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1 PI patients showed higher BOLD activation to SS in the p
2 PI showed hyper-responses to SS in the precentral cortex
3 PI(3,4,5)P3 can be dephosphorylated by 3- or 5-phosphata
4 PI(3,5)P2 is generated from PI3P by the conserved lipid
5 PI(4,5)P2 activation of exocytosis did not depend on the
6 PI-CF subjects had lower acute insulin, C-peptide, and g
7 0:1/18:3), DG(24:1/22:6/0:0), PS(18:2/18:0), PI(16:0/16:0), PS(18:0/18:1), PS(14:1/14:0), dihydroxyac
8 cultures of ileal and colonic mucosa from 10 PI-IBS, diarrhea predominant subtype (D) patients, and 1
11 %), 0.60% (95% PI: 0.08%, 1.11%), 0.24% (95% PI: 0.02%, 0.46%), and 0.29% (95% PI: 0.07%, 0.50%) high
12 ior interval (PI): 0.13%, 0.35%], 0.27% (95% PI: 0.10%, 0.44%), 0.60% (95% PI: 0.08%, 1.11%), 0.24% (
13 0.24% (95% PI: 0.02%, 0.46%), and 0.29% (95% PI: 0.07%, 0.50%) higher daily mortality from all nonacc
14 r respiratory hospitalizations, a 2.57% (95% PI: 0.87%, 4.30%) increase per 10-mug/m(3) increase in P
15 %], 0.27% (95% PI: 0.10%, 0.44%), 0.60% (95% PI: 0.08%, 1.11%), 0.24% (95% PI: 0.02%, 0.46%), and 0.2
16 interval (PI): -0.71%, 1.41%] and 0.98% (95% PI: 0.73%, 1.23%) increases in hospitalization risk per
19 ressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this p
24 ents treated in our health system received a PI-CC during the first ten consecutive years after a nor
25 even in a climate held to 2 degrees C above PI, Karachi (Pakistan) and Kolkata (India) could expect
28 quires both the rhg1-a and Rhg4 alleles, and PI 88788-type soybean, whose resistance requires only th
29 cterium prausnitzii were depleted in EFV and PI compared to HIV SN and negatively correlated with int
31 C), a recently described class of NAADP- and PI(3,5)P2-sensitive Ca(2+)-permeable cation channels in
32 ollowed by 2 expansion cohorts (PI-naive and PI-exposed patients) at the maximum tolerated dose (MTD)
34 sm by which the coincidence of PI(4,5)P2 and PI(3)P in a curved vesicle triggers actin polymerization
35 's phosphoinositide substrates PI(4,5)P2 and PI(3,4,5)P3 accumulated at the transition zone (TZ) in H
36 ethod permitting separation of PI(3,4)P2 and PI(4,5)P2, a technical issue hindering the phosphoinosit
38 ecific interaction between PLC delta1-PH and PI(4,5)P2, encoded within the conformational properties
39 nding has been observed between Akt(PHD) and PI(3,4,5)P3-free nanodiscs, demonstrating that PI(3,4,5)
42 erging evidence suggests that both IMiDs and PIs can have cardiovascular (CV) sequelae, which include
45 as obesity, edema, and tenderness., Arterial PI can be used as a complimentary technique for the dete
47 an PIs were 7.5 in both groups; mean average PIs assessed at 10, 20, and 30 min postadministration we
48 phatidylinositol (PI) by targeting bacterial PI-specific phospholipase C to the PIS domain impairs re
51 ed software SignalP v4.1, TargetP v1.01, Big-PI predictor, TMHMM v2.0 and ProtComp v9.0 were utilized
54 ces Directorate principal investigators (BIO PIs), nearly 90% indicated they are currently or will so
55 ) and phosphatidylinositol 3,4-bisphosphate (PI(3,4)P2), suggesting that the macropinosome is the loc
59 with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the main lipid marker of the plasma membrane
60 main in a phosphoinositide 4,5-bisphosphate (PI(4,5)P2)-dependent manner, ciliary delivery by intrafl
61 te PM phosphatidylinositol 4,5-bisphosphate (PI[4,5]P2) levels, important for localization of STIM1 a
62 ctors phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] and ubiquitin for its activation in vitro We
63 s the phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] precursor phosphatidylinositol between bilaye
64 ially phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], regulate the activities of many actin-bindin
69 translocation is thermodynamically driven by PI(4,5)P2-induced membrane insertion of FGF2 oligomers.
72 f phosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest responses triggered by th
74 pathies, neurological disorders, and cancer, PI-converting enzymes represent potential targets for dr
75 ility of having a potentially inadequate CC (PI-CC, e.g. a CC that was performed earlier that recomme
76 n phase was followed by 2 expansion cohorts (PI-naive and PI-exposed patients) at the maximum tolerat
84 the mechanisms that spatiotemporally control PI conversion in endocytosis and endolysosomal membrane
85 NF1), NF-kappaB signaling (PRKCB, CSNK1A1), PI-3-kinase signaling (PIK3R1, VAV1), RHOA/cytoskeleton
86 Strikingly, lipid recognition by the default PI(4,5)P2 lipid sensor, phospholipase C delta 1 pleckstr
88 a unique cohort of individuals who developed PI-IBS following exposure to contaminated drinking water
94 ith pancreatic-insufficient cystic fibrosis (PI-CF) are at increased risk for developing diabetes.
101 muli (NS) were compared between 14 drug-free PI patients and 18 good sleepers (GS) using functional m
103 ion IMiD pomalidomide, the second-generation PIs carfilzomib and ixazomib, the DACI panobinostat, and
105 ctor attachment protein receptors, that (ii) PI(3)P is required only after the tethering step, and th
107 eighted, and diffusion-weighted (DW) imaging PI-RADS scores was calculated in the peripheral zone (PZ
111 s no statistically significant difference in PI, BOP, PD >/=4 mm, and total CBL among smokers with IL
117 pathways that regulate NKG2D ligands include PI-3 kinase activation, histone acetylation, and the int
121 sulcus bleeding index (mSBI), plaque index (PI), probing depth (PD), and clinical attachment level (
122 mplant soft tissue parameters (plaque index [PI], bleeding on probing [BOP], and probing depth [PD] >
123 ical data (probing depth [PD], plaque index [PI], gingival index [GI], bleeding on probing [BOP], and
124 lesions in vitro at 27 days post-infection (PI), providing new evidence of the role of the parasite
125 main family 4 (RASSF4) positively influences PI(4,5)P2 synthesis through ARF6-dependent regulation of
126 OCRL) deficiencies are reduced by inhibiting PI(3)P production, suggesting PI(3)P kinase inhibitors a
127 fumarate (TDF) without a protease inhibitor (PI) (0.18 [interquartile range {IQR}, 0.08-0.30]; n = 37
128 models to show that HIV protease inhibitor (PI) class ARVs induced neuronal damage and ER stress, le
129 GRL-09510, a novel HIV-1 protease inhibitor (PI) containing a newly-generated P2-crown-tetrahydrofura
130 rferon (IFN; 2003-2010), protease inhibitor (PI; 2011-2013), and direct-acting antiviral (DAA; 2014-2
131 y efficacy of the oral proteasome inhibitor (PI) ixazomib in patients with relapsed/refractory immuno
132 V) or ritonavir-boosted Protease Inhibitors (PI) with the same backbone of Nucleoside Reverse Transcr
133 cleoside RTIs (NNRTIs), protease inhibitors (PIs), and integrase inhibitors (IIs) did not affect HK2,
134 ory drugs (IMiDs) and proteasome inhibitors (PIs) has greatly improved the overall survival of patien
135 atory agents (IMiDs), proteasome inhibitors (PIs), histone deacetylase inhibitors (DACIs), and monocl
138 ressing neurons in the pars intercerebralis (PI) through hugin+ SEZ neurons to the ventral nerve cord
139 ban counties: 0.35% [95% posterior interval (PI): -0.71%, 1.41%] and 0.98% (95% PI: 0.73%, 1.23%) inc
140 sociated with 0.24% [95% posterior interval (PI): 0.13%, 0.35%], 0.27% (95% PI: 0.10%, 0.44%), 0.60%
145 deoxyuridine (BrdU) assay, propidium iodide (PI) staining and growth curves, and blocks cell migratio
146 h phorbol 12-myristate 13-acetate/ionomycin (PI) or lipopolysaccharide (LPS), and stained for Tregs (
147 uggest that the Cryptosporidium lipid kinase PI(4)K (phosphatidylinositol-4-OH kinase) is a target fo
148 ytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads to synergistic accumulati
150 rk demonstrated that the endolysosomal lipid PI(3,5)P2 activates V-ATPases containing the vacuolar a-
151 red with the control group (P <0.001): lower PI and GI, less BOP, less increase in GCF volume, and lo
155 s with 1 and/or 2 thrombosed veins, the mean PI was 6.03+/-0.54 on the side of cDVT and 5.68+/-0.39 o
158 ty of cancer detection than did DCE-negative PI-RADS category 3 lesions (67.8% vs 40.0%, P = .02).
161 f PI-RADS categories 1 and 2, 11.4%-27.1% of PI-RADS category 3, 44.4%-49.3% of PI-RADS category 4, a
162 -27.1% of PI-RADS category 3, 44.4%-49.3% of PI-RADS category 4, and 72.1%-73.7% of PI-RADS category
164 hatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia i
166 that neuronal signaling within the bowel of PI-IBS patients is sensitized 2 years after the initial
167 date a mechanism by which the coincidence of PI(4,5)P2 and PI(3)P in a curved vesicle triggers actin
168 icle endocytosis to the dephosphorylation of PI(4,5)P2, a reaction needed for the shedding of endocyt
169 s in living cells, we show that depletion of PI(4,5)P2 completely prevents Gag PM targeting and assem
171 approaches to optimize the effectiveness of PI-based ART in high-tuberculosis-burden settings are ne
173 (3)P is produced by the INPP4A hydrolysis of PI(3,4)P2, and this is necessary for actin-driven endocy
175 inase domain that lead to elevated levels of PI(3,5)P2 and impair the interaction between the kinase
177 that allows rapidly tunable manipulation of PI(4,5)P2 levels in living cells, we show that depletion
178 Electrokinetic potential measurements of PI(4,5)P2 containing liposomes reveal that Ca(2+) as wel
186 These results reveal an important role of PI(4,5)P2 for HIV-1 morphogenesis beyond Gag recruitment
189 ovel HPLC-MS method permitting separation of PI(3,4)P2 and PI(4,5)P2, a technical issue hindering the
190 traced viral evolution under the pressure of PIs using Gag-protease single genome sequencing and coev
191 e that directly linking the benzene rings of PIs with a single C-C bond is a viable method for genera
197 CBT-I may exert its treatment effects on PI by reducing hyper-responses to SS in the precentral c
200 ids (PIPs) phosphatidylinositol 3-phosphate (PI(3)P) and phosphatidylinositol 4-phosphate (PI(4)P) as
203 e equilibrium between phosphatidylinositide (PI) species within the cell and increases basal autophag
204 embranes containing the phosphatidylinositol PI(4)P, thus possibly explaining the primary residency o
205 thanolamines (PE), and phosphatidylinositol (PI), in newly fertilized individual zebrafish embryos.
206 the predominant Golgi phosphatidylinositol (PI) species, directly interacts with the cytosolic amino
207 C and EDLC was rich in phosphatidylinositol (PI), and contents were 37.8 and 25.2wt%, respectively.
210 ol in spines depends on the phosphoinositide PI(3,4,5)P3 and involves the actin monomer-binding prote
211 al program dependent on the phosphoinositide PI(3,4,5)P3 is sufficient to trigger all steps of myelin
213 By phosphorylating the phosphoinositide- (PI) binding domain of Daple, Akt abolishes Daple's abili
215 unction involved binding to the phospholipid PI(3)P and promoting actin nucleation at nascent autopha
216 eloped a membrane-permeant, photoactivatable PI(4,5)P2, which is loaded into cells in an inactive for
220 ions through ARF6-dependent regulation of PM PI(4,5)P2 levels, pivotal for a variety of physiological
225 hods Two radiologists independently provided PI-RADS V2 scores for the dominant lesion on 343 prostat
226 ion of a series of X-shaped pyromellitimide (PI) oligomers (Xn-R, n = 2-4, R = Hex or Ph) linked toge
227 tations definitively responsible for reduced PI susceptibility have been identified in individuals wi
230 which we term protein interaction by SAMDI (PI-SAMDI), has the advantages that it is applicable to l
231 dy drop in the number of young basic-science PIs and could reduce future US discoveries in fundamenta
232 PI success ratio (fraction of basic-science PIs who are R01 grantees) dropped for younger PIs (below
233 ntify gag and gp41 mutations under selective PI pressure, we sequenced gag and/or gp41 in 61 individu
234 search Award (MIRA) program to reward senior PIs with research time in exchange for less funding, thi
237 by inhibiting PI(3)P production, suggesting PI(3)P kinase inhibitors as a therapeutic strategy in Lo
240 Prostate Imaging Reporting and Data System (PI-RADS) version 2 (V2) decision rules, as well as of pr
241 Prostate Imaging Reporting and Data System (PI-RADS) version 2 score to better understand false-nega
242 Prostate Imaging Reporting and Data System (PI-RADS) version 2; only thereafter, the remaining full
243 {IQR}, 0.08-0.30]; n = 372), LDV/SOF and TDF/PI (0.17 [IQR, 0.04-0.30]; n = 100), and LDV/SOF without
247 aromyces cerevisiae Here we demonstrate that PI(4)P, the predominant Golgi phosphatidylinositol (PI)
248 its activation in vitro We demonstrated that PI(4,5)P2 also induces the oligomerization of ExoU and t
249 (3,4,5)P3-free nanodiscs, demonstrating that PI(3,4,5)P3 is required for membrane binding, CaM displa
253 mouse adrenal chromaffin cells, we show that PI(4,5)P2 uncaging potentiates exocytosis and identify s
256 V and NASH populations increased in both the PI and DAA eras (P < 0.001 for all) whereas HCC WL in HB
258 stance is mechanistically different from the PI 88788-type of resistance that only requires rhg1 We a
259 Listing for DC in HBV also decreased in the PI (-17%; P = 0.002) and DAA eras (-24%; P < 0.001).
260 y, WL for DC in NASH increased by 41% in the PI era (P < 0.001) and 81% in the DAA era (P < 0.001).
261 or DC in HCV patients decreased by 5% in the PI era (P = 0.004) and 32% in the DAA era (P < 0.001) co
262 rs Xn-Hex, reveal that the reductions of the PI units occur at multiple distinct potentials, highligh
264 tivation of exocytosis did not depend on the PI(4,5)P2-binding CAPS-proteins, suggesting that PI(4,5)
266 tion of hydrophobic residues adjacent to the PI(3)P binding site, in addition to electrostatic intera
269 es the oligomerization of ExoU and that this PI(4,5)P2-mediated oligomerization does not require ubiq
272 CRF02_AG population with little exposure to PIs ( 3%), mutations in the Gag P2/NC CS could increase
273 ecedented intrinsic sensitivity of AL PCs to PIs, even higher than that of MM PCs, associated with di
274 with the development of HIV-1 resistance to PIs, we traced viral evolution under the pressure of PIs
275 or phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) and phosphatidylinositol 3,4-bisphosphate (
276 of phosphatidylinositol-3,4,5-trisphosphate (PI(3,4,5)P3) and play important roles in regulating the
280 (HOPS) to (phago)lysosome membranes, whereas PI(3)P is required for membrane association of HOPS only
282 ucose tolerance, adolescents and adults with PI-CF have impairments in functional islet mass and asso
283 ate cancer, and it inversely correlated with PI(3,4)P2 levels across several EGF-stimulated prostate
285 tion that prevents C2E from interacting with PI(4,5)P2-rich membranes, as previously suggested by stu
286 of Stv1NT is essential for interaction with PI(4)P in vitro and in vivo, and interaction with PI(4)P
287 P in vitro and in vivo, and interaction with PI(4)P is required for efficient localization of Stv1-co
289 ial and mutually exclusive interactions with PI(4,5)P2 and heparan sulfates on opposing sides of the
290 TPase a2 isoform specifically interacts with PI(4)P in vitro, consistent with its Golgi localization
298 The donor substrate, which is modified with "PI islands" to become selectively adhesive for the S4s,
300 Is who are R01 grantees) dropped for younger PIs (below 46) and increased for older PIs (above 55).
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