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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
9 as it interacts with membranes containing 2% PI(3)P and 98% phosphatidylcholine.
10         The incidence rate resulted in 30.91 PI-CC per 1000 person-years (95% CI 25.14, 38).
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
17 ons showed FA decreases greater than the 99% PI for zero change.
18   Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo.
19 ressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this p
20 ne CC report and the probability of having a PI-CC.
21                                    KDU731, a PI (4) kinase inhibitor, blocks Cryptosporidium infectio
22                        However, binding of a PI(3,4,5)P3-embedded membrane nanodisc to Akt(PHD) with
23 g and/or gp41 in 61 individuals with VF on a PI/r (n = 40) or NNRTI (n = 20) containing regimen.
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
26                                 In addition, PIs induced beta-amyloid production, indicative of incre
27 ina seed lecithin is a promising alternative PI-rich emulsifier for various food applications.
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
30  to endosomal membranes mediated by GIPC and PI(4,5)P2 are crucial for filopodia formation.
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)
33            Our data show that (i) PI(3)P and PI(4)P are dispensable for the disassembly and activatio
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
37  in addition to the blastodisc, while PE and PI species are mostly absent in the yolk.
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)
40 YO6 to regulate the localization of PIP3 and PI(3)P phosphoinositides and Akt activation.
41                    In contrast, the Rec2 and PI domains tolerate mutation better than other regions.
42 erging evidence suggests that both IMiDs and PIs can have cardiovascular (CV) sequelae, which include
43 TIs (L100I, Y181C, K103N, V108I, Y188L), and PIs (V82L).
44             Apoptosis was confirmed (annexin-PI, SubG1/cell-cycle, apoptotic genes, caspase-3 and pol
45 as obesity, edema, and tenderness., Arterial PI can be used as a complimentary technique for the dete
46                        Lesions classified as PI-RADS category 3 at DW MR imaging and as positive at D
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
49  areas under the curve were compared between PI-RADS versions 1 and 2.
50                     The relationship between PI values of the popliteal artery and the number of thro
51 ed software SignalP v4.1, TargetP v1.01, Big-PI predictor, TMHMM v2.0 and ProtComp v9.0 were utilized
52                                          BIO PIs considered a range of computational needs important
53                                 However, BIO PIs said the most pressing unmet needs are training in d
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
56 ates phosphatidylinositide 4,5 bisphosphate (PI(4,5)P2).
57 PPI phosphatidylinositol (3,5)-bisphosphate (PI(3,5)P2) is essential in multiple organ systems.
58       Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is a negatively charged phospholipid that pla
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
65 ds to phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2].
66 gical failure (VF) while receiving a boosted PI (PI/r)-containing regimen.
67                              TIRAP PBM bound PIs through basic and nonpolar residues with high affini
68                         Shu1 cleavability by PI-PLC and its predicted hydropathy profile strongly sug
69 translocation is thermodynamically driven by PI(4,5)P2-induced membrane insertion of FGF2 oligomers.
70               Ionization energy exhibited by PI, equivalent to 10.8 eV, resulted in significant reten
71 e when compared with DW imaging in the TZ by PI-RADS version 2 criteria.
72 f phosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest responses triggered by th
73 h phosphoinositide-specific phospholipase C (PI-PLC).
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
77                In a buffer solution, E. coli PI-7 displayed a longer lag phase prior to decay and a l
78                    Subpopulations of E. coli PI-7 expressed genes related to dormancy and persister c
79        Virulence functions unique to E. coli PI-7 were also upregulated.
80                         The first is E. coli PI-7, a virulent and antibiotic-resistant strain that wa
81 ctive mechanisms were upregulated in E. coli PI-7.
82 lence and antibiotic resistance than E. coli PI-7.
83 ers cell growth and proteostasis and confers PI sensitivity.
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
87                                 As defective PI conversion underlies human genetic diseases, includin
88 a unique cohort of individuals who developed PI-IBS following exposure to contaminated drinking water
89                                     The DH44 PI-Hugin SEZ circuit controls circadian locomotor activi
90                    If gag and/or gp41 encode PI-resistance mutations, they may not be confined to con
91                          Conclusion Existing PI-RADS V2 decision rules exhibited reasonable performan
92                       The impact of existing PI-RADS V2 decision rules, as well as a series of explor
93 male, pointing to a potential role of female PIs in influencing the gender balance.
94 ith pancreatic-insufficient cystic fibrosis (PI-CF) are at increased risk for developing diabetes.
95                                     Finally, PI(4,5)P2 uncaging triggered the rapid fusion of a subse
96 hemolysis, cell viability, and AnnexinV-FITC/PI staining assays.
97 ncer detection of 15.7%, 16.0%, and 9.2% for PI-RADS category 2, 3, and 4 lesions, respectively.
98 s were detected in areas under the curve for PI-RADS version 2 versus 1.
99      The probability of cancer detection for PI-RADS category 2, 3, 4, and 5 lesions was 15.7%, 33.1%
100            These results point to a role for PI(3,4)P2 in the phenotype caused by loss-of-function mu
101 muli (NS) were compared between 14 drug-free PI patients and 18 good sleepers (GS) using functional m
102                        Viruses released from PI cells induced higher cell-to-cell fusion than the par
103 ion IMiD pomalidomide, the second-generation PIs carfilzomib and ixazomib, the DACI panobinostat, and
104                       Our data show that (i) PI(3)P and PI(4)P are dispensable for the disassembly an
105 ctor attachment protein receptors, that (ii) PI(3)P is required only after the tethering step, and th
106 nly after the tethering step, and that (iii) PI(4)P is required during and after tethering.
107 eighted, and diffusion-weighted (DW) imaging PI-RADS scores was calculated in the peripheral zone (PZ
108                                 Peri-implant PI, BOP, and PD >/=4 mm were recorded, and mesial and di
109 ne third of the minimum clinically important PI difference of two points.
110 rtments contain other functionally important PIs.
111 s no statistically significant difference in PI, BOP, PD >/=4 mm, and total CBL among smokers with IL
112 s during glucose potentiation were higher in PI-CF, suggesting impaired proinsulin processing.
113 d by light, allowing sub-second increases in PI(4,5)P2 levels.
114 higher while IL-10 mRNA levels were lower in PI-IBS D than in HC in both ileum and colon.
115 dulating the inflammatory/immune-response in PI-IBS in an ex-vivo organ culture model.
116 ficantly reduced expression of the SbCAD2 in PI 595743 throughout its growth stages.
117 pathways that regulate NKG2D ligands include PI-3 kinase activation, histone acetylation, and the int
118                      PTEN deletion increased PI(3,4)P2 levels in a mouse model of prostate cancer, an
119          Outcome measures were plaque index (PI), gingival index (GI), bleeding on probing (BOP), PD,
120                  They included plaque index (PI), modified sulcus bleeding index (mSBI), probing dept
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
136                Psychophysiological insomnia (PI) includes arousal to sleep-related stimuli (SS), whic
137                      Average pain intensity (PI) assessed on a 0 to 10 numerical rating scale at 10,
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%
141         We used the 99% prediction interval (PI) for zero change from historical control reproducibil
142 /TUB N terminus, and subsequent release into PI(4,5)P2-deficient ciliary membrane.
143 e faculty member and principal investigator (PI) as both unattainable and undesirable.
144 ic-science faculty [principal investigators (PIs)] younger than 46.
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
149 gnin reduction in the sorghum germplasm line PI 595743.
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
152                              PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol, and loss of PTE
153               Classical ways of manipulating PI(4,5)P2 levels are slower than its metabolism, making
154                Significant reduction in mean PI, GI, PD, and BOP were found after treatment in all gr
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
156                                Baseline mean PIs were 7.5 in both groups; mean average PIs assessed a
157 Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3.
158 ty of cancer detection than did DCE-negative PI-RADS category 3 lesions (67.8% vs 40.0%, P = .02).
159 F moiety sheds lights in the design of novel PIs.
160           Lesions were GS >/=7 in 0%-4.1% of PI-RADS categories 1 and 2, 11.4%-27.1% of PI-RADS categ
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
163 3% of PI-RADS category 4, and 72.1%-73.7% of PI-RADS category 5 lesions.
164 hatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia i
165 man aortic VSMC apoptosis (via activation of PI-3 kinase/Akt signalling) and proliferation.
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
170 er, ezrin can limit the lateral diffusion of PI(4,5)P2 along the lipid bilayer.
171  approaches to optimize the effectiveness of PI-based ART in high-tuberculosis-burden settings are ne
172 aking it difficult to distinguish effects of PI(4,5)P2 from those of its metabolites.
173 (3)P is produced by the INPP4A hydrolysis of PI(3,4)P2, and this is necessary for actin-driven endocy
174 nanodisc, indicating proper incorporation of PI(3,4,5)P3 on the nanodisc surface.
175 inase domain that lead to elevated levels of PI(3,5)P2 and impair the interaction between the kinase
176       First, capabilities and limitations of PI were tested using an authentic mixture of compounds o
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
179 esponse in an ex-vivo organ culture model of PI-IBS D.
180 fecting lipid chain or headgroup moieties of PI(3,4,5)P3.
181                      Multiple copy number of PI 88788-type GmSNAP18, GmAAT, and GmWI12 in one genomic
182         Second, considering the potential of PI for hydrocarbons, base oils, complex mixtures of satu
183  moves on actin filaments in the presence of PI(3,4,5)P3, an activator of myosin-X.
184         Defects in the dynamic regulation of PI(3,5)P2 are linked to human diseases.
185  between bilayers, allowing replenishment of PI(4,5)P2 hydrolyzed during signaling.
186    These results reveal an important role of PI(4,5)P2 for HIV-1 morphogenesis beyond Gag recruitment
187 leasable vesicles, revealing a rapid role of PI(4,5)P2 in fusion triggering.
188                               Mean scores of PI (P <0.05) and PD >/=4 mm (P <0.05) were statistically
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
192                 Here, we review the roles of PIs in different compartments of the endolysosomal syste
193         These findings implicate a subset of PIs as potential mediators of neurodegeneration in HIV-a
194 eatment failure if there is increased use of PIs-based therapy.
195 unger PIs (below 46) and increased for older PIs (above 55).
196 ades-long trend of more money going to older PIs.
197     CBT-I may exert its treatment effects on PI by reducing hyper-responses to SS in the precentral c
198 from age 4.5 to 6 years (P(U,LPS) < 0.001; P(PI) = 0.051; P(FOXP3) < 0.001).
199                             In addition, PD, PI, BOP, MR, and SUP varied significantly according to P
200 ids (PIPs) phosphatidylinositol 3-phosphate (PI(3)P) and phosphatidylinositol 4-phosphate (PI(4)P) as
201 containing phosphatidylinositol-3-phosphate (PI[3]P).
202 I(3)P) and phosphatidylinositol 4-phosphate (PI(4)P) as regulators of PLF.
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.
208           Depletion of phosphatidylinositol (PI) by targeting bacterial PI-specific phospholipase C t
209 phatidylglycerol (PG), phosphatidylinositol (PI), and sulfatides (ST).
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
212 f TIRAP is mediated by its phosphoinositide (PI)-binding motif (PBM).
213    By phosphorylating the phosphoinositide- (PI) binding domain of Daple, Akt abolishes Daple's abili
214                           Phosphoinositides (PIs) are phospholipids that perform crucial cell functio
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
217              In this study, photoionization (PI) was evaluated as the ion source for GCxGC-TOF-MS mea
218 l failure (VF) while receiving a boosted PI (PI/r)-containing regimen.
219                     At clathrin-coated pits, PI(3)P is produced by the INPP4A hydrolysis of PI(3,4)P2
220 ions through ARF6-dependent regulation of PM PI(4,5)P2 levels, pivotal for a variety of physiological
221                 Subsequent restoration of PM PI(4,5)P2 reinduced assembly site formation even in the
222 ucted on nanoholes array textured polyimide (PI) substrates.
223 ng to below 2 degrees C above preindustrial (PI) to prevent dangerous climate change.
224 y 3- or 5-phosphatases, the latter producing PI(3,4)P2.
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
228 the helical structure of TIRAP PBM, reducing PI interactions and cell membrane targeting.
229        However, few mechanisms that regulate PI(3,5)P2 have been identified.
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
235 ed electron is largely localized on a single PI unit.
236         INPP5E's phosphoinositide substrates PI(4,5)P2 and PI(3,4,5)P3 accumulated at the transition
237  by inhibiting PI(3)P production, suggesting PI(3)P kinase inhibitors as a therapeutic strategy in Lo
238 in post-infectious irritable bowel syndrome (PI-IBS) is convincing.
239  prostate imaging reporting and data system (PI-RADS) (version 2).
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
244       The Arabidopsis (Arabidopsis thaliana) PI-PLC gene family is composed of nine members.
245 PHD) with a 10(3)-fold tighter affinity than PI(3,4,5)P3 is able to completely displace CaM.
246 ming a different role in SCN resistance than PI 88788-type GmSNAP18.
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
250             Moreover, our data indicate that PI(4)P is needed to anchor Arl8 (Arf-like GTPase 8) and
251                    Our results indicate that PI(4,5)P2 induces the oligomerization of ExoU, which may
252                                 We show that PI(3,4,5)P3 binding to Akt(PHD) displaces the C-terminal
253 mouse adrenal chromaffin cells, we show that PI(4,5)P2 uncaging potentiates exocytosis and identify s
254 ,5)P2-binding CAPS-proteins, suggesting that PI(4,5)P2 uncaging may bypass CAPS-function.
255 aining the primary residency of Naa60 at the PI(4)P-rich Golgi.
256 V and NASH populations increased in both the PI and DAA eras (P < 0.001 for all) whereas HCC WL in HB
257  developed in gag and in gp41-CD in both the PI- and NNRTI-treated groups.
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
263                    The second version of the PI-RADS guidelines enabled standardized imaging, evaluat
264 tivation of exocytosis did not depend on the PI(4,5)P2-binding CAPS-proteins, suggesting that PI(4,5)
265                        During this time, the PI success ratio (fraction of basic-science PIs who are
266 tion of hydrophobic residues adjacent to the PI(3)P binding site, in addition to electrostatic intera
267           Nonetheless, since 2015 - when the PI-RADS v.2 was published, numerous questions regarding
268 ly orthogonal conformations adopted by their PI units.
269 es the oligomerization of ExoU and that this PI(4,5)P2-mediated oligomerization does not require ubiq
270 ancer diagnosis when stratified according to PI-RADS versions 1 and 2.
271 ng the development of resistance of HIV-1 to PIs.
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
277 nd phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).
278                                Unexpectedly, PI(4,5)P2 depletion also caused loss of pre-assembled Ga
279 ase assay, Hoechst 33342 staining, annexin V/PI staining, and JC-1 staining.
280 (HOPS) to (phago)lysosome membranes, whereas PI(3)P is required for membrane association of HOPS only
281                              To test whether PI sensitivity stems from AL LC production, we engineere
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
284                   Lesions were detected with PI-RADS version 2 and were compared with whole-mount pro
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
288  addition to electrostatic interactions with PI(3)P.
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
291                                     Men with PI-RADS categories 1-2 remained in urologic follow-up fo
292                                     Men with PI-RADS categories 3-5 underwent MR-guided targeted biop
293 onal signaling in the bowel of patients with PI-IBS.
294 enerated from tissue biopsy of patients with PI-IBS.
295 -subunit isoforms interact specifically with PI lipids in their organelles of residence.
296                              MR targets with PI-RADS version 2 category 2, 3, 4, and 5 scores had a p
297 protein sequences in 4 patients treated with PIs over a 9-year period.
298 The donor substrate, which is modified with "PI islands" to become selectively adhesive for the S4s,
299 tage investigator (ESI) policy to fund young PIs at higher rates.
300 Is who are R01 grantees) dropped for younger PIs (below 46) and increased for older PIs (above 55).

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