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1 PAP activity was stimulated by anionic lipids (cardiolip
2 PAP binds to VPg with high affinity (29.5 nm); the react
3 PAP can be classified into different types on the basis
4 PAP has a prevalence of at least 7 cases per million ind
5 PAP I competes with the 3' -> 5' exonucleases for pre-tR
6 PAP is also a cap-binding protein and is a potent antivi
7 PAP levels were specifically elevated in the cytosol of
8 PAP results in progressive dyspnoea of insidious onset,
9 PAP seems to have contributed to the death of only 1 pat
10 PAP(248-286) is a peptide fragment of prostatic acid pho
11 PAP-specific CD8(+)CTLA-4(+) T cells also suppressed T c
12 PAP-specific T cells were detected in both cohorts, incl
14 e, we investigate the requirement of lipin-1 PAP versus coactivator function in the establishment of
15 ry fatty acids into triglycerides, lipin 2/3 PAP activity has a critical role in phospholipid homeost
17 SIGNIFICANCE: Identification of App1p as a PAP enzyme will facilitate the understanding of its cell
19 diac output (CO) measurements to calculate a PAP/CO slope, and exPH defined as a PAP/CO slope >3 mm H
26 e worse for MIP/SOL compared with LEP or ACN/PAP subgroup (P < .01); this remained marginally signifi
28 detection limit of 31 muM for p-aminophenol (PAP) using Pt electrodes and was also used to detect enz
30 We find that in addition to forming amyloid, PAP(248-286) much more readily assembles with lipid vesi
32 ids), PAPS consumption (in the cytosol), and PAP (the stress signaling molecule 3'-phosphoadenosine 5
33 ogether, our results reveal a PAS-guided and PAP-mediated paradigm for gene expression in response to
34 -CSF signaling in surfactant homeostasis and PAP pathogenesis in humans and have therapeutic implicat
35 ochemically active substrates, PNP, ONP, and PAP were determined to be 1.1, 2.8, and 0.5 muM, respect
37 undergo outpatient diagnostic procedures and PAP titration in the sleep laboratory (ideally within 2-
38 d 3T3-L1 cells where total lipin protein and PAP activity levels are down-regulated by the combined d
40 n [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and complement (C3b, C5a, C5b-9) in baboons infus
43 ld-type cells, are rapidly polyadenylated as PAP I levels increase, leading to dramatic reductions in
44 lipid synthesis and composition, as well as PAP activity in various PAP mutant strains, showed the e
47 prevalent clinical form of PAP is autoimmune PAP (aPAP) whereby IgG autoantibodies neutralize GM-CSF.
49 rgets various RNAs, the interactions between PAP and turnip mosaic virus genome-linked protein (VPg)
53 ing a double mutant mouse deficient for both PAP synthesis and hydrolysis, consistent with a mechanis
55 pecific SP components on fibril formation by PAP(248-286) revealed that this effect is primarily due
58 suggest that the polyadenylation of tRNAs by PAP I likely proceeds in a distributive fashion unlike w
60 differ among the various diseases that cause PAP.Conclusions: This insight into the alveolar lipidome
63 arious underlying conditions; and congenital PAP is caused by mutations in genes involved in surfacta
64 ation analysis profile-area under the curve (PAP-AUC) of consecutive methicillin-resistant Staphyloco
66 nity of PARylated PAP in vitro and decreased PAP association with non-heat shock protein-encoding gen
67 d in vitro disease model of CSF2RA-deficient PAP, and introduce gene-corrected iPSC-derived monocytes
68 ylglycerol, is unique among Mg(2+)-dependent PAP enzymes in that its reaction is not involved with de
73 per 10 mm Hg increase; P = 0.022), diastolic PAP - pulmonary capillary wedge pressure (HR, 2.19; 95%
74 per 10 mm Hg increase; P = 0.027), diastolic PAP (HR, 1.83; 95% CI, 1.09-3.08 per 10 mm Hg increase;
75 tolic pulmonary pressure gradient (diastolic PAP minus mean PAWP) <7 mm Hg, a transpulmonary pressure
76 ss of PAP activity, indicating that distinct PAP enzymes in S. cerevisiae are encoded by APP1, PAH1,
77 nce as the primary macrophage defect driving PAP pathogenesis, and support the feasibility of transla
78 ease in hepatic lipin-1 protein and elevated PAP activity, which maintained lipid homeostasis under b
79 ur genes (APP1, DPP1, LPP1, and PAH1) encode PAP activity in yeast, and it has been unclear which gen
80 ata suggest that in the in vivo environment, PAP(248-286) is likely to form fibrils efficiently, thus
84 derstand how the N-Lip and C-Lip combine for PAP function, we determined crystal structures of Tetrah
85 s meets the requirements for new methods for PAP detection and can be used in future feed authenticat
87 Our data suggest a more dynamic role for PAP I in maintaining functional tRNA levels in the cell.
89 tRNAs, which are normally not substrates for PAP I in wild-type cells, are rapidly polyadenylated as
91 ns (lipin 1, lipin 2, and lipin 3) each have PAP activity, but have distinct tissue distributions, wi
92 iPS cells from two children with hereditary PAP (hPAP) caused by recessive CSF2RA(R217X) mutations a
93 ow that human RegIIIalpha (also known as HIP/PAP) binds membrane phospholipids and kills bacteria by
94 m of RNA depurination, and to understand how PAP recognizes and targets various RNAs, the interaction
96 of polyadenylation by poly(A) polymerase I (PAP I) in Escherichia coli leads to toxicity and cell de
98 dosome is required for poly(A) polymerase I (PAP I)-dependent polyadenylation after Rho-independent t
99 t studies suggest that poly(A) polymerase I (PAP I)-mediated polyadenylation in Escherichia coli is h
100 predominant HRCT presentation of idiopathic PAP was interlobular septal thickening and ground glass
102 e: 38+/-14years; 54.3% male) with idiopathic PAP (proved by bronchoalveolar lavage or biopsy) were re
104 es suggest that exercise-induced increase in PAP to a mean higher than 30 mm Hg may be associated wit
106 sis of Arabidopsis thaliana mutant plants in PAP-SAL1 pathway revealed that the ferritin genes AtFER1
108 the Kv1.3-specific small-molecule inhibitor PAP-1, thus highlighting the importance of Kv1.3 in neur
110 iated phosphorylation of Pah1p inhibited its PAP activity by decreasing catalytic efficiency, and the
113 ssion of a truncated lipin 1 protein lacking PAP activity but retaining transcriptional regulatory fu
120 Our findings indicate that borderline mean PAP and an elevated TPG in patients with SSc predict pro
122 Hg, a transpulmonary pressure gradient (mean PAP minus mean PAWP) <12 mm Hg, and pulmonary vascular r
123 L) positively correlated with increased mean PAP (r = 0.5, P = .03) and septal eccentricity index (r
124 ere independently related to mortality: mean PAP (hazard ratio [HR], 1.61; 95% confidence interval [C
126 ean RV E(LL) positively correlated with mean PAP (r = 0.62, P < .0014) and pulmonary vascular resista
127 likely to develop PH than patients with mean PAP</=20 mm Hg (P<0.001 by log rank test, hazard ratio [
129 a suggest that mice lacking lipin 1-mediated PAP activity in skeletal muscle may serve as a model for
131 nsion was ascertained using minute-by-minute PAP and cardiac output (CO) measurements to calculate a
133 ly(ADP-ribose) polymerase 1 (PARP1) modifies PAP and regulates its activity both in vitro and in vivo
136 macrophages differentiated from noncorrected PAP-iPSCs exhibited distinct defects in GM-CSF-dependent
140 of BPNT-1 leads to the toxic accumulation of PAP in yeast and non-neuronal cell types in mice [4, 5].
144 ce and lung histopathology characteristic of PAP; 2) alveolar macrophages from Rasgrp1-deficient mice
146 ples and find that they partially consist of PAP fragments, interact with HIV particles and increase
147 nism, in which a critical surface density of PAP(248-286) on liposomes enables peptide-mediated parti
149 ere the most frequently observed features of PAP in PGA-treated eyes compared with untreated fellow e
152 vities assigned to SEVI, the amyloid form of PAP(248-286), could instead be attributed to a PAP(248-2
153 presents an important organellar importer of PAP, providing a piece of the puzzle in our understandin
154 nd RNase PH, there is a >30-fold increase of PAP I-dependent poly(A) tails that are </=10 nt in lengt
158 triple mutant resulted in a complete loss of PAP activity, indicating that distinct PAP enzymes in S.
162 ies should be educated on the possibility of PAP, especially when initiating monocular PGA therapy.
165 Here, we study the coassembly process of PAP(248-286), a seminal peptide that displays both amylo
167 ore, our data demonstrate that regulation of PAP I is critical not for preventing the decay of mRNAs,
169 n combination, showed that Pah1p is the only PAP involved in the synthesis of triacylglycerol as well
172 This illustrates mechanisms for lipin/Pah PAP function, membrane association, and lipin-related pa
173 histologic pattern-lepidic (LEP), papillary (PAP), acinar (ACN), micropapillary (MIP), or solid (SOL)
174 ts reduced RNA binding affinity of PARylated PAP in vitro and decreased PAP association with non-heat
176 t semen proteins prostatic acid phosphatase (PAP) and semenogelins form amyloid fibrils in vitro.
177 es lipin-1, a phosphatidic acid phosphatase (PAP) controlling the rate-limiting step in the phospholi
178 The lipin phosphatidic acid phosphatase (PAP) enzymes are required for triacylglycerol (TAG) synt
179 and 3) act as phosphatidic acid phosphatase (PAP) enzymes, which are required for triacylglycerol (TA
180 I-816]) encoding prostatic acid phosphatase (PAP) in patients with recurrent, nonmetastatic prostate
181 Lipin 2 is a phosphatidic acid phosphatase (PAP) responsible for the penultimate step of triglycerid
182 report on human prostatic acid phosphatase (PAP), a tumor marker, with a limit of detection of 11 pM
184 mmalian homolog, prostatic acid phosphatase (PAP; also known as ACPP-201) stably associates with muri
185 rs and a phosphatidic acid (PA) phosphatase (PAP) enzyme that catalyzes a critical step in the synthe
187 -1 functions as a phosphatidate phosphatase (PAP) enzyme in the glycerol 3-phosphate pathway for trig
188 The three lipin phosphatidate phosphatase (PAP) enzymes catalyze a step in glycerolipid biosynthesi
189 Mg(2+)-dependent phosphatidate phosphatase (PAP) enzymes with essential roles in lipid biosynthesis.
190 hich functions as phosphatidate phosphatase (PAP) in the yeast Saccharomyces cerevisiae, plays a cruc
191 tes a role of the phosphatidate phosphatase (PAP) in this metabolism; the enzyme produces the diacylg
192 Yeast App1p is a phosphatidate phosphatase (PAP) that associates with endocytic proteins at cortical
193 The PAH1-encoded phosphatidate phosphatase (PAP), which catalyzes the committed step for the synthes
196 olecule is 3'-phosphoadenisine-5'-phosphate (PAP) and it's in vivo levels are regulated by SAL1/FRY1,
197 i-resident 3'-phosphoadenosine 5'-phosphate (PAP) phosphatase (gPAPP) and Bisphosphate 3'-nucleotidas
198 entify the 3'-phosphoadenosine 5'-phosphate (PAP) phosphatase SAL1 as a previously unidentified and c
199 cytosolic 3'-phosphoadenosine 5'-phosphate (PAP), a byproduct of sulfation reactions utilizing the u
201 ing as a phosphatidic acid phosphohydrolase (PAP) enzyme in the triglyceride-synthesis pathway and by
202 Lipin-1 is a phosphatidate phosphohydrolase (PAP) required for the generation of diacylglycerol durin
203 ition of the noncanonical poly(A) polymerase PAP-associated domain-containing 5 (PAPD5) increased TER
204 the catalytic module of poly(A) polymerase (PAP) are recruited by the CPSF30-hFip1 complex in vitro,
205 lation of nascent RNA by poly(A) polymerase (PAP) is important for 3' end maturation of almost all eu
207 the nuclear noncanonical poly(A) polymerase (PAP) speckle targeted PIPKIalpha regulated PAP (Star-PAP
212 s with OHS receive positive airway pressure (PAP), 3) continuous positive airway pressure (CPAP) rath
216 rements of a mean pulmonary artery pressure (PAP) >/=25 mm Hg and mean wedged PAP (PAWP) >15 mm Hg.
217 was found between pulmonary artery pressure (PAP) and AF in these patients, right ventricular functio
218 rease of pulmonary capillary wedge pressure, PAP and RAP were more pronounced in AF than in SR, sugge
219 basis of the pathogenetic mechanism: primary PAP is characterized by the disruption of granulocyte-ma
223 Rationale: Pulmonary alveolar proteinosis (PAP) is characterized by filling of the alveolar spaces
224 atients with pulmonary alveolar proteinosis (PAP) syndrome, disruption of granulocyte/macrophage colo
225 teristic for pulmonary alveolar proteinosis (PAP), it is not specific and has not been compared betwe
226 ption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid composition in alveolar macroph
230 (PAP) speckle targeted PIPKIalpha regulated PAP (Star-PAP) controls E6 mRNA polyadenylation and expr
233 ncoding GM-CSF receptor subunits); secondary PAP results from various underlying conditions; and cong
241 Palpha and PAPgamma) and non-canonical (Star-PAP) PAPs play diverse roles in PAS selection and gene e
242 tures in the BIK 3' UTR uniquely define Star-PAP specificity and may block canonical PAP activity tow
243 role for phosphorylation in determining Star-PAP target mRNA specificity and regulation of 3'-end pro
244 hosphorylation at the catalytic domain, Star-PAP S6 phosphorylation is insensitive to oxidative stres
245 ithin the nucleus which is required for Star-PAP nuclear retention and interaction with PIPKIalpha.
248 c NQO1 mRNA isoforms in the presence of Star-PAP expression, and reverses molecular events of hypertr
249 PIPKIalpha controlled select subset of Star-PAP target messages by regulating Star-PAP-mRNA associat
250 sociated kinases act as coactivators of Star-PAP that regulates its activity and specificity toward m
253 hosphorylated residue (serine 6, S6) on Star-PAP in the zinc finger region, the domain required for P
254 ckle targeted PIPKIalpha regulated PAP (Star-PAP) controls E6 mRNA polyadenylation and expression and
256 alpha, PI4,5P(2), and PKCdelta regulate Star-PAP control of BIK expression and induction of apoptosis
259 timulates PKCdelta association with the Star-PAP complex where PKCdelta is required for Star-PAP-depe
260 ntial for PKCdelta interaction with the Star-PAP complex, and PKCdelta activity is directly stimulate
263 perturbations of gene expression, with Star-PAP impacting lowly expressed mRNAs and long-noncoding R
264 tissue-specific elevations of the substrate PAP, up to 50-fold in liver, repressed translation, and
265 ion, allowing accumulation of its substrate, PAP, a chloroplast stress retrograde signal that regulat
266 C. elegans and, in the mouse nervous system, PAP and Kv3.1b were colocalized in subsets of neurons, i
271 Analysis of crystal structures suggests that PAP binding restricts access to the acceptor-binding poc
277 d in the fry1 papst2 mutant, which lacks the PAP-catabolizing enzyme SALT TOLERANCE 1 and PAPST2.
279 wild type control where the majority of the PAP I synthesized poly(A) tails were after the Rho-indep
281 2-monoacylglycerol and does not require the PAP reaction, making the role of lipin proteins in enter
284 ata suggest that triple elimination of TNAP, PAP, and NT5E is required to block AMP hydrolysis to ade
286 d BHI-V3 plates were stratified according to PAP-AUC interpretive criteria: <0.90 (susceptible [S-MRS
289 position, as well as PAP activity in various PAP mutant strains, showed the essential role of PAH1 in
290 al)), volumetric distribution (VOL(AAP), VOL(PAP), and VOL(MCT)), and percentage of relative volume i
293 olysis, consistent with a mechanism in which PAP accumulation is toxic to tissue function independent
297 ave collected BAL samples from patients with PAP due to autoantibodies against granulocyte-macrophage
299 , resulting in a hypomorphic protein without PAP activity, but which preserved transcriptional coregu