ライフサイエンスコーパス: PPR

1 PPR demonstrated lower HRQoL scores than CSR, but the tw

2 PPR DOM also showed lower SUVA280 at similar weights com

3 PPR domains act as specificity factors through electrost

4 PPR is one of the principal constraints to small ruminan

5 PPR proteins contain tandemly repeated PPR motifs that b

6 PPR proteins have been shown to be sequence-specific RNA

7 PPR proteins influence the editing, splicing, translatio

8 PPR was higher in areas of higher transmission.

9 PPR within 1 radius of the disc margin underwent 7.6 +/-

10 3M Potentially Preventable Readmissions (3M-PPR) software matches clinically related index admission

11 ction and heart failure readmissions, the 3M-PPR software does not distinguish differences in case-le

12 flagged cases (PPR-Yes/PPR-No) using the 3M-PPR software.

13 Whether 3M-PPR software better identifies preventable readmissions

14 this study, plants lacking the SLOW GROWTH 4 PPR protein were characterized.

15 hundreds of proteins, including more than 40 PPR and mTERF domain proteins, and provides a resource f

16 Among more than 80 PPR-type editing factors that have meantime been charact

17 Even if a PPR protein defines the editing site, a DYW domain of th

18 pccmFC sequences in vitro, indicating that a PPR protein with a DYW domain is solely sufficient for c

19 cytes control osteoclast formation through a PPR-mediated mechanism.

20 activate G proteins, Gq and G11, leads to a PPR knockout-like phenotype.

21 Deformations of the disc and adjacent PPR were measured by comparing positions of epipapillary

22 rved antioxidant activity values in ABTS and PPR leaf disc assays were lower than those of convention

23 Observational Procedure: The disc and PPR were imaged by scanning laser ophthalmoscopy in cent

24 se methods to standard invasive sampling and PPR diagnostic methods using field samples collected at

25 xplained by coevolution of editing sites and PPR proteins.

26 ng site, a DYW domain of the same or another PPR protein is believed to catalyze the deamination.

27 The Arabidopsis PPR genes, ELI1 and DOT4, both have DYW deaminase domain

28 lysis has shown that most of the Arabidopsis PPR proteins necessary for RNA editing events include a

29 We demonstrate here that artificial PPR proteins built from consensus PPR motifs selectively

30 These results demonstrate that artificial PPR proteins can be tailored to bind specific endogenous

31 itation sequencing (RIP-seq) that artificial PPR proteins designed to bind the Arabidopsis (Arabidops

32 infarction, 77 of 100 cases were flagged as PPR-Yes.

33 art failure, 86 of 100 cases were flagged as PPR-Yes.

34 sions, we compared processes of care between PPR software-flagged and nonflagged cases.

35 w fluctuations was preserved after blockade, PPR showed that blockade significantly altered the non-l

36 governing the specificity of RNA binding by PPR repeats to infer candidate-binding sites for the mai

37 disease of sheep and goats that is caused by PPR virus, a member of the genus Morbillivirus that incl

38 ection-related mean scores did not differ by PPR status; PPR-Yes versus PPR-No total scores were 61.2

39 ection-related mean scores did not differ by PPR status; respective PPR-Yes versus PPR-No total score

40 many of which are addressed individually by PPR proteins.

41 er day (10 SER patients [one by MRD, nine by PPR]) or 400 mg/m(2) once per day (38 RER patients; 12 S

42 ents; 12 SER patients [three by MRD, nine by PPR]).

43 terminants of nucleotide base recognition by PPR motifs.

44 h this type of function consist of canonical PPR motifs.

45 all-cause readmissions, then flagged cases (PPR-Yes/PPR-No) using the 3M-PPR software.

46 ed differences in the N-terminal and central PPR motifs that explain ecotype-specific variations in c

47 Here, a chloroplast PPR-DYW editing factor, quintuple editing factor 1 (QED1

48 The Arabidopsis chloroplast PPR protein Required for AccD RNA Editing 1 (RARE1) spec

49 The SLO3 protein contains nine classic PPR domains belonging to the P subfamily.

50 plastidial CHLOROPLAST BIOGENESIS 19 (CLB19) PPR editing factor.

51 anied by loss or degeneration of its cognate PPR protein.

52 artificial PPR proteins built from consensus PPR motifs selectively bind the intended RNA in vivo, an

53 3 (PPR2263) encoding a DYW domain-containing PPR protein is required for RNA editing in the mitochond

54 imer of pentatricopeptide repeat-containing (PPR) proteins, termed kinetoplast polyadenylation/uridyl

55 DPP, and PPN to weak stallers, such as CPP, PPR, and PPH, all of which are substrates for EF-P.

56 dings elucidated the common origin of all CS-PPR converter genes except CBL-CIPK converter genes, and

57 its" to its targets according to the current PPR-RNA binding code.

58 long-term synaptic plasticity and decreased PPR at the SC.

59 Previously described PPR proteins with this type of function consist of canon

60 Non-invasive strategies to detect PPR infection without the need for animal handling could

61 thus demonstrating a requirement for direct PPR signaling in T cells.

62 In summary, direct PPR signaling in T cells and the resulting production of

63 These findings demonstrate that direct PPR signaling in T cells plays an important role in PTH-

64 diting, conserved deaminase residues in each PPR protein were mutagenized.

65 ntervention of gene-specific nucleus-encoded PPR trans-factors and that their action does not necessa

66 t abundant cells in adult bone, also express PPR.

67 reduced ratio of paired-pulse facilitation (PPR).

68 tive Arabidopsis thaliana RNA editing factor PPR proteins, RIP2, RIP9, RIP1, OZ1, ORRM1 and ISE2 were

69 h contiguous nucleotides such that the final PPR motif aligns four nucleotides upstream of the edited

70 creates a premature stop codon in the first PPR domain.

71 the tips of it's V-shaped arms, in the first PPR motif and in the NYN domain proximal to the catalyti

72 ereas SU from field strains (FS) such as FIV-PPR cannot.

73 [HV-FIV]), and a less-pathogenic strain, FIV-PPR (referred to here as low-virulence FIV [LV-FIV]).

74 IL-1beta as a potential central mediator for PPR pathogenesis.

75 Patients at HR only for PPR have a favorable outcome.

76 and 74.0% (3.6) in 152 HR patients only for PPR.

77 adication of RP are also largely present for PPR.

78 and ex vivo combined treatment of cells from PPR patient-derived xenografts.

79 l interfering RNA (phasiRNA) production from PPR genes.

80 S)-pentatricopeptide repeat-containing gene (PPR)-small interfering RNA pathway is a highly dynamic a

81 how to engineer these properties in a given PPR.

82 The global PPR situation and technology for its control are summari

83 in children when compared with all gravidae (PPR=1.44, 95% CI 1.29-1.62; I(2)=80%, 57 studies), and a

84 The evolution of HEV PPR, in contrast with that of the rest of the nonstructu

85 y the nucleotide variability seen in the HEV PPR was assumed to be due to high rates of insertion and

86 Synapses with initially high PPR, indicative of low release probability ("weak" synap

87 defects in both organelles with a very high PPR type specificity, indicating that the two proteins a

88 ajor gaps in our knowledge of the multi-host PPR epidemiology.

89 iting factors, DYW1 contains no identifiable PPR motifs but does contain a clear DYW domain.

90 sine kinase (LCK) as aberrantly activated in PPR patients.

91 ver, we observed that LCK hyperactivation in PPR patients upregulates the calcineurin/nuclear factor

92 role of IL-1beta in driving inflammation in PPR.

93 e most significantly upregulated pathways in PPR lesional tissue and aligned with differently express

94 drivers and interaction between pathways in PPR pathology is lacking.

95 ts, which we attribute to oxidized sulfur in PPR DOM that would increase molecular weight without aff

96 ays have been described to be upregulated in PPR, a mechanistic understanding of the key drivers and

97 Notably, the role of wildlife in PPR epidemiology is still not clearly understood.

98 ation; (ii) the k-mer-based tools (including PPR-Hotpep, CUPP and eCAMI) perform better than homology

99 naptic latency but a significantly increased PPR and fraction of synaptic failures.

100 ifference could be because of higher initial PPR in the non-FS neurons.

101 potentiated, while synapses with low initial PPR ("strong" synapses) tended to depress or did not cha

102 haliana is an endoribonuclease that uses its PPR domain to recognize precursor tRNAs (pre-tRNAs) as i

103 tified a protein of unknown function lacking PPR motifs; we named it RNA-editing factor interacting p

104 proteins in paired nonlesional and lesional PPR tissue (n = 5 patients).

105 teomic profiles similar to those of lesional PPR.

106 To address this issue, we studied a maize PPR-SMR protein denoted PPR53 (GRMZM2G438524), which is

107 some of the underlying mechanisms that make PPR wetlands biogeochemical hotspots, which ultimately l

108 In addition, many PPR proteins include a C-terminal DYW deaminase domain w

109 Although many PPR proteins have been functionally studied, few of them

110 Furthermore, in many PPR-DYW editing factors, the truncation of the DYW motif

111 The DYW motif at the C terminus of many PPR editing factors contains residues conserved with kno

112 previously uncharacterized maize (Zea mays) PPR gene, MPPR6, which was isolated from a Mutator-induc

113 SLO4 is a mitochondrial PPR protein that is involved in editing nad4, possibly r

114 KEY MESSAGE: SLO4 is a mitochondrial PPR protein that is involved in editing nad4, possibly r

115 ctivation of G(s)alpha in mice with a mutant PPR that cannot activate G proteins, Gq and G11, leads t

116 The mutant PPR proteins, when expressed in qed1 or rare1 mutant pro

117 However, natural PPR proteins have irregular features that limit the degr

118 e RRM domain of SLIRP and three neighbouring PPR motifs in the second quarter of LRPPRC, which critic

119 deficiency can partially mask the absence of PPR proteins, and that RNase J is capable of processing

120 Alignments of PPR sequences from HEV strains representing all genotype

121 tions suggest that the major consequences of PPR activation are similar in both the fetal and postnat

122 ptimized methods for the direct detection of PPR virus genetic material and antigen in fecal samples.

123 s indicate that the DYW deaminase domains of PPR proteins are involved in editing their cognate editi

124 The epidemiology of PPR and RP as well as the technologies available for the

125 shed single-stranded RNA recognition mode of PPR motifs.

126 ntal to understand the multifunctionality of PPR proteins and the mechanisms governing mRNA translati

127 ected benefits than the current portfolio of PPR conservation.

128 or proper UGGAAexp folding and regulation of PPR translation.

129 However, the physiological relevance of PPR signaling in osteocytes remains to be elucidated.

130 postnatal growth plate; however, the role of PPR signaling in postnatal chondrocytes is unknown.

131 O mice to evaluate the physiological role of PPR signaling in postnatal chondrocytes.

132 hese observations suggest a possible role of PPR signaling in the postnatal growth plate; however, th

133 Here, we show that conditional silencing of PPR in T cells blunts the capacity of iPTH to induce T-c

134 d enhanced short-term plasticity in terms of PPR and Pr.

135 A better understanding of PPR transmission dynamics in multi-host systems is neces

136 The sediment pore waters of PPR wetlands contain some of the highest concentrations

137 methods to determine the detection window of PPR in fecal samples, and compare the sensitivity of the

138 andling could greatly facilitate research on PPR epidemiology and management of the disease in atypic

139 erentially expressed proteins between paired PPR lesional and nonlesional explants.

140 Two moss (Physcomitrella patens) PPR proteins containing DYW-deaminase domains, PPR65 and

141 QED1 and RARE1, another plastid PPR-DYW editing factor, were discovered to require their

142 her suggests that where CSR is not possible, PPR is appropriate in most circumstances.

143 The PRORP1 PPR domain-tRNAPhe structure revealed a conformational c

144 The PRORP1 PPR motifs have evolved strategies for protein-tRNA inte

145 requires pentatricopeptide repeat proteins (PPR proteins) for site recognition and proteins of the m

146 Disruption of this autocrine PTHrP-PPR signaling in these cells leads to defective formatio

147 mation, underscoring importance of the PTHrP-PPR system during root morphogenesis and tooth eruption.

148 This PTHrP-PPR signaling appears to crosstalk with other signaling

149 tion rate (ECAR) and proton production rate (PPR).

150 nalysis to obtain a pooled prevalence ratio (PPR) of malaria in children versus pregnant women (durin

151 m plasticity in terms of paired pulse ratio (PPR) and release probability (Pr), compared to autapses.

152 correlated with initial paired-pulse ratio (PPR), indicative of initial strength of a synapse.

153 (-/-)) show an increased paired-pulse ratio (PPR), which led to the hypothesis that Munc13-3 increase

154 concomitant increase in paired pulse ratio (PPR), which occur in barrel cortex during the third and

155 omitant with a decreased paired-pulse ratio (PPR).

156 ) and its parathyroid hormone/PTHrP receptor PPR.

157 PTH-related peptide (PTHrP) type 1 receptor (PPR), a G-protein-coupled receptor highly expressed in b

158 root surface, and deletion of its receptor (PPR) in these progenitors leads to failure of eruption a

159 lencing of PTH/PTH-related protein receptor (PPR) in T cells abrogates the effects of iPTH, thus demo

160 hormone (PTH)/PTH-related protein receptor (PPR) in T cells.

161 g and acting through the PTH/PTHrP receptor (PPR), is crucial for normal cartilage development.

162 he PTH/PTH-related protein (PTHrP) receptor (PPR) in intramembranous bone formation in the craniofaci

163 go apoptosis in the absence of the receptor (PPR) for parathyroid hormone-related protein.

164 ABTS), and potassium permanganate reduction (PPR) leaf disc assays.

165 he placodes, called the pre-placodal region (PPR), that lies lateral to the neural crest.

166 o the neural plate, the pre-placodal region (PPR).

167 The polyproline region (PPR) and the macro domain of ORF1 protein may modulate v

168 hepatitis E virus (HEV) polyproline region (PPR) is an intrinsically unstructured region (IDR).

169 conservation in the Prairie Pothole Region (PPR) as an example.

170 The Prairie Pothole Region (PPR) of North America is one of the largest wetland comp

171 The Prairie Pothole Region (PPR) of the United States and Canada has undergone exten

172 from wetlands in the Prairie Pothole Region (PPR) using XAD-8, a cation exchange resin, and PPL, a st

173 In the Prairie Pothole Region (PPR), elevated pesticide use and increasing hydrologic c

174 inear method (projection pursuit regression, PPR).

175 and transcriptional effectors that regulate PPR specification and its subdivision into placodal doma

176 Here we report the related PPR proteins mitochondrial editing factor 8 (MEF8) and M

177 on of repeat-associated pentapeptide repeat (PPR) proteins, consistent with observations in SCA31 pat

178 Pentatricopepetide repeat (PPR) proteins are a large family of RNA-binding proteins

179 sses two domains - pentatricopeptide repeat (PPR) and metallonuclease (NYN) - that are present in som

180 main tethered to a pentatricopeptide repeat (PPR) domain by a structural zinc-binding domain.

181 ing factors of the pentatricopeptide repeat (PPR) family show a very high degree of sequence specific

182 ng proteins of the pentatricopeptide repeat (PPR) family, which bind upstream of the editing site in

183 egulating a set of pentatricopeptide repeat (PPR) genes and has been characterized only in Arabidopsi

184 s are modulated by pentatricopeptide repeat (PPR) Kinetoplast Polyadenylation Factors (KPAFs).

185 LS subclass of the pentatricopeptide repeat (PPR) motif-containing family are site-specific recogniti

186 Pentatricopeptide repeat (PPR) motifs are alpha-helical structures known for their

187 The pentatricopeptide repeat (PPR) protein family is a large family of RNA-binding pro

188 PRC belongs to the pentatricopeptide repeat (PPR) protein family, originally defined by their RNA bin

189 by members of the pentatricopeptide repeat (PPR) protein family.

190 We show that the pentatricopeptide repeat (PPR) protein RNA PROCESSING FACTOR 4 (RPF4) supports the

191 that the E(+)-type pentatricopeptide repeat (PPR) protein SLO2, which lacks a C-terminal cytidine dea

192 360 that encodes a pentatricopeptide repeat (PPR) protein.

193 Pentatricopeptide repeat (PPR) proteins (PPRPs) are encoded by a large gene family

194 Pentatricopeptide repeat (PPR) proteins are a large family of helical-repeat prote

195 The pentatricopeptide repeat (PPR) proteins are at the core of this posttranscriptiona

196 Pentatricopeptide repeat (PPR) proteins are helical repeat proteins that bind RNA

197 Pentatricopeptide repeat (PPR) proteins are members of one of the largest nucleus-

198 Nuclear encoded pentatricopeptide repeat (PPR) proteins are required as RNA binding specificity de

199 Pentatricopeptide repeat (PPR) proteins bind RNA via a mechanism that facilitates

200 Pentatricopeptide repeat (PPR) proteins comprise a large family of helical repeat

201 Pentatricopeptide repeat (PPR) proteins constitute a large protein family in flowe

202 sequence-specific pentatricopeptide repeat (PPR) proteins define termini by blocking the 5'-->3' exo

203 a requirement for pentatricopeptide repeat (PPR) proteins for RNA editing.

204 Nuclear encoded pentatricopeptide repeat (PPR) proteins include an RNA binding domain that provide

205 RNA-binding pentatricopeptide repeat (PPR) proteins specifically recognize target sites for C-

206 Pentatricopeptide repeat (PPR) proteins with C-terminal DYW domains are present in

207 proteins, several pentatricopeptide repeat (PPR) proteins, and proteins not typically found in ribos

208 nized by up to 200 pentatricopeptide repeat (PPR) proteins.

209 d approximately 20 pentatricopeptide repeat (PPR) RNA binding proteins.

210 unction, including pentatricopeptide repeat (PPR), tetratricopeptide repeat (TPR), DnaJ, and mitochon

211 a and plastids are pentatricopeptide repeat (PPR)-containing proteins with specific additional C-term

212 ive genes encoding pentatricopeptide repeat (PPR)-like proteins [CELL WALL MAINTAINER 1 (CWM1) and 2

213 PPR proteins contain tandemly repeated PPR motifs that bind specific RNAs, and they are thought

214 d by a stretch of pentatricopeptide repeats (PPR) and a C-terminal extension domain ending with the a

215 ) and 67.0 and 74.8 for parent proxy report (PPR) for the core and brain tumor modules, respectively.

216 rticularly, primary production requirements (PPR) are about equal and constant across all feeds for b

217 res did not differ by PPR status; respective PPR-Yes versus PPR-No total scores were 61.6+/-11.1 and

218 s, classified as prednisone poor responders (PPR), have poorer outcome than do the other pediatric T-

219 translocation, and prednisone poor response (PPR).

220 e substrates of mOGT, including leucine-rich PPR-containing protein and mitochondrial aconitate hydra

221 d with mitochondrion-associated leucine-rich PPR-motif containing protein (LRPPRC) that interacts wit

222 Papulopustular rosacea (PPR) is a chronic inflammatory skin disease with limited

223 ighly contagious peste des petits ruminants (PPR) disease, which is caused by an RNA virus, PPRV, acr

224 Peste des petits ruminants (PPR) is a highly contagious and devastating viral diseas

225 Peste des petits ruminants (PPR) is a highly infectious disease of sheep and goats t

226 Several PPR proteins in plants harbor a carboxy-terminal small-M

227 hanism similar to that described for several PPR proteins lacking SMR motifs.

228 ant across all feeds for both analyses since PPR was driven by fishmeal and oil.

229 t C targets known to be affected by a single PPR protein.

230 gether, these results indicate that the SLO3 PPR protein is a splicing factor of nad7 intron 2 in Ara

231 oteins, a P-type PPR and a member of a small PPR-DYW subfamily, were shown to interact in yeast.

232 tidine deaminase active sites; however, some PPR editing factors lack a DYW motif.

233 d tamoxifen-inducible and cartilage-specific PPR KO mice to evaluate the physiological role of PPR si

234 ed mean scores did not differ by PPR status; PPR-Yes versus PPR-No total scores were 61.2+/-10.8 and

235 ZEA MAYS: PPR10 is amongst the best studied PPR proteins, where sequence-specific binding to two RNA

236 However, other than PPR proteins and the cis-elements on the organelle trans

237 Taken together, these data indicate that PPR signaling in osteocytes is required for bone remodel

238 These findings indicate that PPR signalling in dental mesenchymal progenitors is esse

239 tionary observations support the notion that PPR-RNA mismatches may be essential for proper function

240 The PPR domain of PRORP1 bound to the structurally conserved

241 The PPR phasiRNA production is triggered by different 22-nuc

242 The PPR-deficient progenitors exhibit accelerated cementobla

243 ng-term dataset of pintail counts across the PPR to separate count data into a demographic process an

244 The neural crest domain and the PPR are established in response to signaling events medi

245 pports a mechanistic link between Pr and the PPR, but dissociates Pr from the steady state amplitude

246 The difference between the PPR and the rest of the polyprotein is due to the higher

247 f heterotrimeric G-proteins activated by the PPR.

248 ently, in response to environmental cues the PPR is further subdivided into placodal territories with

249 es heterogeneity in the regions encoding the PPR and the macro domain may facilitate HEV persistence.

250 Like in most RNA editing factors, the PPR array of AEF1 reveals potential for conceptually "im

251 Hence, the PPR is a part of a network for reach decisions and not j

252 Historically, the PPR has been a highly productive area for breeding water

253 t the mutation rate is about the same in the PPR as in the rest of the nonstructural polyprotein.

254 also leads to >22% of all amino acids in the PPR being prolines.

255 MPT instead of simple diversification in the PPR can achieve a value of the conservation objective pe

256 the overall trends for dabbling ducks in the PPR have exhibited increasing abundances since the late

257 ion of columnar chondrocytes, as seen in the PPR knockout, but a remnant of growth cartilage remains,

258 disappearance of the growth cartilage in the PPR knockout.

259 temporal shift and less displacement in the PPR within 1 disc radius (P < .0001) in adduction; the n

260 In the PPR, members of the Six and Eya families, act in part to

261 l and cKO, but no significant changes in the PPR.

262 NA, we determined a crystal structure of the PPR domain in complex with yeast tRNAPhe at 2.85 angstro

263 ture revealed a conformational change of the PPR domain upon tRNA binding and moreover demonstrated t

264 a small fraction of the >400 members of the PPR family in plants.

265 rotein is due to the higher tolerance of the PPR for substitutions at the first and second codon posi

266 re an ancestor, and the carboxyl half of the PPR is more tolerant of mutations than the amino half.

267 ith the stability-conferring function of the PPR proteins PPR10, HCF152 and MRL1, accumulation of the

268 or of the anti-differentiation action of the PPR, while activation of both G(s)alpha and Gq/11alpha i

269 ctly participate in the establishment of the PPR.

270 tylase-4 (HDAC4) partially recapitulates the PPR deletion root phenotype.

271 In Arabidopsis (Arabidopsis thaliana), the PPR protein LPA66 is required for editing at psbF-26.

272 ytic activity and metal binding and that the PPR domain also enhances activity, likely through an int

273 ies atpH, petB and rbcL was reduced when the PPR-encoding genes were silenced.

274 To assess whether the PPR algorithm identifies preventable readmissions, we co

275 led geochemistry and microbiology within the PPR and demonstrates how the conversion of abundant labi

276 al analysis revealed that mutations in these PPR proteins resulted in defective cytochrome c maturati

277 g was used to reduce the expression of three PPR proteins and RNase J, both individually and jointly,

278 nisms underlying the functions attributed to PPR proteins are unknown.

279 gical functions that have been attributed to PPR proteins.

280 , and pathways, which may be contributing to PPR, as well as highlighted a potential role of IL-1beta

281 apable of processing chloroplast mRNAs up to PPR protein-binding sites.

282 lar waveguide particle plasmon resonance (TW-PPR) sensor is demonstrated for label-free biochemical d

283 The TW-PPR sensor can be inexpensively fabricated and has a spe

284 Two PPR proteins, dually targeted to mitochondria and chloro

285 domain, interacts in vivo with the DYW-type PPR protein DYW2 and the P-type PPR protein NUWA in mito

286 stabilization role of NUWA between E(+)-type PPR and DYW2 proteins.

287 nt specificity for sites edited by E(+)-type PPR proteins.

288 the two proteins are core members of E+-type PPR editosomes.

289 These two proteins, a P-type PPR and a member of a small PPR-DYW subfamily, were show

290 the DYW-type PPR protein DYW2 and the P-type PPR protein NUWA in mitochondria, and that the latter en

291 Identifying the targets of PLS-type PPR proteins can help in elucidating the molecular funct

292 The subgroup of PLS-type PPR proteins were found to be the main specificity facto

293 In this study, we utilized PPR skin biopsy explants to integrate both differentiall

294 did not differ by PPR status; PPR-Yes versus PPR-No total scores were 61.2+/-10.8 and 63.4+/-7.0, res

295 fer by PPR status; respective PPR-Yes versus PPR-No total scores were 61.6+/-11.1 and 60.4+/-9.4; P=0

296 st, RNase J reduction alone or combined with PPR deficiency resulted in reduced abundance of polycist

297 Disease type also correlated with PPR core total HRQoL score at the beginning of treatment

298 Toward this goal, we generated mice with PPR deletion in osteocytes (Ocy-PPRKO).

299 ore, MORF proteins interact selectively with PPR proteins, establishing a more complex editosome in p

300 se readmissions, then flagged cases (PPR-Yes/PPR-No) using the 3M-PPR software.