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 is one of the principal constraints to small ruminan

4 PPR proteins are thought to have a major role in the reg

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 ting PPR, seven with OS) or without (n = 14) PPR.

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 hloroplast-targeted protein harboring both a PPR tract and an RNA recognition motif.

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

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

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

20 EMP4 contains nine 35-amino acid PPR motifs and an N-terminal mitochondrion-targeted sequ

21 ding on the spread of the abnormal activity, PPR subgroups have been defined as having either propaga

22 Moreover, the fetal skins of the PTHrP and PPR knockouts (KOs) had reciprocal increases in the leng

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

24 Recent studies have shown that Arabidopsis PPR proteins play an essential, nonredundant role during

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

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

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

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

29 Infection with isolates such as PPR and B2542 was inhibited well by both 7D6 and CD134L,

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

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

32 rly increased trabecular bone volume in both PPR*Tg and control mice, suggesting that trabecular bone

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

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

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

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

37 many of which are addressed individually by PPR proteins.

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

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

40 terminants of nucleotide base recognition by PPR motifs.

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

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

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

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

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

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

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

48 st that the cytoplasmic male sterility (CMS)-PPR interaction is highly conserved across flowering pla

49 3 (PPR2263) encoding a DYW domain-containing PPR protein is required for RNA editing in the mitochond

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

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

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

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

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

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

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

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

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

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

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

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

62 of the pentatricopeptide repeat gene family (PPR), an unusually large gene family in Arabidopsis (app

63 unctions have been determined for only a few PPR proteins, and with few exceptions, substrate RNAs ar

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

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

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

67 For example, clade A FIV-PPR is predominantly neurotropic and causes a mild disea

68 nd unvaccinated cats were infected after FIV-PPR challenge and exhibited similar plasma virus loads.

69 transcription driven by the FIV-C36 and FIV-PPR LTRs were identical.

70 iruses were prepared between FIV-C36 and FIV-PPR, with reciprocal exchanges involving (i) the 3' halv

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

72 challenge with a biological FIV isolate (FIV-PPR) at 13 weeks postimmunization.

73 replicated to levels similar to those of FIV-PPR.

74 roximately 20-fold greater than those of FIV-PPR.

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

76 ironment where FGF activity is favorable for PPR and otic marker expression.

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

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

79 adication of RP are also largely present for PPR.

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

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

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

83 how to engineer these properties in a given PPR.

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

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

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

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

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

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 bone resorption, regulate marrow fibrosis in PPR*Tg mice after treatment of animals with vehicle, OPG

92 as well as the role of dlx3b/4b function in PPR and otic placode induction.

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

94 in cortical bone mineral density with OPG in PPR*Tg mice were associated with greater improvements in

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

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

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

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

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

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

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

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

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

104 al, and bioinformatic data suggest that many PPR proteins influence specific posttranscriptional step

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

106 n empty pericarp4 (emp4), a maize (Zea mays) PPR-encoding gene, confer a seed-lethal phenotype.

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

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

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

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

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

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

113 To gain insight into the mode of action of PPR genes, we generated transgenic petunia plants expres

114 To assay functional activity of PPR + UTR and 5'-UTR regions that either contain or lack

115 Alignments of PPR sequences from HEV strains representing all genotype

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

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

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

119 hanisms within a similarly expanded group of PPR genes.

120 sults provide insight into the mechanisms of PPR specification as well as the role of dlx3b/4b functi

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

122 ected benefits than the current portfolio of PPR conservation.

123 or proper UGGAAexp folding and regulation of PPR translation.

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

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

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

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

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

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

130 emp4 encodes a novel type of PPR protein of 614 amino acids.

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

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

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

134 hosphorylation of Bad at Ser155 in postnatal PPR KO mice.

135 ve been defined as having either propagating PPR or localized, occipital spikes (OS) only.

136 ubjects with (n = 14, seven with propagating PPR, seven with OS) or without (n = 14) PPR.

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

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

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

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

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

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

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

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

145 ion of the PTH/PTH-related peptide receptor (PPR) as a readout failed to provide any lead compounds.

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

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

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

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

150 id hormone-related protein (PTHrP) receptor (PPR) signaling inhibits proliferation and differentiatio

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

152 rathyroid hormone-related protein receptors (PPR*Tg).

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

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

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

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

157 pathogenesis, contains a polyproline region (PPR) that interacts with SH3 domains of redundant kinase

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

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

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

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

162 ory placodes, termed the preplacodal region (PPR).

163 region (DRR) and a proximal promoter region (PPR), which are separated by approximately 2.3 kbp of DN

164 regulated via the proximal promoter region (PPR; -46/-1 in the human sequence; +1 transcription star

165 inear method (projection pursuit regression, PPR).

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

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

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

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

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

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

172 The pentatricopeptide repeat (PPR) family represents one of the largest gene families

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

174 ins in plants, the pentatricopeptide repeat (PPR) family, no physiologically relevant RNA ligands hav

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

176 The pentatricopeptide repeat (PPR) is a degenerate 35-amino acid repeat motif that is

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

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

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

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

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

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

183 k of a chloroplast pentatricopeptide repeat (PPR) protein that we named SUPPRESSOR OF VARIEGATION7 (S

184 We describe a pentatricopeptide repeat (PPR) protein, PPR10, whose binding defines mRNA segments

185 360 that encodes a pentatricopeptide repeat (PPR) protein.

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

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

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

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

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

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

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

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

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

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

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

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

198 of genes encoding pentatricopeptide repeat (PPR) proteins.

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

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

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

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

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

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

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

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

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

208 otosensitivity, or photoparoxysmal response (PPR), is an abnormal EEG reaction to intermittent photic

209 translocation, and prednisone poor response (PPR).

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

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

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

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

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

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

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

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

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

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

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

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

222 utilization of CD134; the prototypic strain PPR requires a minimal determinant in the first cysteine

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

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

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

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

227 The PPR gene family has been implicated in the control of or

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

229 The PPR-deficient progenitors exhibit accelerated cementobla

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

231 understand the precise role of PTHrP and the PPR in the hair cycle, we have evaluated hair growth in

232 pike-evoked GABA release was larger, and the PPR was lower than in wild-type mice.

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

234 /IRF-E2, at the DRR and one AP-1 site at the PPR are required for constitutive expression of TLR9, wh

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

236 f heterotrimeric G-proteins activated by the PPR.

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

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

239 FGF signaling are required to establish the PPR through induction of members of the six/eya/dach, ir

240 ate that dlx3b/4b assist in establishing the PPR through the transcriptional regulation of the BMP an

241 For the PPR and B2542 strains, the replacement of CDR1 of fCD134

242 recognized small molecule antagonist for the PPR.

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

244 /4b results in loss of cv2 expression in the PPR and a transient increase in Bmp4 activity that lasts

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

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

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

248 he size of the tilt aftereffect (TAE) in the PPR group only.

249 of the motion aftereffect was shorter in the PPR group than in the control group.

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

251 disappearance of the growth cartilage in the PPR knockout.

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

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

254 und to this putative signaling domain of the PPR could be altered by chemical modification.

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

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

257 We found that inactivation of the PPR in chondrocytes postnatally leads to accelerated dif

258 rowth plate by postnatal inactivation of the PPR in chondrocytes.

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

260 as well as transgenic overexpression of the PPR ligand PTHrP have suggested that this ligand recepto

261 ght into the functions and substrates of the PPR protein family, we characterized the maize (Zea mays

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

263 peptide that acts as a potent agonist of the PPR, and characterized its activity in ex vivo and in vi

264 e binding to the transmembrane region of the PPR, driven by the assumption that the pharmacological p

265 redundant roles in the specification of the PPR, otic and olfactory placodes.

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

267 ctly participate in the establishment of the PPR.

268 he 3' LTR and Rev2 regions of FIV-C36 on the PPR background.

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

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

271 The binding of SW106 to the PPR was rationalized by using a homology receptor model.

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

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

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

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

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

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

278 gical functions that have been attributed to PPR proteins.

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

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

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

282 Two PPR proteins, dually targeted to mitochondria and chloro

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

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

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

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

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

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

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

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

291 Previous studies using PPR agonists and antagonists as well as transgenic overe

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

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

294 ruitment of additional redundant kinases via PPR-SH3 interactions and PO(3)-Y474-SH2 interactions, wh

295 ist of RNA-related functions associated with PPR proteins and suggest that plastid group II trans-spl

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.