ライフサイエンスコーパス: misexpression

1 tively eliminating the potential for somatic misexpression.

2 edge with a model for the fitness effects of misexpression.

3 the appropriate neurons, with limited if any misexpression.

4 e were studied functionally using retroviral misexpression.

5 f postsynaptic density protein 95 cerebellar misexpression, a major fine cerebellar structural abnorm

6 emselves cell cycle regulated and that their misexpression affects H3 K56-Ac.

7 We argue that their misexpression affects starch degradation indirectly, by

8 c development, depending on context, whereas misexpression after gastrulation leads to expansion of o

9 Interestingly, two misexpression alleles of wallenda (wnd, encoding a leuci

10 Spry2 misexpression also affects development of the vermis, th

11 Zac1 misexpression also blocked neuronal migration, with Zac1

12 Tbx2 misexpression also results in downregulation of Tbx20 wi

13 Misexpression and cytosolic retention of peripheral myel

14 position of such clusters can result in gene misexpression and disease.

15 Based on misexpression and genetic epistasis experiments, we prop

16 pothesis, we establish tools for conditional misexpression and use these to misexpress Ubx in the cru

17 trichoid sensilla using a transgenic in vivo misexpression approach.

18 used avian replication-competent retroviral misexpression approaches to analyze the function of RBPM

19 tive chromosomal contexts to avoid potential misexpression artifacts.

20 Finally, a dominant modifier screen of a nmo misexpression background identified genomic regions that

21 ears to be sensitive to INP1 dosage and INP1 misexpression can affect global exine patterning.

22 Brain TF co-misexpression can drive brain-profile proliferation in t

23 Possibly as a result, SHH or FOXA2 misexpression can transform the MHB into FP and also sup

24 Specifically, PTB misexpression changes AS of PHYTOCHROME INTERACTING FACT

25 periments, including cell-type-specific gene misexpression, conditional RNAi, and fate mapping of pro

26 ins (DIMM(-)/SYT-alpha(-)/SYT-beta(-)), DIMM misexpression conferred accumulation of endogenous SYT-a

27 IR25a-dependent sensory responses, and IR25a misexpression confers temperature-dependent firing of he

28 At the molecular level, GR28B(D) misexpression confers thermosensitivity upon diverse cel

29 However, other dist7 misexpressions could duplicate this phenotype, and the p

30 Notably, Vangl2 misexpression did not randomize bundle orientations but

31 x2b at the AV boundary, and their domains of misexpression directly correlate with the identified val

32 ncing by the polycomb group (PcG) to prevent misexpression during differentiation and development.

33 Fgf misexpression during gastrulation can inhibit or promote

34 -expressed genes in Notch pathway mutant and misexpression embryos.

35 dence, beyond previous Ptf1a inactivation or misexpression experiments in frog embryos, for spatiotem

36 Genetic and misexpression experiments indicated that castor specific

37 Mutant and misexpression experiments indicated that Neurexin IV mem

38 morpholino knockdown, and dominant negative misexpression experiments to demonstrate that Notch sign

39 ion of quantitative measurements and ectopic-misexpression experiments to examine the transcriptional

40 We use targeted misexpression experiments to provide in vivo evidence th

41 Misexpression experiments with CG13196 result in ectopic

42 By combining point mutation analysis and misexpression experiments, we demonstrate that binding o

43 xpression analysis with loss-of-function and misexpression experiments, we provide evidence that the

44 Through misexpression experiments, we show that these genes enco

45 ous localization, conditional knockdown, and misexpression experiments, we uncovered distinct mechani

46 riated muscle development and function, with misexpression frequently associated with impaired contra

47 HEY1 misexpression has limited skeletal impact, female HeyL n

48 ties of putative hair cells induced by Atoh1 misexpression have not been characterized.

49 attempts to study otic induction through Fgf misexpression have yielded widely varying and contradict

50 Elav in non-neural territories is crucial as misexpression here has profoundly adverse consequences.

51 on in most normal adult tissues and frequent misexpression in a variety of malignancies.

52 endrites, whereas TRIP8b(1a) suppressed HCN1 misexpression in axons.

53 from transgenerational transmission of miRNA misexpression in beta-cells.

54 We further found clear signatures of hybrid misexpression in brain, heart, kidney, and liver.

55 antifies the centromere and kinetochore gene misexpression in cancers.

56 ion in human cells and in the resultant gene misexpression in CdLS.

57 Like hyperactivated Stat92E, Chinmo misexpression in CySCs is sufficient to maintain GSCs no

58 ong tissues, it showed no clear signature of misexpression in F(1) hybrids, even though these hybrids

59 a cancer-related gene because of its loss or misexpression in human neoplasias.

60 bute to hybrid dysfunction by giving rise to misexpression in hybrids.

61 pands the period of cone production, whereas misexpression in late-stage RPCs triggers ectopic cone p

62 Gain-of-function phenotypes result from misexpression in leaves.

63 evance of these findings to the role of BDNF misexpression in mood disorders and cognitive decline is

64 Misexpression in mutants is accompanied by an increase i

65 al promoter fragment that prevents transgene misexpression in myocardial progenitor cells.

66 DUX4 is a transcription factor whose misexpression in skeletal muscle causes facioscapulohume

67 sing laser microdissection and targeted gene misexpression in the chicken DM, we show that Pitx2-spec

68 Furthermore, Ken misexpression in the CySC lineage induces the cell-auton

69 we demonstrate a clear length-dependent gene misexpression in the most prevalent neurodegenerative di

70 ndings point to a developmental role of DUX4 misexpression in the pathogenesis of FSHD and should be

71 at these rbe defects are due to AGAMOUS (AG) misexpression in the second whorl.

72 ar to the other mesenchymal neoplasms, HMGA2 misexpression in the smooth muscle cell leads to abnorma

73 The distinct phenotypes resulting from AIL6 misexpression in the transgenic lines described here and

74 Finally, combined HH blockade and FOXA2 misexpression in ventral midbrain induces LMX1B expressi

75 required for hair-cell development, and its misexpression in vitro and in vivo generates hair-cell-l

76 d by exposure to Shh in vitro and transgenic misexpression in vivo.

77 Misexpression in Xenopus of KCNJ2 carrying ATS-associate

78 eviously established injection model of DUX4 misexpression in zebrafish and describe a DUX4-inducible

79 Remarkably, NeuroD2 misexpression induced ganglion cell production even afte

80 Second, direct LGL misexpression induces ectopic HPs identical to those pro

81 pecifies the third-born U3 motoneuron and Kr misexpression induces ectopic U3 cells.

82 Furthermore, we found that MOCOS misexpression induces increased oxidative-stress sensiti

83 n in a photoperiod-dependent manner, and its misexpression influences algal growth and viability.

84 The misexpressions involved are poorly defined.

85 Thus, Ort misexpression is a useful tool for probing functional co

86 oot apical meristem indeterminacy, and their misexpression is sufficient to induce cell division and

87 cell fate within the root meristem, whereas misexpression is sufficient to transform other stem cell

88 ages of hematopoietic development, and their misexpression is the cause of various blood malignancies

89 This misexpression makes these cells vulnerable to influences

90 We show that such Spry2 misexpression moderately reduces FGF signaling, and that

91 diurnal cycle, and characterization of LDAP misexpression mutants indicated that all three LDAPs wer

92 Additionally, misexpression of a BMP antagonist, Noggin, suppresses pr

93 esis on disease pathogenesis is explained by misexpression of a germ line, primate-specific transcrip

94 Transient misexpression of a presumed pancreatic-commitment transc

95 Here, we show that misexpression of a subset of cone genes in the rd7 mouse

96 One possibility invokes misexpression of a transporter.

97 Mutation of R1810 results in the misexpression of a variety of small nuclear RNAs and sma

98 Overexpression or misexpression of a wild-type gene product, however, can

99 Misexpression of ABI3 was sufficient to rescue cold-indu

100 Disrupted ATX1 or CLF function results in misexpression of AG, recognizable phenotypes and loss of

101 Furthermore, misexpression of all three Grs enables salt- or sweet-se

102 On the other hand, misexpression of any two competence factors in Bmp-block

103 Moreover, misexpression of Atoh1 is sufficient to establish ectopi

104 However, co-misexpression of atoh1a with fgf3, fgf8 or sox2, genes n

105 Misexpression of Awh in transgenic silkworms induces ect

106 Misexpression of bbof1 promotes cilia alignment, even in

107 Misexpression of Bclaf1 in late retinal progenitors was

108 However, misexpression of both receptors in GRNs that normally do

109 Loss of Pbx genes resulted in the misexpression of both vasoconstrictors and vasodilators

110 Misexpression of Brn1/2/4 at low dose caused an increase

111 Using misexpression of Brn3a and Pax7 by electroporation in th

112 Dicer mutant mice show misexpression of cardiac contractile proteins and profou

113 ense of later-born fates, whereas precocious misexpression of Casz1 has the opposite effect.

114 The misexpression of CCR5 in epithelial cells, induced upon

115 Upon misexpression of cdc25a, several essential T-box transcr

116 these processes go awry through mutation or misexpression of certain regulatory elements, the subseq

117 Hyperactivation of Stat92E or misexpression of Chinmo results in blood cell tumors.

118 ) immature myeloid population has widespread misexpression of chromatin-remodeling enzymes and myeloi

119 layed or failed in unsynapsed autosomes, and misexpression of chromosome X and chromosome Y genes was

120 Conversely, misexpression of Ci-ephrin-Ad in the endoderm induces ec

121 Misexpression of CNOT6 in the PGCs results in their fail

122 Misexpression of cone genes in rods may represent a nove

123 ten conditional knock-out (cKO) retinas, and misexpression of constitutively active Akt (Akt-CA) in r

124 Conversely, misexpression of constitutively active Babo results in p

125 ence in early larval brains, as indicated by misexpression of Cyclin E.

126 Conversely, misexpression of Dar1 or its mammalian homolog in unipol

127 rucial for proper neuronal specification, as misexpression of dbx in motoneurons dramatically hinders

128 Misexpression of developmental transcription factors occ

129 pe is suppressed by reducing N signaling and misexpression of Dip3 leads to ectopic activity of a N-r

130 Misexpression of DOCK2, WAVE2, and activation of CDC42 r

131 Misexpression of downstream factors Pax2a or Pax8 also e

132 providing direct support for the model that misexpression of DUX4 is a causal factor for FSHD.

133 Our results suggest that the misexpression of DUX4-fl, even at extremely low level, c

134 essed in FSHD, resulting in the pathological misexpression of DUX4-fl.

135 Transgenic misexpression of dysfusion further revealed that Dysfusi

136 and redundant functions of E2F proteins, how misexpression of E2F transcriptional targets promotes ca

137 Misexpression of either MMP inhibits the regulated separ

138 Misexpression of ELAV results in the ectopic synthesis o

139 se models show innervation defects including misexpression of electrical activity-dependent genes and

140 ), and AFL (LAFL) network is associated with misexpression of embryonic characteristics resulting in

141 mental defects spatially associated with the misexpression of ephrin-A1, and that overexpression of e

142 low myofibers in fast and mixed muscles, and misexpression of ephrin-A3 on fast myofibers followed by

143 ly rescues the loss-of-Notch phenotypes, and misexpression of Erm phenocopies the loss of Notch.

144 Furthermore, combined misexpression of Eve target genes is sufficient to parti

145 st that the transcriptomes resulting from co-misexpression of Eyeless+signaling factors provide a mor

146 h lung epithelial hyperplasia was induced by misexpression of FGF7 or FGF10 showed continued expressi

147 In contrast, misexpression of full-length Robo2 prevents many commiss

148 Misexpression of FZR2 is sufficient to drive ectopic or

149 ed impaired sympathetic nervous function and misexpression of genes required for sympathoadrenal line

150 sion analysis, by RNA sequencing, revealed a misexpression of genes that regulate the cell cycle, neu

151 ver regeneration or for robust and sustained misexpression of genetic elements to test their function

152 n approach in transgenic mice and found that misexpression of Gsx2 at early stages of telencephalic n

153 In addition, misexpression of Hau-Six1/2A in the ventrolateral o blas

154 Interestingly, misexpression of Hb can induce Dan and Svp expression in

155 These results show that misexpression of HMGA2 in a differentiated mesenchymal c

156 In vivo studies in transgenic mice show that misexpression of HMGA2 in smooth muscle cells resulted i

157 Misexpression of HMGN1 affects the cellular transcriptio

158 Conversely, misexpression of human jagged 1 (JAG1) represses ventral

159 absent under nonregenerative conditions, but misexpression of human Na(V)1.5 can rescue regeneration

160 ging of transgenic embryos demonstrated that misexpression of human NRG1 type III results in ectopic

161 rate, using a bitransgenic mouse model, that misexpression of human Six1 in adult mouse mammary gland

162 Misexpression of Id1 and Id3 was found to be sufficient

163 to dissect the separate and shared roles for misexpression of Igf2 and H19 in the disease phenotype.

164 ot only dose-dependent upregulation but also misexpression of Ihh, leading to abnormal phalanges, fus

165 us) they die at peri-implantation due to the misexpression of imprinted genes-the genes that are expr

166 summary, we provide extensive evidence that misexpression of individual miRNAs often induces specifi

167 panied by constitutive IRP2 accumulation and misexpression of IRP2 target genes.

168 Misexpression of IRs in different olfactory neurons is s

169 onsistent with this assumption, we show that misexpression of Irx3 in the prethalamus or telencephalo

170 Misexpression of islet1 RNA can compensate for loss of N

171 Misexpression of its modulatory wild-type beta-subunit X

172 Depolarization of embryonic cells by misexpression of KCNE1 non-cell-autonomously induced mel

173 Regulatory mutations that cause the misexpression of key developmental genes may underlie a

174 Misexpression of klu triggers immature INPs to revert to

175 deficient embryos and cells, but we observed misexpression of left-sided marker genes early in develo

176 Misexpression of let-7 microRNAs in NPCs reduced prolife

177 Misexpression of Lhx3b is sufficient to induce ectopic M

178 ormation under stressful conditions, whereas misexpression of lin-42 in the pre-dauer stage inhibits

179 Misexpression of LMO4 leads to ectopic expression of som

180 Significantly, misexpression of Lvalx1 in macromeres (the progenitors o

181 In addition, misexpression of mab-5 in P(1-8).p is sufficient to esta

182 ry thalamus undergo ectopic firing linked to misexpression of membrane ion channels.

183 Moreover, misexpression of miR-14 was sufficient to prematurely in

184 Misexpression of miR-183 cluster in the human retinal ep

185 oncogenes or tumor suppressors, and how the misexpression of miRNAs and dysregulation of factors tha

186 Misexpression of miRNAs is also a major contributor to c

187 normalities, we profiled mRNA, demonstrating misexpression of MYCN in the majority of human MB and ne

188 Misexpression of Nanos1 in oocytes from unlocalized RNA

189 Notably, misexpression of NeuroD genes can direct amacrine cell p

190 Premature misexpression of NeuroD1 in chick partially recapitulate

191 Furthermore, misexpression of NeuroD1 once the EGL is established bot

192 Nevertheless, neurons derived from late misexpression of Neurog2 and, to a lesser extent, Ascl1,

193 Similarly, acute misexpression of Neurog2 in early cortical progenitors p

194 lysolecithin model, coupled with lentiviral misexpression of NFIA.

195 another key transcription factor, leading to misexpression of non-cardiomyocyte genes.

196 Misexpression of Notch in skeletal tissue indicates a ro

197 Misexpression of Nrarp, a downstream target gene and inh

198 Misexpression of one receptor confers bitter responses a

199 ead ectoderm expressing Otx2, and additional misexpression of Otx2 in trunk ectoderm extended the Not

200 Loss of Dmrt1 caused misexpression of overlapping but distinct sets of mRNAs

201 Misexpression of PAX-FOXO1 in myoblasts upregulated Tanc

202 While misexpression of Pax2 leads to ectopic activation of bot

203 Co-misexpression of Pax2/8 with Fgf8 potentiates formation

204 o restrict the domain of gsc expression, and misexpression of Pax2a is sufficient to block delaminati

205 Similarly, misexpression of Pax6 in the midbrain together with Shh

206 duce increased longevity also causes somatic misexpression of PGL-1.

207 Misexpression of Pitx2 on the right side before and duri

208 Misexpression of Pkd2 is sufficient to confer cold respo

209 vascular permeability in the uterus, whereas misexpression of PR in the endothelium of other organs r

210 e eye pigmentation phenotype was modified by misexpression of proteins involved in intracellular prot

211 By blocking HH signaling by in ovo misexpression of Ptc1(Delta)(loop2), we show that HH sig

212 Furthermore, misexpression of Qtzl suppresses defects in the formatio

213 was highly induced, and we hypothesized that misexpression of R-Spondin1 is necessary for AHR activat

214 Misexpression of RBPMS2 in differentiated visceral SMCs

215 utation-expressing neural progenitors showed misexpression of reelin, which led to a non-cell autonom

216 d blocks the induction of Rh5 expression and misexpression of rhomboid leads to the inappropriate ind

217 Finally, misexpression of Rpgr(ex1-19) causes retinal degeneratio

218 At the molecular level, we identify misexpression of several downstream genes, highlighting

219 uction, namely, embryo transfer, can lead to misexpression of several imprinted genes during post-imp

220 Whereas misexpression of several K box miRNAs inhibited Notch pa

221 xin movements may be mediated in part by the misexpression of several PIN-FORMED (PIN) auxin efflux p

222 We show that misexpression of SHH transforms lingual epithelial cell

223 ast growth factor 8a (Fgf8a), and transgenic misexpression of Shha restores fgf8a expression and part

224 ce of P granules is often accompanied by the misexpression of soma-specific proteins and the initiati

225 Here we report that misexpression of Sox21 expands the neural progenitor dom

226 ural patterning; forced hyperpolarization by misexpression of specific ion channels rescues brain def

227 loss of FMRP activity in neurons causes the misexpression of specific mRNAs required for synaptic pl

228 We found that, whereas misexpression of Spry2 alone caused loss of the anterior

229 n increase of finger-like protrusions, and a misexpression of steroidogenic or FLC- and ALC-specific

230 otch signaling in polar cells, we found that misexpression of String can trigger mitosis in existing

231 Consistently, misexpression of Tbr1 in L5 CS neurons suppresses Fezf2

232 previous reports indicate that in addition, misexpression of Tbx2 beyond the limb margin is sufficie

233 In contrast, misexpression of Tbx4 in the forelimb does not result in

234 Importantly, misexpression of Tbx5 throughout the developing myocardi

235 Misexpression of Tfap2a in embryos blocked for Bmp from

236 In the endodermis, misexpression of the ABA insensitive1-1 mutant protein,

237 Misexpression of the Arabidopsis thaliana AtSPL14 SBP do

238 Misexpression of the constitutively active form of Notch

239 roposed that FSHD pathology is caused by the misexpression of the DUX4 (double homeobox 4) gene resul

240 hy (FSHD; MIM158900, MIM158901) is caused by misexpression of the DUX4 transcription factor in skelet

241 Importantly, misexpression of the full-length human ortholog, RNF113A

242 d insulin-like signalling causes the somatic misexpression of the germline-limited pie-1 and pgl fami

243 The eostre phenotype is caused by misexpression of the homeodomain gene BEL1-like homeodom

244 novo DNA methyltransferase Dnmt3a2, causing misexpression of the imprinted genes Igf2, H19, and Igf2

245 within transgenes in plants, as reflected by misexpression of the introduced gene and undesired pheno

246 genic ventroposterior mesendoderm, either by misexpression of the Nodal homologue XNr1 together with

247 hibitor, DAPT, or signaling was activated by misexpression of the Notch intracellular domain (NICD).

248 Finally, misexpression of the Notch modulator Lfng or the Notch l

249 We proposed that the misexpression of the pollen-specific ACT1 in vegetative

250 Misexpression of the posterior Hox proteins transformed

251 monstrate that Muller gliogenesis induced by misexpression of the potently gliogenic Notch pathway tr

252 ome is caused by mutations in the gene Mecp2 Misexpression of the protein MECP2 is thought to contrib

253 ein had different effects, as did continuous misexpression of the proteins.

254 Misexpression of the trailblazer molecular signature by

255 By contrast, misexpression of the Yki target bantam was able to inhib

256 Misexpression of these APC/C substrates, individually, h

257 , plants impaired in EMF1 function displayed misexpression of these genes early in development, which

258 on neocortical development, suggesting that misexpression of this transcription factor in the brain

259 We find that neuron-specific misexpression of TRP-4, the pore-forming subunit of a me

260 o migrating 'ectomesenchyme' by the targeted misexpression of Twist (also known as twist-like 2).

261 Here, we show that the misexpression of very low levels of human DUX4 in zebraf

262 PI4KIIIalpha mutations also cause misexpression of well-established Hippo signaling target

263 We report that misexpression of wild-type or R620W Pep/Lyp in Jurkat ce

264 Misexpression of Wnt and BMP ligands can induce the form

265 ins respond to TCDD during regeneration with misexpression of Wnt signaling pathway members and Wnt t

266 Conversely, misexpression of WOX13 produces, independently from BP a

267 Dp(dist7) fetuses were consistent with known misexpressions of dist7 imprinted genes, the overall phe

268 pe indicates a role for additional undefined misexpressions of imprinted genes.

269 s study, we describe the consequences of Shh misexpression on Class I and Class II gene expression in

270 To assess the consequences of ETS protein misexpression on megakaryopoiesis, we expressed ETS2, ER

271 embryonic axis, which can be rescued by BMP misexpression or by derepressing endogenous BMP signalin

272 Misexpression or inactivating mutations of the BMP recep

273 use of a number of disorders associated with misexpression or mutation in RBPs.

274 en aimed at uncovering modifiers of an Argos misexpression phenotype in the developing eye.

275 iation of Notch (N) signaling since the Dip3 misexpression phenotype is suppressed by reducing N sign

276 tion CRMP mutation modifies both Ras and Rac misexpression phenotypes during fly eye development in a

277 14 proteolysis in spy-3 suppressed all TCP14 misexpression phenotypes, including the enhanced CK resp

278 Conversely, in the distal lung, Notch misexpression prevented the differentiation of alveolar

279 ulation of cell fate by transcription factor misexpression produces functional sensory cells in the p

280 F7 is an essential RNA-binding protein whose misexpression promotes cancer.

281 Moreover, whereas Ascl1 misexpression promotes neurogenesis in dorsal telencepha

282 We report that Hbox12 misexpression provokes DV abnormalities, attenuating nod

283 less abrogates progenitor outgrowth, whereas misexpression redirects it.

284 Notch misexpression resulted in an increase in mucous cells an

285 l1 throughout the avian limb bud using viral misexpression resulted in an oligodactyly phenotype with

286 enhanced death of cardiac NCs, whereas Sdf1 misexpression results in their diversion from their norm

287 e, we outline results from an overexpression/misexpression screen in Drosophila to identify potential

288 Trbl was identified in a misexpression screen in the ovary as an antagonist of bo

289 We isolated Mmp1 in a misexpression screen to identify molecules required for

290 nd that the stage, distribution and level of misexpression strongly influence the response to Fgf.

291 Furthermore, genetic and misexpression studies show an antagonistic relationship

292 We have used an inducible misexpression system to switch on Ubx in the wing epithe

293 parative genomics and heterologous synthetic misexpression to isolate functional cereal microProtein

294 Netrin misexpression was sufficient to induce ectopic dendritic

295 hysiologic consequences resulting from ADAR2 misexpression, we have generated mutant mice expressing

296 The skeletal effects of HES1 misexpression were studied.

297 his early electrical activity by ion channel misexpression with different increases and decreases in

298 tly, this RF-induced misalignment leads to a misexpression (with respect to their normal physiologica

299 ically during junctional neurulation and its misexpression within a limited time period suffices to c

300 we demonstrate instances where H19 and Igf2 misexpression work separately, cooperatively, and antago