ライフサイエンスコーパス: PAR

1 PAR degradation by poly(ADP-ribose) glycohydrolase (PARG

2 PAR is a technically demanding procedure and requires a

3 PAR proteins are initially not competent to polarize but

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

5 PAR-1 deficiency was associated with reduced endothelial

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

7 PAR-2 is normally expressed basolaterally in differentia

8 PAR-6 and PKC-3 are required in the epidermal epithelium

9 PAR-6 is localized to the rosette vertex and dendrite ti

10 PAR-6 was required for the localization of the microtubu

11 PARs are activated by proteolytic cleavage of their rece

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

13 PARs have been the subject of major pharmaceutical resea

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

15 ctor (TF) and protease-activated receptor-1 (PAR-1) were highly expressed in primary KPC pancreatic l

16 NH(2)) of the protease-activated receptor-1 (PAR-1), a thrombin receptor expressed by vECs, neuronal

17 bin receptor, protease activated receptor-1 (PAR-1), as well as deficiency of PAR-1 in all nonhematop

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

19 Protease-activated receptor 2 (PAR-2) is activated by secreted proteases from immune ce

20 Protease-activated receptor 2 (PAR-2) is expressed in various tissues, including lung,

21 Lgmn) cleaves protease-activated receptor-2 (PAR(2)) in the acidic OSCC microenvironment to cause pai

22 ents, cleaves protease-activated receptor-2 (PAR(2)) on neurons to produce OSCC pain.

23 n by cleaving protease-activated receptor-2 (PAR(2)) on nociceptors through distinct mechanisms.

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

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

26 P1 by ADP-ribosylation that is targeted by a PAR-binding E3 ubiquitin ligase, RNF146, leading to 53BP

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

28 ining hemagglutinin and neuraminidase with a PAR-2 agonist peptide (PAR-2AP) in an intranasal prime b

29 Because proteases activate PAR(2) by irreversible cleavage, and activated PAR(2) is

30 We conclude that proteases that activate PAR(2) by canonical and biased mechanisms stimulate PKD

31 R(2) by irreversible cleavage, and activated PAR(2) is degraded in lysosomes, sustained extracellular

32 Lgmn activated PAR(2) by biased mechanisms in HEK293 cells to induce Ca

33 Lgmn activated PAR(2) to induce calcium mobilization, cAMP formation, a

34 is a member of the proteolytically-activated PAR family of G-protein-coupled receptors (GPCR) that re

35 dified OSCC microenvironment, Lgmn activates PAR(2) by biased mechanisms that evoke cancer pain.SIGNI

36 Efficacy outcomes regarding AD, PAR and PAA were collected at baseline and 16 weeks.

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

38 Combined AGO-PAR-CLIP and RNA-seq analysis identified a panel of pote

39 Pathway analysis of AGO-PAR-CLIP-identified miR targets revealed roles in DNA re

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

41 ilial loss and squamous metaplasia may alter PAR-2 polarization.

42 Altered PAR-2 polarization in disease-remodeled epithelia may en

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

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

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

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

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

48 rtical polarity regulators PAR-6, PKC-3, and PAR-3 are essential for the polarization of a broad vari

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

50 Higher PARP1 protein levels and PAR proteins were detected in mtp53 R273H than in wild-t

51 a modified version of the Vienna Package and PAR-CLIP data for HuR (ELAVL1) in humans we characterize

52 t that early TEP peaks (<80 ms) from PFC and PAR reflect stimulation site specific activity that is l

53 e were amplitude differences between PFC and PAR TEPs across a wide time range (15-250 ms), however t

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

55 sponded to apically or basolaterally applied PAR-2 agonists.

56 e used to simplify complex workflows such as PAR-CLIP.

57 ability to survive DNA damage by attenuating PAR synthesis and thus preventing cell death.

58 eration of anti-EGFR fibronectin (FN3)-based PARs with high yield, rapid protein production, predicte

59 res responded to both apical and basolateral PAR-2 stimulation.

60 polyps and turbinates maintained basolateral PAR-2 polarization, suggesting that the calcium response

61 pithelial ALIs responded only to basolateral PAR-2 stimulation, indicated by calcium elevation, incre

62 y emerging evidence for an interplay between PAR-2 and membrane-anchored serine proteases, which may

63 ility of different protease agonists to bias PAR-2 signaling and the newly emerging evidence for an i

64 nocturnal sap flow, was strongly affected by PAR, air temperature and vapor-pressure deficit.

65 Poly(ADP-ribose)ylation (PARylation) by PAR polymerase 1 (PARP1) and PARylation removal by poly(

66 We focus on pathways regulated by PAR in neurodegenerative disease, with emphasis on amyot

67 Lgmn caused PAR(2)-dependent hyperexcitability of trigeminal neurons

68 (OXR) compared to naive parental HT29 cells (PAR).

69 n-S (CS) and neutrophil elastase (NE) cleave PAR(2) at distinct sites and activate it by biased mecha

70 upilumab treatment in patients with comorbid PAR (n = 41) was associated with significant improvement

71 b on PAR in severe AD patients with comorbid PAR.

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

73 on, including the sites that are conjugated, PAR chain length and structure, and the physicochemical

74 Polarization requires that the conserved PAR proteins, which specify polarity in the zygote, be p

75 A1CF functional (RNA-seq) and binding data (PAR-CLIP).

76 es remodeling of the partitioning-defective (PAR) polarity complex and leads to loss of cell polarity

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

78 key enzymes in BER that elongate and degrade PAR polymers on target proteins.

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

80 We also show that macroH2A1-dependent PAR stabilization promotes efficient repair of oxidative

81 culating prothrombin, and tumor cell-derived PAR-1 and further indicate that one key mechanism of thr

82 n vitro evidence that TNKS primarily directs PAR modification to glutamate/aspartate residues.

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

84 SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function.

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

86 synapsis triggers collapse of the elongated PAR structure and, notably, oocytes can be reprogrammed

87 Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI-H5

88 highly similar to those caused by epidermal PAR-6 depletion.

89 A damage to facilitate repair, but excessive PAR synthesis due to extensive DNA damage results in cel

90 affinity tags), ELTA can be used to explore PAR biology with techniques routinely used to investigat

91 fumigatus activates heterologously-expressed PAR-2.

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

93 tumor growth with no adverse effects and FN3-PARs reduced immunosuppressive programmed cell death lig

94 We demonstrated the cytotoxicity of FN3-PARs successfully while evaluating FN3 affinities, CSAN

95 ese results demonstrate the potential of FN3-PARs to direct selective T cell-targeted tumor killing a

96 opic breast cancer model, we showed that FN3-PARs can suppress tumor growth with no adverse effects a

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

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

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

100 Finally, we uncovered a novel role for PAR-6 in organizing non-centrosomal microtubule arrays i

101 curve of experienced pancreatic surgeons for PAR was 15 such procedures.

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

103 iased mechanisms stimulate PKD in the Golgi; PAR(2) mobilization and de novo synthesis repopulate the

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

105 However, PARs are also activated by exogenous application of synt

106 Thus, if PAR proteins can respond to multiple polarizing cues, ho

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

108 Mounting evidence implicates PAR in seeding the abnormal localization and accumulatio

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

110 ng a Rhinitis Control Scoring System) and in PAR Quality of life (QoL) (measured using the Rhinoconju

111 associated with significant improvements in PAR disease control (measured using a Rhinitis Control S

112 The role of Lgmn in PAR(2)-dependent cancer pain is unknown.

113 els either ignore inhibition or only include PAR inhibition.

114 romatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dys

115 ration initiates a fertilization-independent PAR activation program.

116 tase as a model, we show gluten-independent, PAR-2 mediated upregulation of inflammatory pathways in

117 Whereas trypsin induces PAR(2) coupling to Galpha(q), Galpha(s), and beta-arrest

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

119 l, Pillay et al. demonstrate that inhibiting PAR-chain turnover results in cell-cycle arrest, which i

120 ly(ADP-ribose) polymerase 1 (PARP1) inhibits PAR-mediated recruitment of FBXW7 to the DNA damage site

121 ed signaling requires mobilization of intact PAR(2) from the Golgi apparatus or de novo synthesis of

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

123 ) female mice but not in female mice lacking PAR(2) in Na(V)1.8-positive neurons (Par(2)Na(v)1.8), no

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

125 cription of symmetry breaking, wherein local PAR-2-dependent weakening of the actin cortex, together

126 the specific roles of one of four mammalian PARs, namely PAR-2, which is overexpressed in advanced s

127 tributes to robust symmetry breaking by MARK/PAR-1 kinases in diverse cell types.

128 Localization of MARK/PAR-1 kinases to specific regions of the cell cortex is

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

130 The MARK/PAR-1 family of kinases are conserved regulators of cell

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

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

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

134 hown the therapeutic potential of modulating PAR conjugation (PARylation): PAR polymerase (PARP) inhi

135 roles of one of four mammalian PARs, namely PAR-2, which is overexpressed in advanced stage tumors a

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

137 ation, we show that PAR-6 and PKC-3, but not PAR-3, are essential for postembryonic development.

138 Notably, PAR-1-deleted KPC cells (KPC-Par-1(KO)) failed to genera

139 tes that the WD40 domain of FBXW7 is a novel PAR-binding motif that facilitates early recruitment of

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

141 ath by energy depletion and/or activation of PAR-dependent programmed cell death pathways.

142 Thus, Lgmn is a biased agonist of PAR(2) that evokes cancer pain.

143 receptor-1 (PAR-1), as well as deficiency of PAR-1 in all nonhematopoietic cells, also reduces stasis

144 ing to PAR of a defined length, detection of PAR length from proteins and cells, and enrichment of su

145 oss of Xrcc1, a major downstream effector of PAR, also caused persistent PARP1 foci without affecting

146 e secretion, (ii) synergistic enhancement of PAR-mediated activation of the small GTPase RAP1, a regu

147 and the results show striking enrichment of PAR at transcription start sites, depletion of heterochr

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

149 Inhibitors of PAR polymerase (PARP) activity have been developed as ca

150 s show that macroH2A1 alters the kinetics of PAR accumulation following acute DNA damage by both supp

151 2, and distribution and expression-levels of PAR-2, CGRP and c-Fos on day 22.

152 e, we report that asymmetric localization of PAR-1 protein is not essential, and that PAR-1 kinase ac

153 nd protein translation inhibited recovery of PAR(2) responsiveness.

154 While the role of PAR in recruiting and regulating macrodomain-containing

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

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

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

158 n regulation which leads to the synthesis of PAR in the nucleus triggering the release of AIF from th

159 eaved within the extracellular N terminus of PAR(2) at Asn(30) Arg(31), proximal to the canonical try

160 sibly mediated through reduced activation of PARs.

161 Furthermore, expression of PARs and their activators, thrombin and FXa was diminish

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

163 seases, a therapeutic effect of dupilumab on PAR can be expected.

164 We investigated the effect of dupilumab on PAR in severe AD patients with comorbid PAR.

165 nd PKA, but not beta-arrestin recruitment or PAR(2) endocytosis.

166 vation, but not beta-arrestin recruitment or PAR(2) endocytosis.

167 ediatric Admission Record (PAR) was used (OR PAR used compared with PAR not present: 2.41, 95% CI: 1.

168 hal influenza virus over that by virosome or PAR-2AP prime boost alone.

169 rime boost compared with either virosomes or PAR-2AP alone.

170 and TEPs from prefrontal (PFC) and parietal (PAR) cortex were measured before and after administratio

171 of modulating PAR conjugation (PARylation): PAR polymerase (PARP) inhibitors can modulate the format

172 neuraminidase with a PAR-2 agonist peptide (PAR-2AP) in an intranasal prime boost approach increased

173 so induced translocation of a photoconverted PAR(2)-Kaede fusion protein from the Golgi to the plasma

174 Thus, virosomes plus PAR-2AP prevented morbidity as well as mortality.

175 s but not CD4(+) T cells from virosomes plus PAR-2AP-primed mice protected from lethal influenza viru

176 Virosome-plus-PAR-2AP prime boost also resulted in greater percentages

177 from influenza challenge after virosome-plus-PAR-2AP prime boost compared with either virosomes or PA

178 Virosome-plus-PAR-2AP prime boost resulted in greater percentages of T

179 mutual inhibition of anterior and posterior PAR proteins, provides a mechanism for spontaneous symme

180 rected cortical flows and a single posterior PAR-2 domain.

181 mes entirely usually establish two posterior PAR-2 domains, one at each pole.

182 PARP activity and simultaneously protecting PAR chains from degradation.

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

184 f three photosynthetically active radiation (PAR) levels were assessed in fed and unfed specimens of

185 ure and photosynthetically active radiation (PAR) on the synthesis and emission of isoprene, the most

186 ncoming photosynthetically active radiation (PAR) that better represents the response observed at hig

187 tern of photosynthetically active radiation (PAR).

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

189 Protein affinity reagents (PARs), frequently antibodies, are essential tools for ba

190 Agonism of protease-activated receptor (PAR) 1 by activated protein C (APC) provides neuro- and

191 Proteinase-activated receptor (PAR)-4 is a member of the proteolytically-activated PAR

192 (i) priming of protease-activated receptor (PAR)-mediated integrin alpha(IIb)beta(3) activation and

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

194 tivation of the protease activated receptor (PAR)2.

195 GPCR) known as protease-activated receptors (PAR).

196 Proteinase-activated receptors (PARs) are a four-member family of G-protein-coupled rece

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

198 diated through protease activated receptors (PARs).

199 y activating proteinase-activated receptors (PARs).

200 nd function as prosthetic antigen receptors (PARs) allowing selective targeting of tumor antigens whi

201 ods, and when a Paediatric Admission Record (PAR) was used (OR PAR used compared with PAR not present

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

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

204 ologous segment, the pseudoautosomal region (PAR), in which the formation of double-strand breaks (DS

205 target DSBs to the pseudoautosomal regions (PARs) of sex chromosomes.

206 rmally characterize pseudoautosomal regions (PARs) of X and Y chromosomes.

207 The cortical polarity regulators PAR-6, PKC-3, and PAR-3 are essential for the polarizati

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

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

210 b in perennial allergic rhinoconjunctivitis (PAR) and perennial allergic asthma (PAA) caused by indoo

211 main of SIRT1 interact with poly-ADP ribose (PAR) in response to DNA damage, and are responsible for

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

213 vate PARP1/2, which deposit poly-ADP-ribose (PAR) to recruit XRCC1-Ligase3 and other repair factors t

214 Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-Ch

215 s at DNA damage sites in a poly(ADP ribose) (PAR)-dependent manner.

216 alone, it associates with poly(ADP-ribose) (PAR) chains and is recruited to DNA damage sites in a PA

217 ding the complexity of the poly(ADP-ribose) (PAR) chains, low abundance of the modification and lack

218 bility to bind the ends of poly(ADP-ribose) (PAR) chains, the function of the histone variant macroH2

219 in human cancers, binds to poly(ADP-ribose) (PAR) immediately following DNA damage and mediates rapid

220 Poly(ADP-ribose) (PAR) is a nucleic acid-like protein modification that ca

221 Poly(ADP-ribose) (PAR) is rapidly synthesized from NAD(+) at sites of DNA

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

223 The synthesis of poly(ADP-ribose) (PAR) reconfigures the local chromatin environment and re

224 (snoRNAs) as activators of poly(ADP-ribose) (PAR) synthesis, demonstrating that this snoRNA-PAR partn

225 the addition of mono- and poly(ADP-ribose) (PAR)(1-5).

226 olymers, commonly known as poly(ADP-ribose) (PAR), modulate the activities of the modified substrates

227 ication by the addition of poly(ADP-ribose) (PAR), which promotes protein recruitment and localizatio

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

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

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

231 Dupilumab has a therapeutic effect on severe PAR in severe AD patients.

232 R) synthesis, demonstrating that this snoRNA-PAR partnership promotes cancer cell growth independent

233 s on autosome axes and loss of a specialized PAR-axis domain that is highly enriched for DSB-promotin

234 Downregulation of spinal PAR-2 and CGRP levels by EA attenuates the ileitis and r

235 active-cells and expression-levels of spinal PAR-2, CGRP and c-Fos in the EA group were greater (P <

236 firm whether EA attenuates VH through spinal PAR-2 activation and CGRP release, goats received an inj

237 ound here that trypsin, CS, and NE stimulate PAR(2)-dependent activation of protein kinase D (PKD) in

238 owing DNA-damaging treatments that stimulate PAR synthesis during DNA repair.

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

240 el with phosphorylation by PKC-3 to suppress PAR-1 activity in the anterior cytoplasm.

241 nforces proper polarization by synchronizing PAR network activation with cell cycle progression, ther

242 of PAR-1 protein is not essential, and that PAR-1 kinase activity is regulated spatially.

243 ell cycle progression, thereby ensuring that PAR proteins respond specifically to the correct cue.

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

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

246 Our findings indicate that PAR-2AP, a short peptide, may be a new and useful mucosa

247 ically interacts with PAR-6, we propose that PAR-6 promotes non-centrosomal microtubule organization

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

249 inducible protein degradation, we show that PAR-6 and PKC-3, but not PAR-3, are essential for postem

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

251 ells ensure that recombination occurs in the PAR is unknown.

252 ibit spermatocyte-like levels of DSBs in the PAR simply by delaying or preventing synapsis.

253 DSB-promoting factors hyperaccumulate in the PAR, its chromosome axes elongate and the sister chromat

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

255 cis- and trans-acting factors that make the PAR the hottest segment for DSB formation in the male mo

256 We find that, as in human MARK1, the PAR-1 KA1 domain is an auto-inhibitory domain that suppr

257 e we present a dynamic ultrastructure of the PAR and identify controlling cis- and trans-acting facto

258 pose that the repetitive DNA sequence of the PAR confers unique chromatin and higher-order structures

259 hus, the sexually dimorphic behaviour of the PAR is in part a result of kinetic differences between t

260 hich impose a delay in the activation of the PAR network so that it coincides with maturation of the

261 In C. elegans, the roles of the PAR proteins in embryonic development have been extensiv

262 exes in a race between the maturation of the PAR structure, formation of DSBs and completion of pairi

263 ntified FXa as potent, direct agonist of the PAR-1 (protease-activated receptor 1), leading to platel

264 breast tumour xenografts, inhibition of the PAR-complex-mediated SNAI1 degradation mechanism promote

265 ensional organoid cultures, we show that the PAR-atypical protein kinase C (aPKC) polarity complex in

266 KRD31 stabilizes REC114 association with the PAR and elsewhere.

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

268 These PAR-mediated condensates are linked to cancer, viral inf

269 The tissue factor-thrombin-PAR-1 signaling axis in tumor cells promotes PDAC growth

270 KPC-Par-1(KO) cells indicated that thrombin-PAR-1 signaling significantly altered immune regulation

271 indicate that one key mechanism of thrombin/PAR-1-mediated tumor growth is suppression of antitumor

272 as potent platelet agonist that acts through PAR-1.

273 Lgmn evokes pain-like behavior through PAR(2) Exposure of pain-sensing neurons to Lgmn decrease

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

275 ired to generate an action potential through PAR(2) Inhibitors of adenylyl cyclase and protein kinase

276 ophysical measurements of protein binding to PAR of a defined length, detection of PAR length from pr

277 ity to regulate transcription, is coupled to PAR polymerases (PARPs).

278 nt biofouling, and fragments were exposed to PAR levels of 105, 157, or 250 mumol quanta m(-2) s(-1)

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

280 t OAS1 adds AMP residues in 2',5' linkage to PAR, inhibiting its synthesis in vitro and reducing its

281 binates, exhibit apical calcium responses to PAR-2 stimulation.

282 otein targets, are potential alternatives to PARs.

283 oot ganglia neurons with CS, NE, or trypsin, PAR(2) responsiveness initially declined, consistent wit

284 (100%) and 95 of the 195 patients undergoing PAR (48.7%) received neoadjuvant chemotherapy.

285 analyzed 385 consecutive patients undergoing PAR (n = 195) or PAD (n = 190) of the encased artery for

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

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

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

289 Yet, how and when PAR proteins achieve this unpolarized, but responsive, s

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

291 tor Gbetagamma to the Golgi, coinciding with PAR(2) mobilization from the Golgi.

292 rd (PAR) was used (OR PAR used compared with PAR not present: 2.41, 95% CI: 1.98, 2.94, p < 0.001).

293 siveness initially declined, consistent with PAR(2) cleavage and desensitization, and then gradually

294 d R505C) abolish both FBXW7 interaction with PAR and recruitment to DNA damage sites, causing inhibit

295 As NOCA-1 physically interacts with PAR-6, we propose that PAR-6 promotes non-centrosomal mi

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

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

298 enefits of dupilumab for adult patients with PAR and/or PAA associated with msAD.

299 21 severe AD patients with PAR who started dupilumab were enrolled and we devided t

300 In Caenorhabditis elegans zygotes, PAR-1 localizes to the posterior cortex under the influe