ライフサイエンスコーパス: PAP

1 PAP activity was stimulated by anionic lipids (cardiolip

2 PAP binds to VPg with high affinity (29.5 nm); the react

3 PAP is also a cap-binding protein and is a potent antivi

4 PAP seems to have contributed to the death of only 1 pat

5 PAP-AUC testing confirmed only 11 isolates as hVISA (all

6 PAP-specific CD8(+)CTLA-4(+) T cells also suppressed T c

7 PAP/AUC revealed seven VISA and 33 hVISA phenotypes.

8 PAP/AUC test isolate/Mu3 ratios of <0.9, 0.9 to 1.3, and

9 can be rescued by the expression of lipin-1 PAP activity or by inhibition of ERK signaling.

10 e, we investigate the requirement of lipin-1 PAP versus coactivator function in the establishment of

11 ular function has been unknown, confers ~30% PAP activity of wild type cells.

12 SIGNIFICANCE: Identification of App1p as a PAP enzyme will facilitate the understanding of its cell

13 a greater frequency of tumor rejection in a PAP-expressing solid tumor model.

14 raphy/tandem mass spectrometry analysis of a PAP-enriched sample revealed multiple putative phosphata

15 ent include the ProstVac poxviral vaccine, a PAP-encoding DNA vaccine, and immune checkpoint inhibito

16 d then collapsed into three groups (LEP, ACN/PAP, and MIP/SOL).

17 MIP/SOL patients (but not ACN/PAP) derived DFS and SDFS but not OS benefit from ACT (O

18 e worse for MIP/SOL compared with LEP or ACN/PAP subgroup (P < .01); this remained marginally signifi

19 Caenorhabditis elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diver

20 king increase in the immune response against PAP.

21 PNP), o-nitrophenol (ONP), or p-aminophenol (PAP) as products.

22 detection limit of 31 muM for p-aminophenol (PAP) using Pt electrodes and was also used to detect enz

23 G to an electroactive species p-aminophenol (PAP) which could be monitored on an electrode.

24 ively describe PAP depurination activity and PAP-VPg interactions.

25 ogether, our results reveal a PAS-guided and PAP-mediated paradigm for gene expression in response to

26 -CSF signaling in surfactant homeostasis and PAP pathogenesis in humans and have therapeutic implicat

27 ochemically active substrates, PNP, ONP, and PAP were determined to be 1.1, 2.8, and 0.5 muM, respect

28 d 3T3-L1 cells where total lipin protein and PAP activity levels are down-regulated by the combined d

29 would improve the immunogenicity of PSA and PAP, 2 additional versions of MVA-BN-PRO were produced,

30 saccharide and bacteremia but not of TAT and PAP.

31 Anti-PAP antibody titers developed more rapidly and reached l

32 n [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and complement (C3b, C5a, C5b-9) in baboons infus

33 App1p PAP was purified from yeast and characterized with respe

34 Instead, App1p PAP is thought to play a role in endocytosis because its

35 creased prostatic acid phosphatase (PAP), as PAP levels are markedly reduced in Ret-Na(v)1.8 CKO mice

36 ld-type cells, are rapidly polyadenylated as PAP I levels increase, leading to dramatic reductions in

37 lipid synthesis and composition, as well as PAP activity in various PAP mutant strains, showed the e

38 These cases need not have associated PAP.

39 prevalent clinical form of PAP is autoimmune PAP (aPAP) whereby IgG autoantibodies neutralize GM-CSF.

40 To date, all the available PAP structures are from the PAPalpha clade.

41 rgets various RNAs, the interactions between PAP and turnip mosaic virus genome-linked protein (VPg)

42 Furthermore, treatment with MVA-BN-PAP-C1C2 increased the frequency of PAP-specific T cells

43 Treatment of mice with MVA-BN-PAP-C1C2 led to a striking increase in the immune respon

44 either PSA (MVA-BN-PSA-C1C2) or PAP (MVA-BN-PAP-C1C2) to exosomes, while leaving the second transgen

45 h minimal overlap in samples with borderline PAP-AUC.

46 ing a double mutant mouse deficient for both PAP synthesis and hydrolysis, consistent with a mechanis

47 Here, we show that fibril formation by PAP(248-286) is accelerated dramatically in the presence

48 pecific SP components on fibril formation by PAP(248-286) revealed that this effect is primarily due

49 required for normal mRNA polyadenylation by PAP I.

50 The diacylglycerol produced by PAP is used for the synthesis of triacylglycerol as well

51 suggest that the polyadenylation of tRNAs by PAP I likely proceeds in a distributive fashion unlike w

52 Star-PAP specificity and may block canonical PAP activity toward BIK mRNA.

53 In the yeast Saccharomyces cerevisiae, PAP is encoded by PAH1, DPP1, and LPP1.

54 ion analysis profiling-area under the curve (PAP-AUC) analysis.

55 ation analysis profile-area under the curve (PAP-AUC) of consecutive methicillin-resistant Staphyloco

56 ation analysis profile/area under the curve (PAP/AUC) is the gold standard but is cumbersome.

57 tance of sulfur assimilation and cytoplasmic PAP hydrolysis to normal liver function.

58 nity of PARylated PAP in vitro and decreased PAP association with non-heat shock protein-encoding gen

59 d in vitro disease model of CSF2RA-deficient PAP, and introduce gene-corrected iPSC-derived monocytes

60 However, phosphorylation-deficient PAP (PAP-7A) containing alanine substitutions for the se

61 ylglycerol, is unique among Mg(2+)-dependent PAP enzymes in that its reaction is not involved with de

62 hniques were used to quantitatively describe PAP depurination activity and PAP-VPg interactions.

63 P1, LPP1) are responsible for all detectable PAP activity in yeast.

64 CSF-specific autoantibody and do not develop PAP.

65 We have diagnosed PAP among patients with ADA deficiency more commonly in

66 per 10 mm Hg increase; P = 0.022), diastolic PAP - pulmonary capillary wedge pressure (HR, 2.19; 95%

67 per 10 mm Hg increase; P = 0.027), diastolic PAP (HR, 1.83; 95% CI, 1.09-3.08 per 10 mm Hg increase;

68 tolic pulmonary pressure gradient (diastolic PAP minus mean PAWP) <7 mm Hg, a transpulmonary pressure

69 ss of PAP activity, indicating that distinct PAP enzymes in S. cerevisiae are encoded by APP1, PAH1,

70 nce as the primary macrophage defect driving PAP pathogenesis, and support the feasibility of transla

71 ease in hepatic lipin-1 protein and elevated PAP activity, which maintained lipid homeostasis under b

72 ur genes (APP1, DPP1, LPP1, and PAH1) encode PAP activity in yeast, and it has been unclear which gen

73 ata suggest that in the in vivo environment, PAP(248-286) is likely to form fibrils efficiently, thus

74 These data establish PAP-iPSC-derived monocytes and macrophages as a valid in

75 participant received a vaginal examination, PAP smear, and completed a questionnaire.

76 res its RNA binding and, to a lesser extent, PAP-stimulatory functions.

77 andardize and may reduce the requirement for PAP-AUC confirmation.

78 tRNAs, which are normally not substrates for PAP I in wild-type cells, are rapidly polyadenylated as

79 ured RNA derived from tobacco etch virus for PAP binding.

80 However, the SEVI-forming PAP(248-286) peptide is able to produce infection-enhanc

81 iPS cells from two children with hereditary PAP (hPAP) caused by recessive CSF2RA(R217X) mutations a

82 ow that human RegIIIalpha (also known as HIP/PAP) binds membrane phospholipids and kills bacteria by

83 m of RNA depurination, and to understand how PAP recognizes and targets various RNAs, the interaction

84 turation, compete with poly(A) polymerase I (PAP I) for tRNA precursors in wild-type cells.

85 of polyadenylation by poly(A) polymerase I (PAP I) in Escherichia coli leads to toxicity and cell de

86 dosome is required for poly(A) polymerase I (PAP I)-dependent polyadenylation after Rho-independent t

87 predominant HRCT presentation of idiopathic PAP was interlobular septal thickening and ground glass

88 ted tomography (HRCT) features of idiopathic PAP.

89 e: 38+/-14years; 54.3% male) with idiopathic PAP (proved by bronchoalveolar lavage or biopsy) were re

90 Delta mutant exhibited a 10-fold increase in PAP activity.

91 es suggest that exercise-induced increase in PAP to a mean higher than 30 mm Hg may be associated wit

92 macrophages and reduced disease severity in PAP mice.

93 )ation (PARylation) in vitro, which inhibits PAP activity.

94 To examine possible interactions, PAP was changed at different levels of CSP in both studi

95 iated phosphorylation of Pah1p inhibited its PAP activity by decreasing catalytic efficiency, and the

96 nown about the biochemical regulation of its PAP activity.

97 a role in vesicular trafficking through its PAP activity.

98 +) flux stabilizes the tripartite PAP-1:K(+):PAP-1 complex in the pore.

99 ssion of a truncated lipin 1 protein lacking PAP activity but retaining transcriptional regulatory fu

100 Maximum PAP activity was dependent on Triton X-100 (20 mm), PA (

101 Mean PAP was a predictor of mean RV E(LL) (beta = .19, P = .0

102 associated with increased RV afterload (mean PAP and PVRI).

103 The average mean PAP increased from baseline (20.2 mm Hg) to followup (24

104 tients in this study, 86 had borderline mean PAP (21-24 mm Hg) at baseline.

105 Our findings indicate that borderline mean PAP and an elevated TPG in patients with SSc predict pro

106 Patients with borderline mean PAP were more likely to develop PH than patients with me

107 Hg, a transpulmonary pressure gradient (mean PAP minus mean PAWP) <12 mm Hg, and pulmonary vascular r

108 L) positively correlated with increased mean PAP (r = 0.5, P = .03) and septal eccentricity index (r

109 ere independently related to mortality: mean PAP (hazard ratio [HR], 1.61; 95% confidence interval [C

110 A combination of mean PAP and mean PAWP defines postcapillary PH.

111 ean RV E(LL) positively correlated with mean PAP (r = 0.62, P < .0014) and pulmonary vascular resista

112 likely to develop PH than patients with mean PAP</=20 mm Hg (P<0.001 by log rank test, hazard ratio [

113 Loss of lipin 1-mediated PAP activity in adipocytes led to reduced glyceride synt

114 nd inhibited its association with membranes, PAP activity, and triacylglycerol synthesis.

115 PARP1 binds to and modifies PAP by poly(ADP-ribosyl)ation (PARylation) in vitro, whi

116 ly(ADP-ribose) polymerase 1 (PARP1) modifies PAP and regulates its activity both in vitro and in vivo

117 Multipoint PAP-flow relationships are usually described by a linear

118 tal structure of human PAPD1, a noncanonical PAP that can polyadenylate RNAs in the mitochondria (als

119 macrophages differentiated from noncorrected PAP-iPSCs exhibited distinct defects in GM-CSF-dependent

120 cted prior to immunization in the absence of PAP-specific effector responses.

121 of BPNT-1 leads to the toxic accumulation of PAP in yeast and non-neuronal cell types in mice [4, 5].

122 mmunization was prevented by the activity of PAP-specific regulatory cells.

123 By analysis of PAP activity in mutants lacking each of the proteins, we

124 ce and lung histopathology characteristic of PAP; 2) alveolar macrophages from Rasgrp1-deficient mice

125 The complexity of PAP isoforms suggests that they might play different rol

126 ples and find that they partially consist of PAP fragments, interact with HIV particles and increase

127 tvDTH) assay, we found that the detection of PAP-specific effector responses after immunization was p

128 deficiency predisposes to the development of PAP, which could be reversed after enzyme replacement or

129 Two of the seven later developed evidence of PAP.

130 Similar findings of PAP were not found among patients with SCID caused by ot

131 The most prevalent clinical form of PAP is autoimmune PAP (aPAP) whereby IgG autoantibodies

132 h MVA-BN-PAP-C1C2 increased the frequency of PAP-specific T cells 5-fold compared with mice treated w

133 nd RNase PH, there is a >30-fold increase of PAP I-dependent poly(A) tails that are </=10 nt in lengt

134 Further, VPg is a potent inhibitor of PAP depurination of RNA in wheat germ lysate and compete

135 Multiple isoforms of PAP have been identified in vertebrates, which originate

136 The lack of PAP in the pah1Delta mutant highly elevated PSS activity

137 at different levels; increasing the level of PAP from 5 +/- 1 to 33 +/- 3 mmHg significantly increase

138 triple mutant resulted in a complete loss of PAP activity, indicating that distinct PAP enzymes in S.

139 Using site-directed mutagenesis of PAP, we identified Ser(602), Thr(723), and Ser(744), whi

140 trometry to identify interacting partners of PAP I-green fluorescent protein.

141 r macrophages that drive the pathogenesis of PAP in more than 90% of patients.

142 and cholesterol-targeted pharmacotherapy of PAP in vitro and in vivo.

143 g pioglitazone as a novel pharmacotherapy of PAP.

144 The presence of PAP activity in the pah1Delta dpp1Delta lpp1Delta triple

145 The predominant HRCT presentation of PAP was interlobular septal thickening (ILST;100%) and g

146 tus was significantly improved regardless of PAP level.

147 ore, our data demonstrate that regulation of PAP I is critical not for preventing the decay of mRNAs,

148 The 23- to 125-fold selectivity of PAP-1 for Kv1.3 over other Kv1 channels is probably due

149 eviously identified phosphorylation sites of PAP that are within the Ser/Thr-Pro motif.

150 The lung pathology was typical of PAP.

151 n combination, showed that Pah1p is the only PAP involved in the synthesis of triacylglycerol as well

152 gatively regulate either membrane binding or PAP activity.

153 d, targeting either PSA (MVA-BN-PSA-C1C2) or PAP (MVA-BN-PAP-C1C2) to exosomes, while leaving the sec

154 also not substrates for RNase T, RNase PH or PAP I.

155 However, phosphorylation-deficient PAP (PAP-7A) containing alanine substitutions for the seven p

156 mammalian Trf4 orthologues, PAPD5 and PAPD7 (PAP-associated domain containing 5 and 7), suggesting th

157 histologic pattern-lepidic (LEP), papillary (PAP), acinar (ACN), micropapillary (MIP), or solid (SOL)

158 ts reduced RNA binding affinity of PARylated PAP in vitro and decreased PAP association with non-heat

159 vaccine encoding prostatic acid phosphatase (PAP) and a trans-vivo delayed-type hypersensitivity (tvD

160 Prostatic acid phosphatase (PAP) and ecto-5'-nucleotidase (NT5E) hydrolyze extracell

161 t semen proteins prostatic acid phosphatase (PAP) and semenogelins form amyloid fibrils in vitro.

162 es lipin-1, a phosphatidic acid phosphatase (PAP) controlling the rate-limiting step in the phospholi

163 Lipin 2 is a phosphatidic acid phosphatase (PAP) responsible for the penultimate step of triglycerid

164 report on human prostatic acid phosphatase (PAP), a tumor marker, with a limit of detection of 11 pM

165 tigen (PSA), and prostatic acid phosphatase (PAP), and is derived from the highly attenuated modified

166 ted by decreased prostatic acid phosphatase (PAP), as PAP levels are markedly reduced in Ret-Na(v)1.8

167 T, an autologous prostatic acid phosphatase (PAP)-loaded dendritic cell immunotherapy, in men with me

168 (NT5E, CD73) or prostatic acid phosphatase (PAP, ACPP).

169 mmalian homolog, prostatic acid phosphatase (PAP; also known as ACPP-201) stably associates with muri

170 de fragment of prostatic acidic phosphatase (PAP), dramatically enhances the infectivity of human imm

171 rs and a phosphatidic acid (PA) phosphatase (PAP) enzyme that catalyzes a critical step in the synthe

172 Phosphatidate phosphatase (PAP) catalyzes the dephosphorylation of phosphatidate to

173 -1 functions as a phosphatidate phosphatase (PAP) enzyme in the glycerol 3-phosphate pathway for trig

174 The three lipin phosphatidate phosphatase (PAP) enzymes catalyze a step in glycerolipid biosynthesi

175 Mg(2+)-dependent phosphatidate phosphatase (PAP) enzymes with essential roles in lipid biosynthesis.

176 hich functions as phosphatidate phosphatase (PAP) in the yeast Saccharomyces cerevisiae, plays a cruc

177 tes a role of the phosphatidate phosphatase (PAP) in this metabolism; the enzyme produces the diacylg

178 Phosphatidate phosphatase (PAP) plays diverse roles in lipid metabolism and cell si

179 Yeast App1p is a phosphatidate phosphatase (PAP) that associates with endocytic proteins at cortical

180 The PAH1-encoded phosphatidate phosphatase (PAP), which catalyzes the committed step for the synthes

181 avage product of prostatic acid phosphatase, PAP(248-286)).

182 mplex with 3'-phosphoadenosine 5'-phosphate (PAP) alone and together with the Gl sinigrin.

183 i-resident 3'-phosphoadenosine 5'-phosphate (PAP) phosphatase (gPAPP) and Bisphosphate 3'-nucleotidas

184 entify the 3'-phosphoadenosine 5'-phosphate (PAP) phosphatase SAL1 as a previously unidentified and c

185 cytosolic 3'-phosphoadenosine 5'-phosphate (PAP), a byproduct of sulfation reactions utilizing the u

186 Lipin-1 is a phosphatidate phosphohydrolase (PAP) required for the generation of diacylglycerol durin

187 ition of the noncanonical poly(A) polymerase PAP-associated domain-containing 5 (PAPD5) increased TER

188 lation of nascent RNA by poly(A) polymerase (PAP) is important for 3' end maturation of almost all eu

189 Poly(A) polymerase (PAP) is the enzyme that catalyzes the poly(A) addition r

190 the nuclear noncanonical poly(A) polymerase (PAP) speckle targeted PIPKIalpha regulated PAP (Star-PAP

191 Star-PAP is a poly (A) polymerase (PAP) that is putatively required for 3'-end cleavage and

192 a non-canonical, nuclear poly(A) polymerase (PAP) that is regulated by the lipid signaling molecule p

193 a nuclear non-canonical poly(A) polymerase (PAP) that shows specificity toward mRNA targets.

194 Poly(A) polymerase (PAP), the enzyme that catalyzes the formation of the tai

195 c subunit of cytoplasmic poly(A) polymerase (PAP).

196 ing protein, PABPN1, and poly(A) polymerase (PAP).

197 mic parameters [pulsatile arterial pressure (PAP) and heart rate (HR)].

198 al increases in pulmonary arterial pressure (PAP) induced significant increases in SPP (+39.1 +/- 10.

199 s defined as mean pulmonary artery pressure (PAP) >/= 25 mm Hg.

200 rements of a mean pulmonary artery pressure (PAP) >/=25 mm Hg and mean wedged PAP (PAWP) >15 mm Hg.

201 was found between pulmonary artery pressure (PAP) and AF in these patients, right ventricular functio

202 rease of pulmonary capillary wedge pressure, PAP and RAP were more pronounced in AF than in SR, sugge

203 Ser-10 should be dephosphorylated for proper PAP function.

204 Pokeweed antiviral protein (PAP) from Phytolacca americana is a ribosome-inactivatin

205 features of pulmonary alveolar proteinosis (PAP) in patients with ADA deficiency.

206 Pulmonary alveolar proteinosis (PAP) is a rare lung syndrome caused by the accumulation

207 atients with pulmonary alveolar proteinosis (PAP) syndrome, disruption of granulocyte/macrophage colo

208 teristic for pulmonary alveolar proteinosis (PAP), it is not specific and has not been compared betwe

209 ption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid composition in alveolar macroph

210 er developed pulmonary alveolar proteinosis (PAP).

211 re secondary pulmonary alveolar proteinosis (PAP).

212 ruli in the Proximal-Antennal-Protocerebrum (PAP) forming a thermotopic map in the brain.

213 We purified PAP from the pah1Delta dpp1Delta lpp1Delta triple mutant

214 (PAP) speckle targeted PIPKIalpha regulated PAP (Star-PAP) controls E6 mRNA polyadenylation and expr

215 nhibition of either CTLA-4 or IL-35 reversed PAP-specific suppression of tvDTH response.

216 to changes in CSP were influenced by setting PAP at different levels; increasing the level of PAP fro

217 Patient-specific PAP-iPSCs were generated from CD34(+) bone marrow cells

218 Star-PAP activity is stimulated by lipid messenger phosphatid

219 Star-PAP directly associated with cleavage and polyadenylatio

220 Star-PAP is a non-canonical, nuclear poly(A) polymerase (PAP)

221 Star-PAP is a nuclear non-canonical poly(A) polymerase (PAP)

222 Star-PAP is a poly (A) polymerase (PAP) that is putatively re

223 Palpha and PAPgamma) and non-canonical (Star-PAP) PAPs play diverse roles in PAS selection and gene e

224 We show that in addition to CKIalpha, Star-PAP associates with another CKI isoform, CKIepsilon in t

225 tures in the BIK 3' UTR uniquely define Star-PAP specificity and may block canonical PAP activity tow

226 role for phosphorylation in determining Star-PAP target mRNA specificity and regulation of 3'-end pro

227 hosphorylation at the catalytic domain, Star-PAP S6 phosphorylation is insensitive to oxidative stres

228 ithin the nucleus which is required for Star-PAP nuclear retention and interaction with PIPKIalpha.

229 complex where PKCdelta is required for Star-PAP-dependent BIK expression.

230 This identifies Star-PAP as a potential drug target for the treatment of HPV-

231 CKI isoforms alpha and epsilon modulate Star-PAP activity and regulates Star-PAP target messages.

232 siRNA knockdown of Star-PAP abolished cleavage of HO-1, and this phenotype could

233 well as the polyadenylation activity of Star-PAP in vitro.

234 PIPKIalpha controlled select subset of Star-PAP target messages by regulating Star-PAP-mRNA associat

235 expression and the 3'-end processing of Star-PAP targets similar to the CKI activity inhibitors.

236 equivalently inhibit the expression of Star-PAP targets.

237 sociated kinases act as coactivators of Star-PAP that regulates its activity and specificity toward m

238 In the absence of Star-PAP, treatment of cells with the chemotherapeutic drug V

239 tes the CKI mediated phosphorylation of Star-PAP, which is critical for both its polyadenylation acti

240 between VP-16 treatment and the loss of Star-PAP.

241 hosphorylated residue (serine 6, S6) on Star-PAP in the zinc finger region, the domain required for P

242 ckle targeted PIPKIalpha regulated PAP (Star-PAP) controls E6 mRNA polyadenylation and expression and

243 he Star-PAP complex that phosphorylates Star-PAP and complements the loss of CKIalpha.

244 lpha associates with and phosphorylates Star-PAP in its catalytic domain.

245 PI4,5P(2)-regulated poly(A) polymerase Star-PAP downstream of DNA damage.

246 enotype could be rescued by recombinant Star-PAP but not PAPalpha.

247 alpha, PI4,5P(2), and PKCdelta regulate Star-PAP control of BIK expression and induction of apoptosis

248 odulate Star-PAP activity and regulates Star-PAP target messages.

249 Star-PAP target messages by regulating Star-PAP-mRNA association.

250 We show Star-PAP-specific PAS usage regulates the expression of the e

251 another CKI isoform, CKIepsilon in the Star-PAP complex that phosphorylates Star-PAP and complements

252 timulates PKCdelta association with the Star-PAP complex where PKCdelta is required for Star-PAP-depe

253 ntial for PKCdelta interaction with the Star-PAP complex, and PKCdelta activity is directly stimulate

254 The Star-PAP-mediated APA of PTEN is essential for DNA damage-ind

255 This pathway is distinct from the Star-PAP-mediated oxidative stress pathway indicating signal-

256 hibitors (IC261 and CKI7) block in vivo Star-PAP activity, but the knockdown of CKIalpha did not equi

257 The data support a model where Star-PAP binds to the RNA, recruits the CPSF complex to the 3

258 perturbations of gene expression, with Star-PAP impacting lowly expressed mRNAs and long-noncoding R

259 tissue-specific elevations of the substrate PAP, up to 50-fold in liver, repressed translation, and

260 ion, allowing accumulation of its substrate, PAP, a chloroplast stress retrograde signal that regulat

261 C. elegans and, in the mouse nervous system, PAP and Kv3.1b were colocalized in subsets of neurons, i

262 dependent translation and potentially target PAP to uncapped IRES-containing RNA.

263 We demonstrate that PAP activity supplied by lipin-1, lipin-2, or lipin-3, b

264 We provide the first in vivo evidence that PAP I interacts with the mRNA degradosome during both ex

265 In vivo we show that PAP is PARylated during heat shock, leading to inhibitio

266 Collectively, these data showed that PAP activity controls the expression of PSS for membrane

267 coupled with immunoblot analysis showed that PAP-7A was highly enriched in the membrane fraction.

268 Analysis of crystal structures suggests that PAP binding restricts access to the acceptor-binding poc

269 The PAP activity shown by App1p heterologously expressed in

270 The PAP-AUC of 616 clinical samples was consistent with S-MR

271 The PAP/AUC was measured for all isolates according to the m

272 In fluorescence spectroscopy analysis, the PAP-7A showed tighter association with phospholipid vesi

273 n an equilibrium between free PNPase and the PAP I polyadenylation complex.

274 Here, we examined the PAP-mediated regulation of CHO1-encoded phosphatidylseri

275 segregation of hot and cold responses in the PAP, and show that silencing the hot- or cold-sensing ne

276 Lipid analysis of cells lacking the PAP genes, singly or in combination, showed that Pah1p i

277 This was due to the lack of the PAP activity of lipin 1 in adipocytes after day 4 of dif

278 wild type control where the majority of the PAP I synthesized poly(A) tails were after the Rho-indep

279 an important role in the maintenance of the PAP I-degradosome association during stationary phase.

280 easing CSP produced a rightward shift of the PAP-RSNA relationship, although the effect on reflex gai

281 'set point' and saturation pressures of the PAP-SPP relationship were higher than those with CSP at

282 These PAP-specific CD8(+)CTLA-4(+) suppressor T cells expresse

283 r, we demonstrate that the majority of these PAP I interactions are formed via protein-protein intera

284 ata suggest that triple elimination of TNAP, PAP, and NT5E is required to block AMP hydrolysis to ade

285 Moreover, our data reveal that TNAP, PAP, and NT5E are the main AMP ectonucleotidases in prim

286 d BHI-V3 plates were stratified according to PAP-AUC interpretive criteria: <0.90 (susceptible [S-MRS

287 vely; they may be reasonable alternatives to PAP/AUC.

288 ir biophysical properties and sensitivity to PAP-1 by whole-cell patch-clamp.

289 ise with an average upstream transmission to PAP in a close to one-for-one mm Hg fashion.

290 ation of K(+) flux stabilizes the tripartite PAP-1:K(+):PAP-1 complex in the pore.

291 n expressed on a low copy plasmid, wild type PAP could not complement the pah1Delta mutant in the abs

292 on with phospholipid vesicles than wild type PAP.

293 Each method was evaluated using PAP-AUC as the reference method.

294 position, as well as PAP activity in various PAP mutant strains, showed the essential role of PAH1 in

295 y pressure (PAP) >/=25 mm Hg and mean wedged PAP (PAWP) >15 mm Hg.

296 This raises the question whether PAP thereby affects the expression and activity of enzym

297 olysis, consistent with a mechanism in which PAP accumulation is toxic to tissue function independent

298 The toxicity associated with PAP I is exacerbated by the absence of either RNase T an

299 fication of various pathogens coincided with PAP in 3 of these patients.

300 row cells of a CSF2RA-deficient patient with PAP.

301 patients with ADA deficiency with or without PAP.

302 A novel yeast PAP is identified as the actin patch protein encoded by