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1                                              PI4K-IIIalpha co-localized with NS5A and double-stranded
2 y, Vps74 (the orthologue of human GOLPH3), a PI4K effector required to maintain residence of a subset
3                                     Although PI4K-IIIalpha siRNAs decreased HCV replication and virus
4 onist-induced phospholipase C activation and PI4K inhibition, but not isolated PtdIns(4,5)P(2) deplet
5 dent of phosphoinositide kinase 3 (PI3K) and PI4K.
6 versely, lowering PIP2 synthesis by blocking PI4K or using the PIP2 scavengers polylysine or bovine s
7 e-III phosphatidylinositol 4-kinase enzymes (PI4Ks).
8 l 4-kinase beta (PI4KB) is one of four human PI4K enzymes that generate phosphatidylinositol 4-phosph
9 soform of the recently characterized type II PI4K (PI4KII) family.
10 annel indirectly as a substrate for type III PI4Ks.
11 t of subtype-specific inhibitors of type-III PI4Ks and help to better understand the significance of
12                       Inhibition of type-III PI4Ks with 10 microM wortmannin (Wm) significantly reduc
13  chemically distinct agents known to inhibit PI4K, resulted in both an inhibition of agonist-induced
14 , neither LIS1 nor phosphoinositol-4 kinase (PI4K) were detected in any of the purified tagged 3A sam
15 7 cells during manipulations of PI 4-kinase (PI4K) activities.
16 that type III phosphatidylinositol-4-kinase (PI4K) activity is required.
17           We report here that a PI 4-kinase (PI4K) activity previously reported on synaptic vesicles
18 osely related phosphatidylinositol 4-kinase (PI4K) PI4Kbeta1 and PI4Kbeta2 lipid kinases.
19 wo classes of phosphatidylinositol 4-kinase (PI4K), designated as Types II and III, that phosphorylat
20  patches in a phosphatidylinositol 4-kinase (PI4K)-dependent manner.
21       Because phosphatidylinositol 4-kinase (PI4K)-mediated phosphatidylinositol 4-phosphate (PI(4)P)
22 e activity of phosphatidylinositol-4-kinase (PI4K).
23 Plasmodium phosphatidylinositol-4-OH kinase (PI4K)-specific inhibitor KDU691.
24              Phosphatidylinositol 4-kinases (PI4K) catalyze the first step in the synthesis of phosph
25              Phosphatidylinositol 4-kinases (PI4Ks) and small guanosine triphosphatases (GTPases) are
26          Two phosphatidylinositol 4-kinases (PI4Ks) have been localized to the Golgi complex in mamma
27 hat distinct phosphatidylinositol 4-kinases (PI4Ks) play important roles at multiple steps in the tra
28  vesicles by phosphatidylinositol 4-kinases (PI4Ks) that produce phosphatidylinositol 4-phosphate (Pt
29 bit type III phosphatidylinositol 4-kinases (PI4Ks).
30 egulation of phosphatidylinositol 4-kinases (PI4Ks).
31 parison of type II and type III PI4-kinases, PI4Ks were not required for HCV entry, and only PI4K-III
32 respect to the kinetic effects of modulating PI4K activity on polarized biosynthetic traffic in MDCK
33 IIalpha, which also accounts for the bulk of PI4K activity in brain extracts, is concentrated at syna
34 er, the structural basis for coordination of PI4K, GTPases, and their effectors is unknown.
35                             Determination of PI4K activity in subcellular fractions of SH-SY5Y cells
36  that the activity of a WT-sensitive form of PI4K, such as PI4Kbeta, is required.
37 ailed study of novel selective inhibitors of PI4K IIIbeta, which exert antiviral activity against a p
38  distribution of the 110-kDa beta isoform of PI4K, as determined by Western blot analysis.
39 zyme results in the arrest of replication of PI4K IIIbeta-dependent viruses.
40 Ks were not required for HCV entry, and only PI4K-IIIalpha was required for HCV replication.
41 confirmed that phospholipase C activation or PI4K inhibition greatly reduced I(CRAC) currents.
42 tidylinositol 4-kinases (PtdIns 4-kinases or PI4Ks) are at the apex of the phosphoinsitide cascade.
43 nt firing by proBDNF relies on a p75NTR-Rac1-PI4K pathway.
44           To convert their lipid substrates, PI4Ks must be recruited to the correct membrane compartm
45                              We propose that PI4K-IIIalpha plays an essential role in membrane altera
46 initial HCV RNA translation, suggesting that PI4K-IIIalpha functions at a posttranslational stage.
47                   We previously reported the PI4K inhibitor PIK93, and this compound has defined key
48            Therefore, the inhibition of this PI4K isoform leads to the arrest of viral replication.
49 ts under dynamic conditions and that various PI4Ks regulate PI(4)P synthesis in distinct cellular com
50 localized PtdIns4P production by the various PI4Ks isoforms in specific cellular compartments.
51                            Pretreatment with PI4K-IIIalpha siRNAs greatly reduced the accumulation of

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