ライフサイエンスコーパス: PAR

1 PAR activation contributes to the inflammatory response

2 PAR complex dynamics are linked to the cell cycle by Pol

3 PAR is frequently associated with allergic asthma (AA).

4 PAR proteins constitute a highly conserved network of sc

5 PAR(2) activates transient receptor potential (TRP) chan

6 PAR-1 antagonist treatment significantly decreased pulmo

7 PAR-1 deficiency also reduced leukemogenicity of AML1-ET

8 PAR-1 protects NMY-2 from being moved across the cortex

9 PAR-2 activation induces G protein-alpha-mediated signal

10 PAR-2 activation was blocked in murine model by administ

11 PAR-2 is activated by proteases secreted by airway neutr

12 PAR-2 is activated via proteolytic cleavage by trypsin-l

13 PAR-4 was also found on gastrin-releasing peptide (GRP)-

14 PAR-CLIP is a recently developed Next Generation Sequenc

15 PAR-CLIP, a CLIP-seq protocol, derives a transcriptome w

16 PARs are activated by proteolysis of the N terminus to r

17 PARs are implicated in a wide range of diseases, such as

18 PARs have been the subject of major pharmaceutical resea

19 oblasts via proteinase-activated receptor 1 (PAR-1) and mammalian target of rapamycin complex 1 (mTOR

20 proteolysis, protease-activated receptor-1 (PAR-1) expressed by stromal cells and the extracellular

21 both HAM-1 and its target, the kinase PIG-1 [PAR-1(I)-like Gene], leads to abnormal dopaminergic head

22 st cells, and protease-activated receptor 2 (PAR-2).

23 s that cleave protease-activated receptor-2 (PAR(2)) at Arg(36) downward arrowSer(37) reveal a tether

24 pled receptor protease-activated receptor-2 (PAR-2) plays a key role in inflammation.

25 signaling via protease-activated receptor-2 (PAR-2), and promoted fibroblast activation, proliferatio

26 mm Hg or higher (OR 2.98, 99% CI 2.72-3.28; PAR 47.9%, 99% CI 45.1-50.6), regular physical activity

27 conserved polarity effector proteins PAR-3, PAR-6, CDC-42, and atypical protein kinase C (aPKC) form

28 Inhibition of protease-activated receptor-4 (PAR-4), but not PAR-2, blocked the effects of MET-1.

29 t, specialized aPKC-containing assemblies: a PAR-3-dependent assembly that responds to polarity cues

30 he amount of common backgrounds present in a PAR-CLIP dataset, and we provide the user the option to

31 The only marketed drug targeting a PAR is vorapaxar, a selective antagonist of PAR1 used to

32 In addition, we found that a PAR-1 antagonist, SCH, prevented LPS-induced excessive m

33 al hormone therapy use was associated with a PAR% of 34.6% (95% confidence interval: 22.7, 45.4).

34 Little is known, however, about PAR-2 regulation of inflammation-related microRNAs.

35 Meanwhile, PAR-3 stabilizes NMY-2 against PAR-2 and PAR-6 dynamics on the cortex.

36 on the in-house Ago2-dataset and on an Ago2-PAR-CLIP dataset in human stem cells.

37 These genes were added to an ancestral PAR of the sex chromosome pair in two distinct events pr

38 the PAR (one gene that was in the ancestral PAR and two from each of the added regions).

39 ile its downregulation suppresses PARP-1 and PAR protein expression and cisplatin resistance.

40 In conclusion, PAR-1 and PAR-2 are involved in FXa-mediated intracellular Ca(2+)

41 Antagonism of PAR-1 and PAR-2 reduced FXa-induced Ca(2+) release.

42 In addition, we find that PAR-1 and PAR-3 are necessary for inhibiting movement of NMY-2 acr

43 Codepletion of ATX-2 and PAR-5 rescued the localization of ZEN-4 at the spindle m

44 le, PAR-3 stabilizes NMY-2 against PAR-2 and PAR-6 dynamics on the cortex.

45 We find that PAR-3 and PAR-6 concentrate CDC-42-dependent NMY-2 in the anterior

46 the posterior domain by inhibiting PAR-3 and PAR-6.

47 hanisms through which PARP1 is activated and PAR is robustly synthesized are not fully understood.

48 n comparison to zero of 18,055 autosomal and PAR genes (Fisher's exact P < 0.0001).

49 the direct thrombin inhibitor lepirudin and PAR-4 deficiency attenuate hepatotoxicity.

50 id thrombin-antithrombin complex levels) and PAR-1 immunostaining were increased in this model of bac

51 ncoded latency membrane protein 1 (LMP1) and PAR levels that was dependent upon PARP1.

52 onjugated ADP-ribose, including both MAR and PAR.

53 sion, our results demonstrate that PARP1 and PAR actively, and in some instances differentially, regu

54 ifferential responses to PARylated PARP1 and PAR.

55 the effects that PARP1, PARylated PARP1, and PAR have on RECQL5 and WRN, using both in vitro and in v

56 m68, DNA damage-triggered PAR production and PAR-dependent DNA repair signaling were dramatically dim

57 Using AGO2 RIP-seq and PAR-CLIP-seq, we show that the DNA damage-induced increa

58 kt-mTor proliferation/survival signaling and PAR-2-Galphai-NFkappaB inflammatory signaling.

59 When testisin and PAR-2 are co-expressed in HeLa cells, GPI-anchored testi

60 ome activation and that mimicking biased aPC PAR-1 signaling using parmodulins may be a feasible ther

61 Here, we assess PAR-2 expression and function in OSCC cell lines and tis

62 nt mice, implicating stromal cell-associated PAR-1 as one thrombin target important for tumor outgrow

63 Targeting biased PAR-1 signaling via parmodulin-2 restricted mTORC1 and N

64 caused edema and mechanical hyperalgesia by PAR(2)- and TRPV4-mediated mechanisms.

65 lspindlin oligomers is globally inhibited by PAR-5/14-3-3.

66 al modification predominantly synthesized by PAR polymerase-1 (PARP-1) in genome maintenance.

67 r estrogen receptor-negative breast cancers (PAR% = 27.9%).

68 r estrogen receptor-positive breast cancers (PAR% = 39.7%) than for estrogen receptor-negative breast

69 Elastase caused PAR(2)-dependent sensitization of TRPV4 currents in Xeno

70 Moreover, cellular PAR levels were up to 2-fold greater in type III than ty

71 Although proteases that cleave PAR(2) at non-canonical sites can trigger distinct signa

72 pment of three distinct versions: HITS-CLIP, PAR-CLIP and iCLIP.

73 In conclusion, PAR-1 and PAR-2 are involved in FXa-mediated intracellul

74 for DNA damage-initiated and PARP1-conferred PAR production.

75 Caenorhabditis elegans embryos, the cortical PAR proteins (including the small guanosine triphosphata

76 We found that the cortical PAR proteins are required for the retention of anillin a

77 ively, our results suggest that the cortical PAR proteins coordinate the establishment of cell polari

78 chemical activity of partitioning-defective (PAR) proteins.

79 polarity machinery (partitioning defective [PAR] proteins) controls the unequal inheritance of key c

80 imilar to the effect of Runx1/Cbfb deletion, PAR-1 overexpression induced CDKN1A/p21 expression and a

81 We took advantage of newly discovered PAR antagonists to contrast the contribution of PAR1 and

82 Analysis of EBV PAR-CLIP miRNA targetome data sets combined with pathway

83 Upregulated Sam68 coincides with elevated PAR production and NF-kappaB-mediated anti-apoptotic tra

84 We also evaluate PAR inhibitory actions on leishmanial growth and ribosom

85 ls within the tunica muscularis that express PARs and the mechanisms leading to contractile responses

86 Finally, PAR-6 is necessary to localize polarity proteins such as

87 miR-23b, and miR-200c was observed following PAR-2 stimulation.

88 nding the structural rearrangement following PAR activation and how PARs are allosterically controlle

89 tilization (MRU) and related direct cost for PAR, with or without concomitant AA, in France.

90 y three zinc finger motifs are essential for PAR recognition.

91 cally greater than all pharmacotherapies for PAR.

92 and 3.7%, 4.8%, and 11.2%, respectively, for PAR trials.

93 ether, these data demonstrate a key role for PAR-1 during S. pneumoniae lung infection that is mediat

94 these data revealed a multifaceted role for PAR-1 in leukemogenesis, and highlight this receptor as

95 Using real time PCR, we found PARs to be expressed in smooth muscle cells (SMCs), inte

96 ng miRNAs, we analyze multiple datasets from PAR-CLIP experiments in conjunction with RNA-Seq data.

97 this article is to review how signaling from PARs is influenced by alternative cleavage sites and the

98 les were harvested at low as opposed to high PAR, the leaf content was higher in DM, protein, K, Ca a

99 d, and red lettuce, were observed under high PAR.

100 EBV-infected B cells had higher PAR levels than EBV-negative B cells.

101 Substantially higher PARs were obtained when the low-risk group was compared

102 Homogeneous PAR oligomers and unnatural variants produced from chemi

103 al. (2017) in Nature Cell Biology, show how PAR protein oligomerization can dynamically couple prote

104 Here we analyze how PARs regulate the behavior of the cortical motor protein

105 arrangement following PAR activation and how PARs are allosterically controlled within the plasma mem

106 mplement recent efforts that investigate how PARs regulate the Rho GTPase CDC-42, which in turn regul

107 hanced crosslinking and immunoprecipitation (PAR-CLIP), we isolated RNAs associated with Argonaute 2

108 Re-expression of PAR-1 in PAR-1-deficient cells combined with a limiting-dilution

109 dentify the presence of common background in PAR-CLIP datasets is not yet available.

110 quality of life were significantly higher in PAR compared with healthy control subjects (P < 0.0001).

111 Colonic adenocarcinoma growth was reduced in PAR-1-deficient mice, implicating stromal cell-associate

112 els either ignore inhibition or only include PAR inhibition.

113 e detection is coupled to a massive increase PAR production, primarily attached to PARP-1 (automodifi

114 ition in the catalytic domain that increases PAR production.

115 ains could also recognize DNA damage-induced PAR.

116 romoted DNA damage accumulation, inefficient PAR removal, and persistent PARP-1 residency on chromati

117 Accordingly, inhibiting PAR-1 signaling, but not the anticoagulant properties of

118 NMY-2 in the posterior domain by inhibiting PAR-3 and PAR-6.

119 e in DDR via regulating DNA damage-initiated PAR production.

120 efficiency of conversion of that intercepted PAR (varepsilonc ) are major opportunities for genetic i

121 ough thrombin and factor Xa, which are known PAR agonists, and cause microthrombosis in liver microci

122 diversity patterns of five such S. latifolia PAR boundary genes with their orthologues in S. dioica,

123 dependent role of PAR-1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemic proliferation when there

124 me evident: the enzyme used to transform MAR/PAR into phosphoribose must be purified from the rattles

125 tential of a tag-based pipeline in which MAR/PAR is hydrolyzed down to phosphoribose, leaving a 212 D

126 , including the CaMKK-like Ssp1 and the MARK/PAR-1 family kinase Kin1, that are required for polarize

127 the 14-3-3-family protein Bmh1 and the MARK/PAR-kinase Kin4.

128 In contrast to the SDR, the maternal PAR recombination rate is much higher than the rates of

129 Meanwhile, PAR-3 stabilizes NMY-2 against PAR-2 and PAR-6 dynamics

130 Mechanistically, PAR-1 increased the adherence properties of MLL-AF9 cell

131 thelial cells (HUVEC) following FXa-mediated PAR activation and investigated whether FXa reactive IgG

132 e data support a model wherein KLK5-mediated PAR-2 activation regulates the expression of inflammatio

133 d higher protein carbonyls, 3-nitrotyrosine, PAR, lactate dehydrogenase and proteins in bronchoalveol

134 otease-activated receptor-4 (PAR-4), but not PAR-2, blocked the effects of MET-1.

135 Several novel PAR-binding domains have been recently identified.

136 In the absence of PAR, the RING domain is unable to bind and activate a ub

137 olving aberrant expression and activation of PAR-2-mediated pathways, characterizes younger patients

138 Thus, the elastase-biased agonism of PAR(2) causes Galphas-dependent activation of adenylyl c

139 her neutrophil elastase, a biased agonist of PAR(2), causes inflammation and pain by activating PAR2

140 ATX-2 does this by regulating the amount of PAR-5 at mitotic structures, particularly the spindle, c

141 Antagonism of PAR-1 and PAR-2 reduced FXa-induced Ca(2+) release.

142 or testisin and that proteolytic cleavage of PAR-2 by recombinant testisin activates downstream signa

143 The cleavage of PAR-2 by testisin induces activation of the intracellula

144 (EHRs), we identified in 2010 two cohorts of PAR patients, based on General Practitioners' diagnoses

145 Costs of PAR with or without AA are poorly documented.

146 Here, we show that the N-terminal domain of PAR-2 is a substrate for testisin and that proteolytic c

147 catalytic activity, although the effects of PAR on PARP-1 structure are poorly understood.

148 No molecular or functional evidence of PAR-4 was observed.

149 much focus has been given to exploration of PAR activities in bacteria, its mechanism of action in L

150 Re-expression of PAR-1 in PAR-1-deficient cells combined with a limiting-

151 n vitro, while pharmacological inhibition of PAR 1 similarly slowed both the growth and migration of

152 ffects appear to be related to inhibition of PAR-1, and represents a novel neuroprotective strategy t

153 This ultimately controls the initiation of PAR signaling.

154 nd biochemical studies on the interaction of PAR with its many protein binding partners.

155 ediment to understanding the interactions of PAR with poly(ADP-ribose) glycohydrolase (PARG) and othe

156 g ATX-2 function leads to elevated levels of PAR-5, enhanced chromatin and centrosome localization of

157 ced chromatin and centrosome localization of PAR-5-GFP, and ultimately a reduction of ZEN-4-GFP at th

158 olo-like kinase 1 and govern the movement of PAR proteins to establish polarity.

159 We uncovered striking regulation of PAR complex composition and stoichiometry during Caenorh

160 iating the posttranscriptional regulation of PAR-5.

161 The observed robustness of PAR domain dimensions in embryos of different sizes is i

162 d activation of TRPV4 and expand the role of PAR(2) as a mediator of protease-driven inflammation and

163 demonstrated the cell-dose-dependent role of PAR-1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemi

164 st a novel and previously overlooked role of PAR-2 in airway physiology, adding to our understanding

165 -treated mice and BMDCs indicating a role of PAR-2-mediated signalling.

166 s a clear increase in costs with severity of PAR and control of AA.

167 yses were performed according to severity of PAR and level of AA control.

168 H2B were rapidly depleted from the sites of PAR accumulation.

169 The rate-limiting step of PAR signaling is determined by the efficiency of proteol

170 Stimulation of PAR-2 activates Nf-kappaB signaling, resulting in RelA n

171 we have demonstrated that the suppression of PAR-1 leads to down-regulation of inflammatory factors i

172 diates the localization of ZEN-4 upstream of PAR-5.

173 ed signaling to the molecular arrangement of PARs in the cell membrane and to determine how these may

174 uence, the genetic and epigenetic control of PARs and their cofactors in physiologic and pathophysiol

175 varied from 111euro to 188euro depending on PAR severity.

176 o claims data collected valid information on PAR management, with or without concomitant AA, and on r

177 The optimized PAR condition permits the acquisition of high signal-to-

178 lood mononuclear lymphocytes with lithium or PAR.

179 spray (MFNS; 200 mug daily, n = 2140) SAR or PAR trials.

180 etermination in the presence of paracetamol (PAR) and caffeine (CAF).

181 Paromomycin (PAR), a broad-spectrum aminoglycoside antibiotic, has be

182 hmania ribosome in complex with paromomycin (PAR), a highly potent compound recently approved for tre

183 hium and the antidepressant (AD) paroxetine (PAR) functionally synergize with FKBP51, as revealed by

184 s much higher than the rates of the paternal PAR or autosomes, culminating in an elevated chromosome-

185 al population attributable risk percentages (PAR%) by combining the relative risks and the observed p

186 nduced liver injury, independent of platelet PAR-4 signaling.

187 is required for both anterior and posterior PAR complexes.

188 kinesin ZEN-4/MKLP1 and the polarity protein PAR-6.

189 The conserved polarity effector proteins PAR-3, PAR-6, CDC-42, and atypical protein kinase C (aPK

190 ol protein 42), associated polarity proteins PAR-6 (Partitioning defective 6) and PKC-3/atypical prot

191 We use published PAR-CLIP data to demonstrate the advantages of our appro

192 ni ) of photosynthetically active radiation (PAR) and the efficiency of conversion of that intercepte

193 gen and photosynthetically active radiation (PAR).

194 ense photosynthetically available radiation (PAR), but the effects on ocean productivity have receive

195 nd high Photosynthetically Active Radiation; PAR) at time of harvest were determined.

196 including the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-del

197 VI and thrombin protease-activated receptor (PAR) 1.

198 we examined the protease-activated receptor (PAR)-2, a GPCR previously shown to regulate airway cell

199 Protease-activated receptor (PAR)-2, Toll-like receptor (TLR), and C-type lectin rece

200 is a ligand for protease-activated receptor (PAR)1 and PAR4.

201 Thrombin-activated receptor (PAR-1) expression is increased in HIV-infected ART recip

202 activation of protease-activated receptors (PAR) leads to increased intracellular calcium (Ca(2+)).

203 y activating proteinase-activated receptors (PARs) 1 and 4.

204 Protease-activated receptors (PARs) are a family of G-protein-coupled receptors (GPCRs

205 Protease-activated receptors (PARs) can activate HSCs through thrombin and factor Xa,

206 ed family of proteinase-activated receptors (PARs).

207 responses via protease-activated receptors (PARs).

208 y activating proteinase-activated receptors (PARs).

209 ized (15)N-(15)N proton assisted recoupling (PAR) mixing period and a (13)C dimension for improved re

210 The S. latifolia pseudoautosomal region (PAR) includes several genes extremely closely linked to

211 Six of 783 non-pseudoautosomal region (PAR) X-chromosome genes (ATRX, CNKSR2, DDX3X, KDM5C, KDM

212 ally elevated in the pseudoautosomal region (PAR).

213 LSCs, while a small number of LSCs required PAR-1 for their efficient growth.

214 For individual cancers, the respective PARs in women and men were 82% and 78% for lung, 29% and

215 Perennial allergic rhinitis (PAR) represents a global and public health problem, due

216 nitis (SAR) and perennial allergic rhinitis (PAR).

217 ymers of adenosine diphosphate (ADP)-ribose (PAR) chains, primarily catalyzed by poly(ADP-ribose) pol

218 NA repair factors via their poly ADP-ribose (PAR) binding domains.

219 interacts with and attaches poly-ADP-ribose (PAR) chains to EZH2.

220 NA damage-stimulated polymers of ADP-ribose (PAR) production and the PAR-dependent NF-kappaB transact

221 mono-ADP-ribose (MAR) and poly(ADP-ribose) (PAR) chain removal (de-MARylation and de-PARylation, res

222 associated with accessing poly(ADP-ribose) (PAR) in a homogeneous form has been an impediment to und

223 histone H1 accumulated on poly(ADP-ribose) (PAR) in vivo.

224 Poly(ADP-ribose) (PAR) is a posttranslational modification predominantly s

225 DNA double-strand breaks, poly(ADP-ribose) (PAR) is quickly and heavily synthesized to mediate fast

226 ion or genetic deletion of poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) is protective against toxic i

227 sion stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and cisplatin resistance while i

228 ears ago, the discovery of poly(ADP-ribose) (PAR) set a new field of science in motion-the field of p

229 Pr), the smallest internal poly(ADP-ribose) (PAR) structural unit, binds between the WWE and RING dom

230 translational modification poly(ADP-ribose) (PAR) to facilitate repair.

231 NA repair that possesses a poly(ADP-ribose) (PAR)-binding macro domain.

232 or in polymeric chains as poly(ADP-ribose) (PAR).

233 he zinc finger domain and poly (ADP-ribose) (PAR).

234 of RNS), poly(adenosine diphosphate-ribose) (PAR, marker of PARP activation) and IL-6, in the broncho

235 calculated the population-attributable risk (PAR) by comparing incidence and mortality of total and m

236 estimation of population attributable risk (PAR) suggested that nsVT was the strongest predictor for

237 nt cancers and population-attributable risk (PAR).

238 The population attributable risks (PARs) were 0.41, 0.40 and 0.38 for total, CVD and cancer

239 OR) and their population attributable risks (PARs) were calculated, with 99% confidence intervals.

240 n mice, which was prevented by the selective PAR-4 antagonist (pepducin P4pal-10).

241 score that reflects its presence in several PAR-CLIP datasets.

242 lavage were assessed in subjects with severe PAR (n = 46) and healthy control subjects (n = 19).

243 Elastase stimulated PAR(2)-dependent cAMP accumulation and ERK1/2 activation

244 hed the utility of this approach by studying PAR polarity proteins, which mediate polarization of man

245 To our surprise, PAR-1 deficiency also prevented leukemia development ind

246 1 binds to damaged chromatin and synthesizes PAR chains to signal DNA damage and recruit the DNA repa

247 functional role for thrombin and its targets PAR-1 and fibrinogen in the pathogenesis of colonic aden

248 We find that PAR signaling fulfills two roles: localizing NMY-2 to th

249 In addition, we find that PAR-1 and PAR-3 are necessary for inhibiting movement of

250 We find that PAR-3 and PAR-6 concentrate CDC-42-dependent NMY-2 in th

251 We find that PAR-4/LKB1 impinges on myosin via two pathways, an anill

252 We found that PAR-2 is expressed basolaterally, where it stimulates bo

253 tively targeted in the RISC, indicating that PAR-CLIP more accurately defines meaningful targeting in

254 We further show that PAR interferes with several aspects of cytosolic transla

255 The PAR polymerase PARP1 binds to damaged chromatin and synt

256 The PAR% for modifiable factors was higher for estrogen rece

257 Despite sequence homology across the PAR isoforms, discovery of PAR2 antagonists has been les

258 l risk factors (and controlled for age), the PAR% for invasive breast cancers was 70.0% (95% confiden

259 ymers of ADP-ribose (PAR) production and the PAR-dependent NF-kappaB transactivation of anti-apoptoti

260 We further assessed the PAR at the national scale by comparing the low-risk grou

261 Deletion of FKBP51 blunted the PAR- or lithium-induced increase in pGSK3beta(S9) in cel

262 ng molecular players and interactions in the PAR network have begun to merge with biophysical, theore

263 os could favor elevated recombination in the PAR to remove deleterious mutations on the W.

264 unique as well as conserved elements in the PAR-binding pocket that can serve as hotspots for the de

265 several ASM mitogenic factors, including the PAR-2 ligands, mast cell tryptase, trypsin, tissue facto

266 . dioica, including all three regions of the PAR (one gene that was in the ancestral PAR and two from

267 hese risk factors accounted for 90.7% of the PAR for all stroke worldwide (91.5% for ischaemic stroke

268 ollectively associated with about 90% of the PAR of stroke in each major region of the world, among e

269 tein kinase C (aPKC) form a core unit of the PAR protein network, which plays a central role in polar

270 g cascades, the functional importance of the PAR(2)-biased agonism is uncertain.

271 -anchored testisin specifically releases the PAR-2 tethered ligand.

272 Moreover, our study suggests that the PAR-mediated fast recruitment of EXO1 facilities early D

273 an interlocked feedback loop, which uses the PAR DOMAIN PROTEIN 1epsilon (PDP1epsilon) activator and

274 also consider some of the ways in which the PAR network has evolved to polarize cells in different c

275 Close linkage with the PAR boundary must have evolved since these additions, be

276 ks cue-sensing and effector roles within the PAR network to ensure robust establishment of polarity.

277 The PARs were 4% and 12% for breast cancer incidence and mor

278 Within the 2 cohorts, the PARs for incidence and mortality of total carcinoma were

279 For example, the PARs in women and men were 41% and 63% for incidence of

280 act the excitability of DRG neurons, through PAR-4 activation.

281 ing evidence suggests that signaling through PAR-1 is involved in inflammation, however, its function

282 increases the binding of the macro domain to PAR and simulates the demodification activity.

283 Per a 10 leads to PAR-2 activation on BMDCs resulting in downstream activa

284 to characterize the integrated responses to PAR activation in whole muscles.

285 n the absence of Sam68, DNA damage-triggered PAR production and PAR-dependent DNA repair signaling we

286 etion diminishes gamma-irradiation-triggered PAR synthesis and NF-kappaB activation in colon epitheli

287 a 10-administered mice and was reduced upon PAR-2 blockage.

288 evels in mouse lungs, which was reduced upon PAR-2 blockage.

289 d the Zinc Finger Protein 598 (ZNF598) using PAR-CLIP and revealed that it cross-links to tRNAs, mRNA

290 rmediates of our synthesis to access various PAR fragments, and evaluation of these compounds as subs

291 kly recruited to the sites of DNA damage via PAR-binding.

292 s of AGO2 cross-linking sites identified via PAR-CLIP-seq.

293 endent NMY-2 in the anterior cortex, whereas PAR-2 inhibits CDC-42-dependent NMY-2 in the posterior d

294 d remodeling, whereas it was associated with PAR-2 overexpression and higher alveolar tryptase (P </=

295 that all human RecQ helicases interact with PAR noncovalently.

296 est number of binding sites overlapping with PAR-CLIP with maximum F-Score of 0.337.

297 by social security system for a patient with PAR, and no AA was 159euro in 2013.

298 For patients with PAR and concomitant AA, the median annual cost varied be

299 colorectal cancers per 100000 person-years (PAR, 17.0%) among those who had not undergone a lower en

300 colorectal cancers per 100000 person-years (PAR, 8.5%) among those who had.