cation from the endoplasmic reticulum to the endolysosome, thus allowing proper activation by microbi

217 or pathogens, exogenous Ags preprocessed in endolysosomes, thus shaping the peptidome available for

218 ing TLRs are strategically positioned in the endolysosome to detect incoming nonself RNA.

219 LR) 9 requires proteolytic processing in the endolysosome to initiate signaling in response to DNA.

220 vity, indicating that virus trafficking from endolysosomes to autophagosomes is not a prerequisite fo

221 4 as ARL8 effectors that promote coupling of endolysosomes to dynein-dynactin for retrograde transpor

222 uitination for proteolytic degradation, onto endolysosomes to facilitate VCP/p97 function.

223 recruitment of several effectors that couple endolysosomes to kinesins for anterograde transport alon

224 Long-range movement involves coupling of the endolysosomes to motor proteins that carry them along mi

225 ular trafficking, secretion, and function of endolysosomes to promote adaptive immune responses.

226 acilitating the reprogramming of a subset of endolysosomes to replicate some functions of lysosome-re

227 tion, in part, by sorting the virus from the endolysosomes to the endoplasmic reticulum (ER), a criti

228 we show that the sorting nexin SNX19 tethers endolysosomes to the endoplasmic reticulum (ER), decreas

229 mation of a phagosome, the events related to endolysosome-to-phagosome fusion do not significantly di

230 Similar results were observed by activating endolysosome Toll-like receptor 3 (TLR3) and TLR7/8.

231 mechanisms and signaling pathways regulating endolysosome transport and maturation to maintain axonal

232 e control of both anterograde and retrograde endolysosome transport.

233 endogenous alpha-syn to PFFs in the lumen of endolysosomes, triggering aggregation.

234 Upon acidification of endolysosomes, two-thirds of the hemes are released from

235 ibutes to the juxtanuclear redistribution of endolysosomes upon cytosol alkalinization.

236 nd cells that lack TRPML1 exhibited enlarged endolysosomes/vacuoles and trafficking defects in the la

237 ytosolic NADP(+) is transported to acidified endolysosomes via connexin 43 (Cx43) and gated by cAMP-E

238 BLOC-2 is recruited to endolysosomes via its HPS3 subunit.

239 that increased sequestration of Ca(2+) into endolysosomes was an intermediary in the regulation of l

240 receptors have been shown to be targeted to endolysosomes, we used intracellular microinjection and

241 IFITM3 localizes to endolysosomes where it prevents virus fusion, although m

242 arker vimentin, the nanoparticles target the endolysosome, where the carrier is degraded and the carg

243 hout blocking trafficking of VLPs to NPC1(+) endolysosomes, where EBOV fuses.

244 nsing TLRs from the endoplasmic reticulum to endolysosomes, where the TLRs encounter their respective

245 tion mutations result in the accumulation of endolysosomes which are positive for the membrane damage

246 complete fusion results in the formation of endolysosomes, which are hybrid organelles from which ly

247 nd become entrapped and then degraded within endolysosomes, which can significantly impair their ther

248 amino acid transporter, SLC3A2, and MTOR on endolysosomes, which directly activates mTORC1 by co-opt

249 tor protein complex 2 (AP-2) for delivery to endolysosomes while TLR7, TLR11, TLR12, and TLR13 utiliz

250 The rapid accumulation of Wnt-induced endolysosomes within 30 minutes was inhibited by the dep