ライフサイエンスコーパス: PCD

1 PCD can be a means to maintain homeostasis, prevent or p

2 PCD can result in the export of fitness from the cell to

3 PCD diagnostic quality was higher than EID diagnostic qu

4 PCD images were also used to calculate iodine concentrat

5 PCD is characterized by clinical variability and extensi

6 PCD provides spectral information, which may be used for

7 PCD-causing mutations have been identified in 20 genes,

8 Furthermore, we found that 24 PCD stage-specific miRNAs are aberrantly overexpressed i

9 ge analysis was performed in a family with a PCD subject.

10 d in ETI are well studied, how they activate PCD and confer disease resistance remains elusive.

11 GmNAC30 cooperates with GmNAC81 to activate PCD through the induction of the cell death executioner

12 sensitive test of airway disease in advanced PCD.

13 ey account for only approximately 65% of all PCDs.

14 dynamic hot spot." Kinetic regulation allows PCD to adopt two distinct functions.

15 Although PCD is common throughout the nervous system, its influen

16 nd biochemical methods to detect and analyze PCD processes in vivo and in planta.

17 the molecular participants in apoptotic and PCD cascades, successful identification of early master

18 of large and small airway disease in CF and PCD.

19 t its variants cause ciliary dysmotility and PCD with laterality defects.

20 Dose-reduced spiral unenhanced lung EID and PCD CT examinations were performed in 30 asymptomatic vo

21 -enhanced spiral and axial abdominal EID and PCD scans were acquired.

22 ents in the context of SI-induced events and PCD.

23 e leaves (in which perforation formation and PCD are occurring) as compared to all other leaf develop

24 different between HL and NHL; whereas LE and PCD occur almost exclusively in patients with HL, sensor

25 ember, resulted in a frameshift mutation and PCD.

26 esent the native 3D structures of normal and PCD-causing RSPH1-mutant human respiratory cilia in unpr

27 the group level via re-usable resources and PCD may also provide a mechanism for how groups beget ne

28 gative regulators of jasmonate signaling and PCD.

29 One difference between plant and animal PCD is the absence of phagocytosis in plants.

30 While the molecular control of some animal PCD forms such as apoptosis is known in great detail, we

31 biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogen

32 d significantly during senescence-associated PCD.

33 negatively regulates ETI and the associated PCD through a physical interaction with cyclin-dependent

34 Autophagy, PCD and DNA damage related proteins were also identified

35 ts were not differentially expressed between PCD and NPCD cells.

36 nses, and the mechanistic interfaces between PCD, cell stress and virus infection pathways.

37 a versatile caspase inhibitor, p35, blocked PCD of bursCCAP neurons, suggesting caspase-dependent ap

38 nd to be S-nitrosylated at the onset of both PCDs.

39 uals from two unrelated families affected by PCD.

40 re at first intervention, sepsis reversal by PCD within a week, number of organs failed, organ failur

41 Canonical PCDs play an important role in amino acid hydroxylation,

42 three-dimensional fold similar to canonical PCDs, although the prominent active site cleft present i

43 he crystal structure of an alpha-carboxysome PCD-like protein from the chemoautotrophic bacterium Thi

44 nzymes is disrupted in the alpha-carboxysome PCD-like protein.

45 Multiple causative PCD mutations account for only 65% of cases, suggesting

46 ts demonstrate that mutations in SPAG1 cause PCD with ciliary ODA+IDA defects and that exome sequenci

47 To identify mutations that cause PCD, we performed exome sequencing on six unrelated prob

48 ify mutations in additional genes that cause PCD, we performed exome sequencing on three unrelated pr

49 s in two genes (DNAI2, DNAH5) known to cause PCD, including an Ashkenazi Jewish founder mutation in D

50 ls with SPAG1 mutations had a characteristic PCD phenotype, including 8 with situs abnormalities.

51 As a coactivator, PCD is known as DCoH or dimerization cofactor of the tra

52 We conclude that this conserved PCD-like protein, renamed here alpha-carboxysome RuBisCO

53 Thus, whether conserved PCD regulatory mechanisms include plant apoptosis remain

54 tors negatively regulate ethylene-controlled PCD in the lace plant.

55 Mammalian core PCD genes, such as caspases, are not present in plant ge

56 Programmed cell death (PCD) and associated pathway genes, which are triggered b

57 hown how instrumental programmed cell death (PCD) can be in innate and adaptive immune responses.

58 ing limb development, programmed cell death (PCD) contributes to separation of the digits.

59 Programmed cell death (PCD) functions in a variety of processes including growt

60 atured high levels of programmed cell death (PCD) in a concentration-dependent manner as measured by

61 Programmed cell death (PCD) in multicellular organisms is a vital process in gr

62 ed immunity (ETI) and programmed cell death (PCD) in plants, is a novel transmembrane nucleoporin.

63 i (AAL) toxin induces programmed cell death (PCD) in susceptible tomato (Solanum lycopersicum) leaves

64 ed the involvement of programmed cell death (PCD) in the process.

65 Programmed cell death (PCD) induced by endoplasmic reticulum (ER) stress is imp

66 Programmed cell death (PCD) is a crucial process both for plant development and

67 Programmed cell death (PCD) is a crucial process for plant innate immunity and

68 Programmed cell death (PCD) is an important mechanism for destroying cells in a

69 Programmed cell death (PCD) is central to organism development and for a long t

70 Programmed cell death (PCD) is critical for development and responses to enviro

71 Programmed cell death (PCD) is essential for several aspects of plant life, inc

72 Programmed cell death (PCD) is essential for several aspects of plant life, inc

73 Programmed cell death (PCD) is usually considered a cell-autonomous suicide pro

74 Programmed cell death (PCD) occurs in several forms including apoptosis and nec

75 to trigger selective programmed cell death (PCD) of at least lung, breast, and colorectal cancer cel

76 ty, is able to induce programmed cell death (PCD) of CD38(+) multiple myeloma tumor cell lines when c

77 ns is associated with programmed cell death (PCD) of the infected cell.

78 on can lead to either programmed cell death (PCD) or acclimation.

79 s is a RIP1-dependent programmed cell death (PCD) pathway that is distinct from apoptosis.

80 well appreciated that programmed cell death (PCD) plays critical roles in the life cycle of diverse b

81 In mammalian cells, programmed cell death (PCD) plays important roles in development, in the remova

82 A plethora of diverse programmed cell death (PCD) processes has been described in living organisms.

83 everal indicators for programmed cell death (PCD) that are often observed in phytoplankton in respons

84 to triggers localized programmed cell death (PCD) upon recognition of Pseudomonas syringae effectors

85 xanthus cells undergo programmed cell death (PCD) whereby 80% of vegetative cells die.

86 ssing neurons undergo programmed cell death (PCD) within 24 hours after adult eclosion.

87 nity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pa

88 , we show that during programmed cell death (PCD), induced by both heat shock (HS) or hydrogen peroxi

89 lopmentally regulated programmed cell death (PCD).

90 e 7% of RBCs undergo programmed cell death (PCD).

91 al and hypersensitive programmed cell death (PCD).

92 ysEP) associated with programmed cell death (PCD).

93 often associated with programmed cell death (PCD).

94 progenitors or their programmed cell death (PCD).

95 ling pathway known as programmed cell death (PCD).

96 stress, UPR promotes programmed cell death (PCD).

97 for paraneoplastic cerebellar degeneration (PCD) in HL and dermato/ polymyositis in both HL and NHL,

98 to pterin-4alpha-carbinolamine dehydratase (PCD) enzymes.

99 Pterin-4a-carbinolamine dehydratase (PCD) is a highly conserved enzyme that evolved a second,

100 H)/pterin-4alpha-carbinolamine dehydratases (PCD)-like protein is the causative mutation in a seedlin

101 leaves due to salicylic acid (SA)-dependent PCD, revealing roles for myoinositol or inositol derivat

102 leaves due to salicylic acid (SA)-dependent PCD.

103 by the lack of reliable reporters to detect PCD processes.

104 nvestigate whether photon-counting detector (PCD) technology can improve dose-reduced chest computed

105 Developmental PCD in the Drosophila ovary is an intriguing example of

106 ic promoter-reporter lines for developmental PCD in Arabidopsis.

107 t the large-scale nonapoptotic developmental PCD in the Drosophila ovary occurs by an alternative cel

108 ed a robust down-regulation of developmental PCD genes and an up-regulation of the genes involved in

109 Moreover, different cases of developmental PCD share a set of cell death-associated genes.

110 ry conserved core machinery of developmental PCD.

111 Why did PCD evolve?

112 ound in cells subjected to the two different PCD-inducing stimuli: low in H2O2-treated cells and high

113 ng human normal plasma cell differentiation (PCD).

114 up approach, percutaneous catheter drainage (PCD) with saline irrigation is reported to be effective.

115 ype of childhood primary ciliary dyskinesia (PCD) and ultrastructural defects and genotype is poorly

116 to diagnosis of primary ciliary dyskinesia (PCD) in the United Kingdom consists of assessing ciliary

117 Primary ciliary dyskinesia (PCD) is a genetically heterogeneous recessive disorder o

118 Primary ciliary dyskinesia (PCD) is a genetically heterogeneous, autosomal-recessive

119 Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently cause

120 Primary ciliary dyskinesia (PCD) is an inherited chronic respiratory obstructive dis

121 Primary ciliary dyskinesia (PCD) is caused when defects of motile cilia lead to chro

122 Primary ciliary dyskinesia (PCD) is characterized by dysfunction of respiratory cili

123 common cause of primary ciliary dyskinesia (PCD), a congenital disorder of ciliary beating, characte

124 otype resembling primary ciliary dyskinesia (PCD), a disorder characterized by chronic airway disease

125 been linked with primary ciliary dyskinesia (PCD), a disorder characterized by ciliary dysmotility; y

126 e major cause of primary ciliary dyskinesia (PCD), an inherited disorder of ciliary and flagellar dys

127 m flagella cause primary ciliary dyskinesia (PCD), characterized by chronic airway disease, infertili

128 tile cilia cause primary ciliary dyskinesia (PCD), characterized by recurrent respiratory infections

129 diatric syndrome primary ciliary dyskinesia (PCD).

130 diseases such as primary ciliary dyskinesia (PCD).

131 lung disease in primary ciliary dyskinesia (PCD).

132 iopathy known as primary ciliary dyskinesia (PCD).

133 heir silencing inhibited Pto/AvrPto-elicited PCD.

134 deletion of the mazF gene does not eliminate PCD in wild-type strain DK1622 as originally seen in DZF

135 Enhanced PCD due to hyperglycemia was specific to necroptosis as

136 ential regulatory mechanism specific for ETI/PCD induction.

137 ditional bacteria, and found no evidence for PCD enzymatic activity.

138 Image noise was significantly lower for PCD images in all BMI groups (P < .001 for groups 1 and

139 x and the limitations of certain methods for PCD diagnosis.

140 tically active chloroplasts are required for PCD to occur in mips1, but this process is independent o

141 amiana Cbl10 and Cipk6 are also required for PCD triggered by other plant resistance genes and virus,

142 nce is a highly specific diagnostic test for PCD, and it improves the speed and availability of diagn

143 labeled antibodies as a diagnostic tool for PCD.

144 er onset of daily wet cough than typical for PCD, and better lung function (FEV1), compared with 75 a

145 ion and evolutionary dynamics resulting from PCD and public goods production may be a key to the succ

146 Furthermore, PCD is a means for solving a central problem of group li

147 Homozygous mice have PCD characterized by hydrocephalus, male infertility, an

148 omatography-post column derivatisation (HPLC-PCD) system detected a dense collection of high antioxid

149 rt the association between ZMYND10 and human PCD, given that zmynd10 knockdown in zebrafish caused ci

150 cylic acid (SA) signaling and hypersensitive PCD, BiP overexpression further induced NRP-mediated cel

151 tion of the genes involved in hypersensitive PCD triggered by nonhost-pathogen interactions.

152 data indicate that during the hypersensitive PCD, BiP positively regulates the NRP cell death signali

153 The identified PCD genes account for about half of PCD incidences and t

154 In plant innate immunity, PCD is believed to prevent the spread of pathogens from

155 other phytohormone pathways and/or important PCD components.

156 y demonstrate early onset of lung disease in PCD, with abnormal air flow mechanics by age 6-8 years t

157 toxic compounds that have been implicated in PCD, also depended on interdigital vascular patterning.

158 gene encoding DRC1, CCDC164, are involved in PCD pathogenesis.

159 is still unclear whether they participate in PCD onset, execution, or both.

160 h the prominent active site cleft present in PCD enzymes is disrupted in the alpha-carboxysome PCD-li

161 tion of low nasal nitric oxide production in PCD and (2) discovery of biallelic mutations in multiple

162 epidermal growth factor-related receptor) in PCD and mGluR5 in limbic encephalitis (LE).

163 a unique genotype-phenotype relationship in PCD, and suggests that mutations in RSPH1 may be associa

164 Consistent with a role in PCD, GmNAC81 and GmNAC30 bind in vivo to and transactiva

165 ntuitive positive role of the vasculature in PCD.

166 her of the two ZmHbs is sufficient to induce PCD through a pathway initiated by elevated NO and Zn(2+

167 g root apical meristems from hypoxia-induced PCD through mechanisms initiated by nitric oxide and med

168 hat OXI1 is a new regulator of (1)O2-induced PCD, likely acting upstream of jasmonate.

169 During SI-induced PCD, we previously observed a major acidification of the

170 integral and essential event for SI-induced PCD.

171 of cathepsin B and PBA1 in ER-stress-induced PCD (ERSID).

172 Jasmonate (JA) promotes AAL toxin induced PCD in a COI1 (coronatine insensitive 1, JA receptor)-de

173 endent JA pathway enhances AAL toxin induced PCD through regulating the redox status of the leaves, o

174 NO increased in both experimentally induced PCDs, although with different intensities.

175 ammaR-mediated cross-linking of DARA induces PCD of CD38-expressing multiple myeloma tumor cells, whi

176 Suppression of ZmHb2 induces PCD in the anchoring cells, allowing the embryos to deve

177 tion in interdigital vessel number inhibited PCD, resulting in syndactyly, whereas an increment in ve

178 tion in both ROS production and interdigital PCD.

179 asculature positively regulates interdigital PCD.

180 limb development in regulating interdigital PCD by ROS production.

181 core of more than 7.5 at first intervention (PCD) had the ability to predict surgery with a sensitivi

182 PCD, APACHE II score at first intervention (PCD), and organ failure within a week of the onset of di

183 the miRNA-30b/c/d-mediated regulation of key PCD factors (IRF4, PRDM1, ELL2 and ARID3A).

184 ational analyses have identified several key PCD components, and we recently identified the mips1 mut

185 reas suppression of ZmHb1 results in massive PCD, leading to abortion.

186 FEV1), compared with 75 age- and sex-matched PCD cases (73.0 vs. 61.8, FEV1 % predicted; P = 0.043).

187 FcgammaRs induce DARA cross-linking-mediated PCD.

188 discovery of biallelic mutations in multiple PCD-causing genes.

189 guing example of nonapoptotic, nonautonomous PCD, providing insight on the diversity of cell death me

190 dynamic expression modulation during normal PCD.

191 al changes in their expression during normal PCD.

192 gulating networks of significance for normal PCD and malignant plasma cell biology.

193 CP loss is seen in up to 28% of PCD cases, in whom laterality determination specified by

194 at local glucose levels alter the balance of PCD pathways, and that clinically relevant outcomes may

195 The molecular basis of PCD regulation in the lace plant is unknown, however eth

196 The genetic causes of PCD are still evolving, while the diagnosis is often dep

197 Thus, the party in control of PCD has a distinct advantage in these battles.

198 Here, we examine the ecological effects of PCD in different microbial scenarios and conclude that P

199 The curative efficacy of PCD alone was in 27 patients (48%).

200 also provided insight into the evolution of PCD in unicellular photoautotrophs, the impact of PCD on

201 ution resulted in elevation and expansion of PCD.

202 a subject with typical clinical features of PCD.

203 ls with RSPH1 mutations had some features of PCD; however, nasal nitric oxide levels were higher than

204 n up new avenues of research in the field of PCD and developmental tissue remodeling.

205 H1D3 are responsible for an X-linked form of PCD causing disruption of early axonemal dynein assembly

206 In animals and plants, different forms of PCD play crucial roles in development, immunity, and res

207 entified PCD genes account for about half of PCD incidences and the underlying mechanisms remain poor

208 cum), as monitored by measuring hallmarks of PCD in plants.

209 n unicellular photoautotrophs, the impact of PCD on the fate of natural phytoplankton assemblages and

210 one is compelled to consider the impacts of PCD beyond the cell, for death obviously lowers the fitn

211 The estimated incidence of PCD is approximately 1 per 15,000 births, but the preval

212 e are relatively few documented instances of PCD in bacteria.

213 By using zebrafish morpholino knockdown of PCD candidate genes as an in vivo screening platform, we

214 h should improve diagnosis and management of PCD.

215 e homologs of caspases, the key mediators of PCD in animals.

216 Using a fly model of PCD, we conclude that ZMYND10 is a cytoplasmic protein r

217 es the gene-trapped allele as a new model of PCD.

218 ither as a negative or positive modulator of PCD events.

219 Interestingly, prior to the onset of PCD, the autopod vasculature undergoes extensive pattern

220 The performance of PCD showed no statistically significant difference compa

221 y 1 per 15,000 births, but the prevalence of PCD is difficult to determine, primarily because of limi

222 nterdigital areas, as the genetic program of PCD provides the first layer and vascular patterning ser

223 or inositol derivatives in the regulation of PCD.

224 Here, we identified a suppressor of PCD by screening for mutations that abolish the mips1 ce

225 The treatment of PCD is not standardized, and there are no validated PCD-

226 Our understanding of PCD regulation in plants has advanced significantly over

227 Reversal of sepsis within a week of PCD, APACHE II score at first intervention (PCD), and or

228 omatic embryogenesis through their effect on PCD.

229 es may depend on glucose-mediated effects on PCD.

230 xyl-propylene carbonate-graft-dodecanol; PEG-PCD) to prepare micelles.

231 wer Ni concentrations than our physiological PCD assay and that the results are predictive of physiol

232 To study tonoplast rupture, a plant PCD feature, both confocal and electronic microscopies w

233 ommonly regulated genes during diverse plant PCD processes in Arabidopsis (Arabidopsis thaliana).

234 oplasts may play a central role during plant PCD as for mitochondria in animal cells, but it is still

235 pressed in plants, successfully impact plant PCD.

236 Here, we identified a regulator of plant PCD by screening for mutants that display transcriptomic

237 the regulation of the diverse types of plant PCD.

238 uch regulators can trigger or suppress plant PCD.

239 In plants, PCD occurs during development as well as in response to

240 Here we describe a potential PCD pathway in Pseudomonas aeruginosa that enhances the

241 une responses and avoid detection to prevent PCD and allow infection.

242 n Initial human experience with dose-reduced PCD chest CT demonstrated lower image noise compared wit

243 ose a double safety mechanism that restricts PCD to interdigital areas, as the genetic program of PCD

244 es, suggest a mechanism for the milder RSPH1 PCD phenotype and demonstrate that cryo-electron tomogra

245 ring several key hallmark features of the SI PCD signaling pathway, notably activation of a DEVDase/c

246 fore we hypothesized that PTI might suppress PCD.

247 ception with 1-methylcyclopropene suppressed PCD, increased BAX inhibitor-1, an effective attenuator

248 ferent microbial scenarios and conclude that PCD can increase biological complexity.

249 We present evidence that PCD operates alongside differentiation to regulate cereb

250 Here we report that PCD triggered by the mycotoxin fumonisin B1 (FB1) can be

251 Recent research has revealed that PCD is complex, with at least a dozen cell death modalit

252 The PCD Foundation is developing a network of clinical cente

253 netic and transgenic analyses to dissect the PCD mechanisms of bursCCAP neurons.

254 CCDC65, was absent in airway cells from the PCD subject and CCDC65-silenced cells.

255 in the spinal canal, which was lower in the PCD than the EID images because of beam hardening (20 HU

256 proteins formed upon exposure to both of the PCD-inducing stimuli.

257 vered that heterologous co-expression of the PCD-like protein from Halothiobacillus neapolitanus with

258 but they are not sufficient to carry out the PCD fully.

259 l-based complementation assay, we tested the PCD-like proteins from T. intermedia and two additional

260 SPT activity and sensitivity to the PCD-inducing mycotoxin fumonisin B1 (FB1) were increased

261 mutant strain putatively indicates that the PCDs are a result of genomic DNA damage.

262 These PCD indicators represent a powerful resource that can be

263 higher transcript levels in NPCD compared to PCD cells.

264 he range of ciliary defects that can lead to PCD.

265 as part of the signaling pathway leading to PCD is discussed.

266 Plant effector-triggered PCD also shares with mammalian apoptosis the involvement

267 This effector-triggered PCD is partly analogous to pyroptosis, an inflammatory h

268 SI in field poppy (Papaver rhoeas) triggers PCD in incompatible pollen.

269 candidate genes in 70 genetically undefined PCD patients.

270 els were also determined in cells undergoing PCD and cells not undergoing PCD (NPCD cells).

271 as it does not benefit the cells undergoing PCD.

272 ells undergoing PCD and cells not undergoing PCD (NPCD cells).

273 vegetative and generative tissues undergoing PCD.

274 eived medical management and later underwent PCD and surgery as per the indication.

275 Thus, host and pathogen each may use PCD as a survival-promoting strategy.

276 In particular, plants and animals utilize PCD to control pathogen invasion and infected cell popul

277 not standardized, and there are no validated PCD-specific therapies.

278 nscript levels in mature stage leaves, where PCD is not occurring.

279 y lysis or other means can be harmful, while PCD can evolve by providing advantages to relatives.

280 es from the data reviewed here is that while PCD carries an obvious cost to the cell, it can be a dri

281 h PCD and normal staining in all 252 in whom PCD was considered highly unlikely.

282 n 413 unrelated probands, including 325 with PCD and 88 with idiopathic bronchiectasis, revealed bial

283 Sepsis reversal was achieved with PCD alone in 62.5%.

284 h plant hormone signaling is associated with PCD and PTI, both FB1-triggered cell death and suppressi

285 Here we report a novel gene associated with PCD but without ciliary ultrastructural abnormalities ev

286 se activity, which have been associated with PCD in other phytoplankton species.

287 members of critical pathways associated with PCD.

288 scovery cohort of 35 patients diagnosed with PCD by ciliary ultrastructure, and a diagnostic accuracy

289 of enhanced kidney tissue was improved with PCD iodine mapping compared with EID (5.2 +/- 1.3 vs 4.0

290 Analysis of 295 individuals with PCD identified recessive truncating mutations of C21orf5

291 In the remaining 5 individuals with PCD who underwent exome sequencing, we identified mutati

292 sequencing of 67 additional individuals with PCD with ODA defects from 58 families revealed CCDC114 m

293 tion DYX1C1 mutations in 12 individuals with PCD.

294 participants younger than 19 years old with PCD were evaluated prospectively at six centers in North

295 ccessfully identified 22 of 25 patients with PCD and normal staining in all 252 in whom PCD was consi

296 ore accurate identification of patients with PCD has also allowed definition of a strong clinical phe

297 ide levels were higher than in patients with PCD with other gene mutations (98.3 vs. 20.7 nl/min; P <

298 of 127 patients with CF and 33 patients with PCD, all of whom had spirometry and LCI, of which a subs

299 c cause is not defined for all patients with PCD.

300 kinocilia, and establish a useful zebrafish PCD model.