ライフサイエンスコーパス: endolysosome

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

2 ructural collapse of the nanocarriers in the endolysosome.

3 mbrane undergoes rapid recycling through the endolysosome.

4 or ubiquitin-dependent TLR9 targeting to the endolysosome.

5 DNase II digests DNA in endolysosomes.

6 fined mechanisms of amino acid transfer into endolysosomes.

7 ease in the concentration of Cu localized to endolysosomes.

8 endent of receptor and ligand trafficking in endolysosomes.

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

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

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

12 by agonist endocytosis and delivery into the endolysosomes.

13 ivering CpG-oligodeoxynucleotides to TLR9 in endolysosomes.

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

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

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

17 in the periphery for eventual processing in endolysosomes.

18 brane and accumulation of the transporter in endolysosomes.

19 ell surface, further suggesting the role for endolysosomes.

20 that probably depends on the alkalization of endolysosomes.

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

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

23 Endolysosomes also accumulated acidotropic probes and co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 itutively ubiquitinated and recruited to the endolysosome for degradation.

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

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

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

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

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

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

47 r VAMP8 interaction to promote autophagosome-endolysosome fusion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Whole-endolysosome patch clamping presents new opportunities t

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

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

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

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

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

69 trafficking and organelle tubulation in the endolysosome system.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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