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1 n, whereas the shorter chain species di-14:0 LBPA had little effect on cholesterol clearance in NPC1-
2 rotection, generated the enantiomers of 2,2'-LBPA.
3 omal phospholipid lyso-bisphosphatidic acid (LBPA) (also known as bismonoacylglycerol phosphate).
4 omal phospholipid lyso-bisphosphatidic acid (LBPA), suggesting an important role for LBPA in NPC2-med
5  endosomal marker lyso-bisphosphatidic acid (LBPA).
6  analogue of (S,S)-lysobisphosphatidic acid (LBPA) and its enantiomer were synthesized from the same
7 SCRTs but requires lysobisphosphatidic acid (LBPA) in vivo, and can be reconstituted on supported bil
8  It was found that lysobisphosphatidic acid (LBPA) is required for release of PS-ASOs from LEs.
9 identify endosomal lysobisphosphatidic acid (LBPA) presented by the CD1d-like endothelial protein C r
10 us enrichment with lysobisphosphatidic acid (LBPA), also known as bis-monoacylglycerol phosphate, eit
11 ntiomerically pure lysobisphosphatidic acid (LBPA), bisether analogues, and phosphorothioate analogue
12 LE/LY phospholipid lysobisphosphatidic acid (LBPA).
13  the anionic lipid lysobisphosphatidic acid (LBPA; also called bis(monoacylglycerol)phosphate) via tr
14  polyunsaturated acyl chains showed that all LBPA species containing one 18:1 chain significantly red
15                      Inside LEs, PS-ASOs and LBPA were co-localized in punctate, dot-like structures,
16 gate functional interaction between NPC2 and LBPA in cholesterol trafficking.
17              Deactivation of LBPA using anti-LBPA antibody significantly decreased PS-ASO activities
18 lysosomal bis(monoacylglycero)phosphate (BMP/LBPA) lipid levels were significantly decreased.
19      The (R,R) and (S,S) enantiomers of both LBPA and phosphorothioate LBPA were synthesized from (S)
20 n properties of ILVs, which are supported by LBPA, contribute to PS-ASO intracellular release from LE
21 vide a mechanistic basis supporting cellular LBPA as a potential new target for therapeutic intervent
22        Furthermore, Alix reduction decreased LBPA levels and limited co-localization of LBPA with PS-
23 pecific pharmacological interruption of EPCR-LBPA signaling attenuates major aPL-elicited pathologies
24             The engagement of aPLs with EPCR-LBPA expressed on innate immune cells sustains interfero
25 cid (LBPA), suggesting an important role for LBPA in NPC2-mediated cholesterol trafficking.
26 also led to robust and specific increases in LBPA species with polyunsaturated acyl chains, potential
27 s and an NPC1 mouse model that PG incubation/LBPA enrichment significantly improved the compromised a
28 analogues, and phosphorothioate analogues of LBPA from solketal.
29  configuration and acyl chain composition of LBPA on cholesterol clearance in NPC1-deficient cells.
30                              Deactivation of LBPA using anti-LBPA antibody significantly decreased PS
31 critically dependent upon the interaction of LBPA with functional NPC2 protein.
32 d LBPA levels and limited co-localization of LBPA with PS-ASOs at ILVs inside LEs.
33 e recycling, EGFR accumulates in a subset of LBPA-rich perinuclear multivesicular bodies (MVBs) disti
34 equirements for potential therapeutic use of LBPA as an option for addressing NPC disease.
35                                           PG/LBPA enrichment specifically enhanced the late stages of
36             Finally, we demonstrated that PG/LBPA treatment efficiently cleared cholesterol and toxic
37 CRT complex, the unconventional phospholipid LBPA, and other known endocytosis regulators.
38 nantiomers of both LBPA and phosphorothioate LBPA were synthesized from (S)- and (R)-solketal, respec
39               We find that S,R, S,S, and S,R LBPA stereoisomers behaved similarly, with all 3 compoun
40                       Examination of several LBPA molecular species containing one or two monounsatur
41                     Here we demonstrate that LBPA enrichment in human NPC2-deficient cells, either di
42 -deficient cells, supporting the notion that LBPA is the active agent promoting late endosome/lysosom
43 ycerol phosphate, either directly or via the LBPA precursor phosphatidylglycerol (PG), has been inves
44 G analogs to determine whether conversion to LBPA is required for sterol clearance, or whether PG its
45 PG species were not appreciably converted to LBPA and showed virtually no cholesterol clearance effic
46 that enrichment of NPC1-deficient cells with LBPA results in cholesterol clearance.
47 emonstrate that NPC2 interacts directly with LBPA and identify the NPC2 hydrophobic knob domain as th
48 internalization and became co-localized with LBPA by 2 hours in LEs.