ライフサイエンスコーパス: molt

1 d at many locations there were exuviae (cast molts).

2 that apl-1 is required for each transitional molt.

3 nization and replication during a subsequent molt.

4 his gene activity is required to transit the molt.

5 ds to shed their cuticle at the end of every molt.

6 ticks or survive through the larval-nymphal molt.

7 A was most abundant prior to the pupal-adult molt.

8 izing hypodermis coincident with each larval molt.

9 retraction is not completed before the adult molt.

10 ed a loss of br mRNA at the precocious adult molt.

11 val molting as they initiate a supernumerary molt.

12 to the first larval stage and were unable to molt.

13 commitment to form pupal cuticle at the next molt.

14 GL-intact hamsters exhibited seasonal pelage molt.

15 h level of ecdysone secretion that induces a molt.

16 quired for the second to third instar larval molt.

17 quitoes during the vulnerable stages of each molt.

18 e of ecdysone that initiates the metamorphic molt.

19 hange or the rate of the fall brown-to-white molt.

20 c mortality occurred during the larval-pupal molt.

21 ed their old exoskeleton at the end of every molt.

22 then remain constant in size until the next molt.

23 le components or hormones that occurs during molts.

24 of lin-42a in the epidermis peaks during the molts.

25 tart and completion, respectively, of larval molts.

26 , including mid-embryogenesis and the larval molts.

27 mRNA expression during the larval and pupal molts.

28 t retain their stickiness for months between molts.

29 ologs during the continuous growth and dauer molts.

30 ut is low or undetectable after the tick has molted.

31 hypoxia leads to growth and ecdysone-induced molting.

32 o the surrounding matrices and fluids during molting.

33 ynthesis, imaginal cell size, and control of molting.

34 enesis, early larval development, and larval molting.

35 egradative and biosynthetic process known as molting.

36 on hormone (EH), a neuropeptide regulator of molting.

37 ng the lethargus period that precedes larval molting.

38 g pads without affecting isometric growth or molting.

39 clear hormone receptors essential for larval molting.

40 terial found between the two cuticles during molting.

41 erized by defects in pharyngeal function and molting.

42 near the end of juvenile instars, and during molting.

43 r T-lineage leukemia cell lines, Jurkat, H9, Molt 3 and HUT 78.

44 Treatment of the leukemia lines Ha and Molt 3, with the methylation inhibitor, 5-aza-2'-deoxycy

45 MOLT-3 cells, synchronized by double-thymidine block, wh

46 ta 1-integrin substrates in the T-cell lines MOLT-3, Jurkat, and H9 and in the Daudi B-cell line.

47 h DRMs in 293T cells and in the T-cell line, MOLT 4.

48 en shown to infect established T cell lines (Molt-4 and Jurkat) and primary human naive CD4(+) T cell

49 p101 was overexpressed in human T-cell lines Molt-4 and Jurkat.

50 Two model human Ph(-) ALL cell lines (T-cell MOLT-4 and pre-B-cell Reh) were treated with LBH589 and

51 n human testicular cells and leukemic cells (MOLT-4 and TF-1a).

52 ononuclear cells and in the T-lymphoblastoid MOLT-4 cell line exposed to various cytokines, suggestin

53 d-type EWI-2 overexpression had no effect on MOLT-4 cell tethering and adhesion strengthening on the

54 hly specific as seen by the absence of other MOLT-4 cell-surface proteins.

55 Thus, the present work has tested on MOLT-4 cells (human T cell acute lymphoblastic leukemic)

56 n contrast, HLA-ABC and CD49e marked >95% of MOLT-4 cells but were not expressed on human spermatogon

57 Overexpression of EWI-2 in MOLT-4 cells caused reorganization of cell-surface CD81,

58 Induction of apoptosis in MOLT-4 cells did not require new protein synthesis and w

59 SB-HCV-infected Molt-4 cells expressed a significantly lower level of th

60 In addition, EFA selectively rescued MTAP+ MOLT-4 cells from L-alanosine toxicity at 25 microM with

61 fter Fas ligand stimulation, SB-HCV-infected Molt-4 cells had increased cleavage of caspase 8 and 3 a

62 Wild-type Molt-4 cells have moderate oxygen consumption rates, whi

63 rk shows that EERB induces cellular death in MOLT-4 cells in a dose-dependent way (0-10mg/mL) but not

64 cell extracts prepared from gamma-irradiated Molt-4 cells in the presence of okadaic acid.

65 This effect of dGal-1 on HL-60 and MOLT-4 cells is enhanced by pretreatment of the cells wi

66 AIF-1 polymerized nonmuscle actin and MOLT-4 cells overexpressing AIF-1 migrated 95% more rapi

67 d in conditioned media from AIF-1-transduced MOLT-4 cells proliferated 99% more rapidly than vascular

68 HL-60 and MOLT-4 cells treated with dGal-1 continue to grow normal

69 Flow cytometric analysis of MOLT-4 cells treated with EERB showed the presence of de

70 The binding of HCV E2 to MOLT-4 cells was not enhanced when it was preincubated w

71 To determine AIF-1 function, MOLT-4 cells were stably transduced by AIF-1 retrovirus.

72 Incubation of Jurkat and MOLT-4 cells with CTA056 resulted in the inhibition of t

73 h apoptosis, the dGal-1-treated HL-60 cells, MOLT-4 cells, and activated neutrophils do not undergo a

74 hecin-treated HL-60 cells, etoposide-treated MOLT-4 cells, and anti-Fas-treated neutrophils exhibit e

75 human promyelocytic HL-60 cells, T leukemic MOLT-4 cells, and fMet-Leu-Phe-activated, but not restin

76 SB-HCV was used to infect Molt-4 cells, and their cellular proliferation and CD44

77 cantly reduced in CFSE-high, SB-HCV-infected Molt-4 cells.

78 ial electron transport, relative to parental MOLT-4 cells.

79 20 with LPs did not enhance gp120 binding to MOLT-4 cells.

80 nditioned media from empty vector-transduced MOLT-4 cells.

81 n of phorbol 12-myristate 13-acetate-treated MOLT-4 cells.

82 ated the oxygen consumption rates only in WT Molt-4 cells.

83 is expressed by human spermatogonia but not MOLT-4 cells.

84 e compounds show a selective toxicity toward MOLT-4 compared to HeLa cells that correlate well with i

85 ced ROS production was diminished by >75% in MOLT-4 rho(0) cells, which lack mitochondrial electron t

86 tion is confirmed by reduced core binding on Molt-4 T cells treated with gC1qR-silencing small interf

87 partner, a 70-kDa protein, was isolated from MOLT-4 T leukemia cells, using anti-alpha4beta1 integrin

88 ogonia) and EpCAM-/HLA-ABC+/CD49e+ (putative MOLT-4) cell fractions.

89 both HCV E2 and LPs to CD4+ lymphoblastoid (MOLT-4) cells, foreskin fibroblasts, and hepatocytes.

90 ytotoxicity studies were performed in MCF-7, Molt-4, and rhabdomyosarcoma cell lines.

91 A multiparameter sort of MOLT-4-contaminated human testicular cell suspensions wa

92 have characterized an essential peroxidase, MoLT-7 (MLT-7), that is responsible for proper cuticle m

93 leton that occurs in insects at the end of a molt (a process called ecdysis) is typically followed by

94 microbiomes in newly engorged nymphs, newly-molted adults, and aged adults, as well as ticks exposed

95 Molting after the normal first instar period was restore

96 al alterations are maintained as the animals molt and mature.

97 ation whereas E75D has roles both during the molt and pupal commitment.

98 on worms arrest as larvae that are unable to molt and this phenotype is also seen with pan-1(RNAi) in

99 rdinated movement, adult sterility, abnormal molting and aberrant collagen deposition.

100 al ecdysteroid agonists for EcR that disrupt molting and can be used as safe pesticides.

101 In premolt, a preparation stage for upcoming molting and energy consumption, highly expressed genes w

102 n mutant background partially rescues larval molting and growth.

103 We studied the regulation of molting and metamorphosis in bed bugs with a goal to ide

104 Ecdysteroids initiate molting and metamorphosis in insects via a heterodimeric

105 e orthologs of NR genes that function during molting and metamorphosis in insects.

106 expression of genes known to be involved in molting and metamorphosis showed high levels of Kruppel

107 ing developmental transitions such as larval molting and metamorphosis through its active metabolite

108 (HaCHI) gene, critically required for insect molting and metamorphosis was selected as a potential ta

109 ing developmental transitions such as larval molting and metamorphosis.

110 ecdysone, a steroid hormone that stimulates molting and metamorphosis.

111 developmental events in arthropods including molting and metamorphosis.

112 n of insects from microbial infection during molting and metamorphosis.

113 s several developmental processes, including molting and morphogenesis, and results in larval lethali

114 T-7), that is responsible for proper cuticle molting and re-synthesis.

115 vity was capable of affecting O. volvulus L3 molting and that the presence of both activities in a si

116 This positive system that promotes molting and the negative control via the critical weight

117 ontrols growth, and at high levels it causes molting and tissue differentiation.

118 roteins, and a significant reduction in both molting and viability of third-stage larvae.

119 ock gene PERIOD (PER), results in arrhythmic molts and continuously abnormal epidermal stem cell dyna

120 ion of lin-42a leads to anachronistic larval molts and lethargy in adults.

121 changes in gene expression initiate periodic molts and metamorphosis during insect development.

122 n chromosome 10 (PTEN) (such as Jurkat, CEM, Molt) and, concomitantly, elevated PI-3,4,5-P(3) levels

123 variables and the sequence of blood feeding, molting, and aging.

124 ar receptor cofactor required for viability, molting, and numerous morphological events.

125 g acquired by ticks, persisting through tick molting, and reinfecting new mammalian hosts.

126 cally expressed nuclear hormone receptors in molting, and to analyze meiosis-specific roles for prote

127 Images of juveniles, discarded molts, and precopulatory behavior, as well as gravid fem

128 hophora + Tardigrada + Arthropoda) and other molting animals (Ecdysozoa), we analyzed the transcripto

129 oins nematodes with arthropods in a clade of molting animals, Ecdysozoa.

130 Molts are coordinated with successive transitions in the

131 sely timed betaFTZ-F1 expression late in the molt as steroids decline.

132 let-7 express genes characteristic of larval molting as they initiate a supernumerary molt.

133 ssed transiently during the larval and pupal molts as the ecdysteroid titer begins to decline and aga

134 It was known that juveniles molt at regular 8-10 hr intervals, but the anticipated p

135 We show that low oxygen tension induces molting at smaller body size, consistent with the hypoth

136 C. elegans molts at the end of each of its four larval stages but t

137 lting suggests that after summer had passed, molt began in the adults that had just bred; the timing

138 RNA genes mir-48 and mir-84 exhibit retarded molting behavior and retarded adult gene expression in t

139 calize with peptide hormones known to elicit molting behavior, suggesting the involvement of novel re

140 survival rate was observed, together with a molting block, These findings confirm the important regu

141 evelopment and is maintained at each nymphal molt but then disappears at the molt to the adult.

142 h weak alleles of pqn-47 complete the larval molts but fail to exit the molting cycle at the adult st

143 ity in the rate of the spring white-to-brown molt, but not in either the initiation dates of color ch

144 the tracheal system are set in size at each molt, but then remain constant in size until the next mo

145 In contrast, induction of a precocious adult molt by application of precocene II to third-stage nymph

146 v-SPI proteins play a vital role in nematode molting by controlling the activity of an endogenous ser

147 For example, Haemonchus contortus molts by digesting a ring of cuticle at the tip of the n

148 During larval molts, C. elegans undergoes a period of profound behavio

149 eurohormone bursicon, which, after the final molt, coordinates the plasticization and tanning of the

150 The molt culminates in ecdysis, an ordered sequence of behav

151 mplete the larval molts but fail to exit the molting cycle at the adult stage.

152 mir-84 and let-7 promote exit from the molting cycle by regulating targets in the heterochronic

153 We propose that the molting cycle of C. elegans involves the dynamic assembl

154 During each molting cycle of insect development, synthesis of new cu

155 The molting cycle of nematodes involves the periodic synthes

156 To complete each molting cycle, insects display a stereotyped sequence of

157 fic changes in Cas-PMCA abundance during the molting cycle, with peak expression occurring during pre

158 e distinct but interconnected aspects of the molting cycle.

159 abolism and physiological responses during a molting cycle.

160 . elegans development, in synchrony with the molting cycle.

161 that LIN-42A and affiliated factors regulate molting cycles in much the same way that PER-based oscil

162 C. elegans molting cycles involve rhythmic cellular and animal beha

163 fluctuate in a reiterated pattern during the molting cycles, reminiscent of the expression hierarchy

164 e molting program including the cessation of molting cycles.

165 The molting defect induced by Ce-imp-2 deficiency was mimick

166 t abnormalities, appeared independent of the molting defect.

167 s eliminated in larvae carrying mutations in molting defective (mld), a gene encoding a nuclear zinc

168 Comparison to molting-defective lrp-1(ku156) mutants revealed that the

169 ans, which emerged from a genetic screen for molting-defective mutants sensitized by low cholesterol.

170 n apl-1(yn5) background caused lethality and molting defects at all larval stages, suggesting that ap

171 n chitinase-dependent loss of chitin, severe molting defects, and lethality at all developmental stag

172 y others in screens for genes causing larval molting defects, is identified here as a novel P-granule

173 ll differentiation contributes to peb-1(cu9) molting defects.

174 ed mutant phenotypes such as burst vulva and molting defects.

175 rig mutants display defects in molting, delayed larval development, larval lethality, d

176 the adults that had just bred; the timing of molt derived from bone histology is also corroborated by

177 nge of body morphology defects, most notably molt, dumpy, and early larval stage arrest phenotypes th

178 attern; its levels oscillate relative to the molts during postembryonic development.

179 ct growth and metamorphosis is punctuated by molts, during which a new cuticle is produced.

180 Insect growth is punctuated by molts, during which the animal produces a new exoskeleto

181 tive action of chitinases and possibly other molting enzymes.

182 Nymphs reared in pairs molted fewer times than solitary nymphs and, thus, becam

183 The molting fluid enzyme chitinase, which degrades the matri

184 t to serve as a physical barrier, preventing molting fluid enzymes from accessing the new cuticle and

185 ection of the newly synthesized cuticle from molting fluid enzymes has long been attributed to the pr

186 In D. immitis, molting from the third to the fourth larval stage can be

187 As a consequence, excreta and molts from this marine mammal colony, and presumably oth

188 mulates ecdysteroid production by crustacean molting glands (Y-organs).

189 uth of their core sub-Antarctic breeding and molting grounds.

190 they use sea ice as a breeding, foraging and molting habitat.

191 We show that interinstar molting has the same size-related oxygen-dependent mecha

192 ates sterol homeostasis and is essential for molting hormone (20-hydroxyecdysone; 20E) biosynthesis.

193 s degrees by feeding the mutants the steroid molting hormone 20-hydroxyecdysone, or the precursors of

194 teps in the conversion of cholesterol to the molting hormone 20-hydroxyecdysone.

195 ophila polytene chromosomes initiated by the molting hormone 20-hydroxyecdysone.

196 ecdysteroids, herbal analogues of the insect molting hormone and their semisynthetic derivatives, wer

197 with a molt, triggered by release of steroid molting hormone ecdysone from the prothoracic gland (PG)

198 , growth ceases in response to a peak of the molting hormone ecdysone that coincides with a nutrition

199 The molting hormone ecdysone triggers chromatin changes via

200 TTH), which stimulates the production of the molting hormone ecdysone via an incompletely defined sig

201 Because the PGs produce the molting hormone ecdysone, we hypothesized that ecdysone

202 stage can be induced in vitro by the insect molting hormone, 20-hydroxyecdysone, suggesting that thi

203 functions as a receptor for the ecdysteroid molting hormones of insects.

204 racteristic concentration of the ecdysteroid molting hormones that regulate metamorphosis.

205 The prepupal peak of ecdysteroids (molting hormones) triggers the regression of APR dendrit

206 ing Pn.p cells die around the time of the L1 molt in a manner that often resembles the programmed cel

207 ation of the hypodermis and the cessation of molting in C. elegans.

208 olism and biological processes pertaining to molting in crustaceans.

209 ties have also been found to be critical for molting in O. volvulus L3 larvae.

210 ion level of chitinase 1 and caused abortive molting in the insects.

211 ity of reaching adulthood in fewer than four molts increased with birth weight: the heavier neonates

212 PIXR abrogation also impairs larval molting, indicative of its role in tick biology.

213 ae were fed on EMLA-infected mice, and after molting, infected nymphs were used to infest naive anima

214 hormone (CHH) neuropeptide family including molt-inhibiting hormone (MIH) and CHH.

215 At the end of each molt, insects shed their old cuticle by performing the e

216 Molting is a critical developmental process for crustace

217 Crustacean molting is known to be regulated largely by ecdysteroids

218 Molting is required for progression between larval stage

219 n regulating the timing and nature of insect molts is well-established.

220 leaves the timing of first and second instar molts largely unchanged, but triples duration of the thi

221 o Ov-spi transcripts are up-regulated in the molting larvae and adult stages of the development of th

222 exta increase up to ten-fold in mass between molts, leading to increased oxygen need without a concom

223 y avoidance of octanol and quiescence during molting lethargus.

224 as arousal thresholds and quiescence during molting lethargus.

225 DA1877 affects cyclic gene expression during molting, likely through the nuclear hormone receptor NHR

226 During molt, males show little or no aggression and no reproduc

227 jor aspects of insect development, including molting, metamorphosis, and reproduction.

228 n suggests that the function of CPZ-1 during molting might be conserved in other nematodes.

229 The phenology of the annual cycles of molt, migration, and breeding for these Argentine-breedi

230 Neither the timing of the metamorphic molt nor the duration of larval growth was affected by t

231 he presence of A. phagocytophilum as freshly molted nymphs.

232 osantel was found also to completely inhibit molting of O. volvulus infective L3 stage larvae.

233 vae also show defects in tracheal growth and molting of their tracheal cuticle.

234 with keratin in 'pristine' sheds, or natural molts of the adhesive toe pad and non-adhesive regions o

235 T5, was found to be required for pupal-adult molting only.

236 crust expression with gender, social status, molting or feeding, dominant animals show significantly

237 singly, PTTH production is not essential for molting or metamorphosis.

238 In both sexes, lep-2 mutants fail to cease molting or produce an adult cuticle.

239 The monophyly of Ecdysozoa, molting organisms, was not supported by any of the analy

240 mutant suggests that cpz-1 has a role in the molting pathways.

241 MeHg concentrations in seawater, and HgT in molted pelage of M. angustirostris, at the Ano Nuevo Sta

242 (Mirounga angustirostris), whose excreta and molted pelage, in turn, constitute a source of environme

243 s in diet, time elapsed between the previous molt period and sampling, sample size, and/or external c

244 Alaska (1998-2010), sampled during breeding/molting periods.

245 ction acting on wide individual variation in molt phenology might enable evolutionary adaptation to c

246 es, we found strong selection on coat colour molt phenology, such that animals mismatched with the co

247 p-2 leads to embryonic death and an abnormal molting phenotype in Caenorhabditis elegans.

248 We have identified a regulator of molting, pqn-47.

249 tor, were maintained in ticks throughout the molting process (larvae to nymphs), were tick transmitte

250 ecdysone and/or ponasterone A initiates the molting process through binding to its conserved heterod

251 chitinase family genes, primarily during the molting process, and provide a biological rationale for

252 gest that pqn-47 executes key aspects of the molting program including the cessation of molting cycle

253 Mmp1 also degrades old cuticle at molts, promotes apical membrane expansion in larval trac

254 pation but was dispensable for larval-larval molting, pupation, and adult eclosion.

255 ytic domains, prevented embryo hatch, larval molting, pupation, and adult metamorphosis, indicating a

256 er attain the critical weight but eventually molt regardless.

257 r understand the role of ecdysteroids in the molt regulation, the full-length cDNAs of the blue crab,

258 Na(+)K(+)/ATPases, and strong inhibitions of molt-related proteins such as chitinase and JHE-carboxyl

259 high as 9.5 pM during the M. angustirostris molting season.

260 anugo pups, Hg concentrates in the hair, and molting serves as a main detoxification route.

261 e a developmental arrest at the first larval molt, showing that this gene activity is required to tra

262 or: camouflage mismatch in seasonally colour molting species confronting decreasing snow cover durati

263 will be critical for hares and other colour molting species to keep up with climate change.

264 ed in both Y-organs and eyestalks at various molt stages.

265 ified differentially expressed genes at four molting stages of Chinese mitten crab (Eriocheir sinensi

266 erentially expressed genes amongst different molting stages, provide novel insights into the function

267 mice, and (iii) able to persist through tick molting stages.

268 s differentially expressed amongst different molting stages.

269 ly control the production and release of the molting steroid ecdysone.

270 Our results demonstrate that the molting steroid hormone ecdysone in adult Drosophila is

271 scued larvae arrest at the subsequent larval molt, suggesting that amon is also required for the seco

272 ring breeding and non-breeding compared with molt, suggesting that the VMH may play a role in the est

273 Histological evidence of molting suggests that after summer had passed, molt bega

274 originally discovered and characterized as a molt termination signal in insects through its regulatio

275 At each molt the cuticle fails to open sufficiently at the anter

276 At the molt, the tracheal system is shed and replaced with a ne

277 At the adult molt, these postecdysial processes include expansion and

278 -1, was identified through the analysis of a molting third-stage larvae expressed sequence tag datase

279 e basal layer of the cuticle of third-stage, molting third-stage, and fourth-stage larvae, the body c

280 us, while loss of PAN-1 in the soma inhibits molting, this report demonstrates that PAN-1 is also a P

281 metamorphosis suggests that larvae possess a molt timer that establishes a minimal time to metamorpho

282 At the final molt to adulthood, this synchronization mechanism is jet

283 ganisms persisted in these ticks through the molt to nymphs.

284 All arthropods periodically molt to replace their exoskeleton (cuticle).

285 each nymphal molt but then disappears at the molt to the adult.

286 ponsive to this action of insulin during the molt to the fifth instar together with the ability to be

287 on these mice, where it persists through the molt to the nymph stage.

288 trains was capable of persisting through the molt to the nymphal stage as analyzed by culture.

289 lus microplus ticks could acquire and, after molting to the adult stage, transmit B. equi to naive ho

290 PCR positive, after feeding on the sheep and molting to the next instar, increased marginally with in

291 each of the three larval instars ends with a molt, triggered by release of steroid molting hormone ec

292 This mechanism enables exoskeletal molting, tube expansion, and epithelial integrity.

293 its biological activities on O. volvulus L3 molting was investigated.

294 Consistent with a function in molting, we found that PEB-1 was detectable in all hypod

295 gland cells have prominent functions during molting, we suggest defective gland cell differentiation

296 cted larvae underwent numerous supernumerary molts, which could be terminated with injection of eithe

297 functions of LIN-42 may coordinate periodic molts with successive development of the epidermis.

298 ruitment, inhibits reproduction, and induces molting, with no change in plasma prolactin levels.

299 ydroxyecdysone (20E) during larval and pupal molts, with E75A also increasing at pupal commitment.

300 uctor-A causes severe defects during cuticle molting, wound protection, tube expansion and larval gro