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

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

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

8 Spry2 misexpression also affects development of the vermis, th

9 Zac1 misexpression also blocked neuronal migration, with Zac1

10 Tbx2 misexpression also results in downregulation of Tbx20 wi

11 Misexpression analysis suggests that D-Six4 and its like

12 Misexpression and cytosolic retention of peripheral myel

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

14 Based on misexpression and genetic epistasis experiments, we prop

15 he activity of the genes was modulated using misexpression and RNAi-mediated silencing.

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

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

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

22 Specifically, PTB misexpression changes AS of PHYTOCHROME INTERACTING FACT

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

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

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

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

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

28 Notably, Vangl2 misexpression did not randomize bundle orientations but

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

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

31 Fgf misexpression during gastrulation can inhibit or promote

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

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

34 Genetic and misexpression experiments indicated that castor specific

35 Mutant and misexpression experiments indicated that Neurexin IV mem

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

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

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

39 Misexpression experiments with CG13196 result in ectopic

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

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

42 Through misexpression experiments, we show that these genes enco

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

44 HEY1 misexpression has limited skeletal impact, female HeyL n

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

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

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

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

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

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

51 antifies the centromere and kinetochore gene misexpression in cancers.

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

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

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

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

56 reover, loss of Gli3 expression induces Gli1 misexpression in mammary mesenchyme.

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

58 Misexpression in mutants is accompanied by an increase i

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

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

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

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

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

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

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

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

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

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

69 Misexpression in Xenopus of KCNJ2 carrying ATS-associate

70 Remarkably, NeuroD2 misexpression induced ganglion cell production even afte

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

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

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

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

75 shown to induce Tbx2, and we found that Tbx2 misexpression inhibited the expression of both Hey1 and

76 The misexpressions involved are poorly defined.

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

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

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

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

81 This misexpression makes these cells vulnerable to influences

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

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

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

85 Transient misexpression of a presumed pancreatic-commitment transc

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

87 One possibility invokes misexpression of a transporter.

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

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

90 Misexpression of ABI3 was sufficient to rescue cold-indu

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

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

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

94 Moreover, misexpression of Atoh1 is sufficient to establish ectopi

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

96 Misexpression of Awh in transgenic silkworms induces ect

97 Misexpression of bbof1 promotes cilia alignment, even in

98 Misexpression of Bclaf1 in late retinal progenitors was

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

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

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

102 Using misexpression of Brn3a and Pax7 by electroporation in th

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

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

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

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

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

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

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

110 Misexpression of CNBP induced the expression of BF-1, Si

111 Misexpression of CNOT6 in the PGCs results in their fail

112 Misexpression of cone genes in rods may represent a nove

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

114 Conversely, misexpression of constitutively active Babo results in p

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

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

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

118 Misexpression of developmental transcription factors occ

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

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

121 Misexpression of dominant-negative forms of Tbx5 results

122 Misexpression of downstream factors Pax2a or Pax8 also e

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

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

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

126 Transgenic misexpression of dysfusion further revealed that Dysfusi

127 Misexpression of eight of nine genes tested caused pheno

128 cally, misactivation of Notch2 signaling, or misexpression of either Hey1 or Hey2, repressed Bmp2.

129 Misexpression of either MMP inhibits the regulated separ

130 Misexpression of ELAV results in the ectopic synthesis o

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

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

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

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

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

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

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

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

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

140 Misexpression of FZR2 is sufficient to drive ectopic or

141 Errors cause misexpression of genes and aberrant development.

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

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

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

145 se of transcriptional deregulation caused by misexpression of growth-suppressive, inflammatory, and p

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

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

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

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

150 To determine whether misexpression of HMGA2 in differentiated mesenchymal cel

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

152 Misexpression of HMGN1 affects the cellular transcriptio

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

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

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

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

157 Misexpression of Id1 and Id3 was found to be sufficient

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

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

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

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

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

163 Misexpression of IRs in different olfactory neurons is s

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

165 Misexpression of islet1 RNA can compensate for loss of N

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

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

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

169 Misexpression of klu triggers immature INPs to revert to

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

171 Misexpression of let-7 microRNAs in NPCs reduced prolife

172 Misexpression of Lhx3b is sufficient to induce ectopic M

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

174 Misexpression of LMO4 leads to ectopic expression of som

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

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

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

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

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

180 Misexpression of miRNAs is also a major contributor to c

181 ome ventralized by late gastrulation whereas misexpression of msxB dorsalizes the embryo.

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

183 Misexpression of Nanos1 in oocytes from unlocalized RNA

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

185 Premature misexpression of NeuroD1 in chick partially recapitulate

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

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

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

189 lysolecithin model, coupled with lentiviral misexpression of NFIA.

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

191 Misexpression of Notch in skeletal tissue indicates a ro

192 Misexpression of Nrarp, a downstream target gene and inh

193 Misexpression of one receptor confers bitter responses a

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

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

196 Misexpression of PAX-FOXO1 in myoblasts upregulated Tanc

197 While misexpression of Pax2 leads to ectopic activation of bot

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

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

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

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

202 Misexpression of Pitx2 on the right side before and duri

203 Misexpression of Pkd2 is sufficient to confer cold respo

204 Misexpression of Ppa inhibits the formation of neural cr

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

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

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

208 Furthermore, misexpression of Qtzl suppresses defects in the formatio

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

210 Misexpression of RBPMS2 in differentiated visceral SMCs

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

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

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

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

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

216 Whereas misexpression of several K box miRNAs inhibited Notch pa

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

218 We show that misexpression of SHH transforms lingual epithelial cell

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

220 ingle-mutant mothers are inviable due to the misexpression of SKN-1, a transcription factor that can

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

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

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

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

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

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

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

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

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

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

231 Importantly, misexpression of Tbx5 throughout the developing myocardi

232 Misexpression of Tfap2a in embryos blocked for Bmp from

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

234 Misexpression of the Arabidopsis thaliana AtSPL14 SBP do

235 Misexpression of the constitutively active form of Notch

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

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

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

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

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

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

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

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

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

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

246 or and a gain-of-function disease, caused by misexpression of the PAX3-FKHR or PAX7-FKHR fusion oncop

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

248 Misexpression of the posterior Hox proteins transformed

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

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

251 nase, thus allowing it to induce conditional misexpression of the tagged gene.

252 Misexpression of the trailblazer molecular signature by

253 Furthermore, transgenic misexpression of the truncated version of HMGA2, contain

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

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

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

257 Importantly, we show misexpression of this receptor in non-T1 neurons, normal

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 2) is a tetraspan membrane glycoprotein, the misexpression of which is associated with hereditary dem

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

265 Misexpression of Wnt and BMP ligands can induce the form

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

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

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

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

270 this growth, and the effects of Eph receptor misexpression on axonal growth across the midline.

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

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

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

274 Misexpression or inactivating mutations of the BMP recep

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

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

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

278 f Imp activity partially suppresses a gurken misexpression phenotype, indicating that Imp does act in

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

280 14 proteolysis in spy-3 suppressed all TCP14 misexpression phenotypes, including the enhanced CK resp

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

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

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

284 less abrogates progenitor outgrowth, whereas misexpression redirects it.

285 Notch misexpression resulted in an increase in mucous cells an

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

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

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

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

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

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

292 Furthermore, genetic and misexpression studies show an antagonistic relationship

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

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