ライフサイエンスコーパス: molt

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

2 elopmental parameters (survival, weight, and molting).

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

4 then remain constant in size until the next molt.

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

6 nization and replication during a subsequent molt.

7 his gene activity is required to transit the molt.

8 ticks or survive through the larval-nymphal molt.

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

10 izing hypodermis coincident with each larval molt.

11 teroid peak into the different phases of the molt.

12 retraction is not completed before the adult molt.

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

14 val molting as they initiate a supernumerary molt.

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

16 commitment to form pupal cuticle at the next molt.

17 quitoes during the vulnerable stages of each molt.

18 GL-intact hamsters exhibited seasonal pelage molt.

19 c mortality occurred during the larval-pupal molt.

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

21 h level of ecdysone secretion that induces a molt.

22 e of ecdysone that initiates the metamorphic molt.

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

24 le components or hormones that occurs during molts.

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

26 tart and completion, respectively, of larval molts.

27 , including mid-embryogenesis and the larval molts.

28 mRNA expression during the larval and pupal molts.

29 t retain their stickiness for months between molts.

30 ologs during the continuous growth and dauer molts.

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

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 ir outermost structures during growth and/or molting.

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

38 ng the lethargus period that precedes larval molting.

39 g pads without affecting isometric growth or molting.

40 mately 97% of larval survival and successful molting.

41 clear hormone receptors essential for larval molting.

42 terial found between the two cuticles during molting.

43 erized by defects in pharyngeal function and molting.

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

45 hypoxia leads to growth and ecdysone-induced molting.

46 e specification, animal size regulation, and molting.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 20 with LPs did not enhance gp120 binding to MOLT-4 cells.

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

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

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

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

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

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

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

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

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

84 y phase of the AcMNPV infection cycle, newly molted 5th-instar T. ni larvae were orally infected with

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

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

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

88 Molting after the normal first instar period was restore

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

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

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

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

93 Normally, ecdysone positively regulates both molting and antimicrobial peptide production, so the ina

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

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

96 n mutant background partially rescues larval molting and growth.

97 inates growth and maturation, represented by molting and metamorphosis [2].

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

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

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

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

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

103 ing developmental transitions such as larval molting and metamorphosis.

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

105 developmental events in arthropods including molting and metamorphosis.

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

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

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

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

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

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

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

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

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

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

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

117 ation results in a failure of host larvae to molt, and probably a reduced antimicrobial response.

118 that supports approximately 97% survival and molting, and a 150% increase in larval weight after 10 d

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

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

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

122 on of three life history parameters (weight, molting, and survival).

123 the epidermal epithelium for animal growth, molting, and the proper pattern of seam-cell divisions.

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

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

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

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

128 be monophyletic and placed within a clade of molting animals, the ecdysozoans, with nematodes and six

129 Molts are coordinated with successive transitions in the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Here, we block the molt by genetically dampening ecdysone production, creat

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 filling of the diverticula is linked to the molting cycle and possibly involved therein.

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

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

154 of JHSB3 were studied during the 10-day long molting cycle of 4(th) instar nymph, between a blood mea

155 es of the JH biosynthetic pathway during the molting cycle of 4(th) instar.

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

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

158 The molting cycle of nematodes involves the periodic synthes

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

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

161 e distinct but interconnected aspects of the molting cycle.

162 abolism and physiological responses during a molting cycle.

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

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

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

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

167 e molting program including the cessation of molting cycles.

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

169 t abnormalities, appeared independent of the molting defect.

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

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

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

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

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

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

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

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

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

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

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

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

182 tive action of chitinases and possibly other molting enzymes.

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

184 The molting fluid enzyme chitinase, which degrades the matri

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

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

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

188 Invertebrates molt, furry mammals shed, and human skin exfoliates.

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

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

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

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

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

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

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

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

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

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

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

200 The molting hormone ecdysone triggers chromatin changes via

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

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

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

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

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

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

207 olism and biological processes pertaining to molting in crustaceans.

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

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

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

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

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

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

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

215 Molting is a critical developmental process for crustace

216 Crustacean molting is known to be regulated largely by ecdysteroids

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

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

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

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

221 y avoidance of octanol and quiescence during molting lethargus.

222 as arousal thresholds and quiescence during molting lethargus.

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

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

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

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

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

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

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

230 Frequent molting of the shrimp may be explained by an intensified

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

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

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

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

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

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

237 l size, concomitant with the larval-to-pupal molt orchestrated by the steroid hormone ecdysone.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 er attain the critical weight but eventually molt regardless.

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

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

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

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

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

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

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

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

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

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

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

266 s differentially expressed amongst different molting stages.

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

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

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

270 of winter-gray individuals during the autumn molt suggests that regulatory changes may underlie the c

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

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

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

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

275 udy biomineralization because they regularly molt their exoskeletons and grow new ones in a relativel

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

277 -1, was identified through the analysis of a molting third-stage larvae expressed sequence tag datase

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

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

280 The ecdysteroids induce and direct molting through the ecdysone receptor (EcR), a nuclear h

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

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

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

293 ctor, NHR-23/NR1F1, in regulating C. elegans molting, we discovered that NHR-23/NR1F1 is also constit

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