ライフサイエンスコーパス: loss of

1 ow-up with a mean difference in child weight loss of 0.001 (95% CI, -0.06 to 0.06).

2 were used to identify risk factors for BCVA loss of 1 line or more over 1 year.

3 vention trial and achieved an average weight loss of 10.5 kg (10% of initial body weight).

4 itored by mass spectrometry indicated that a loss of 4-5 kJ/mol/protomer in the N3 domain that is per

5 Thermogravimetric analysis showed a weight loss of 85.81+/-0.52% and a decomposition temperature of

6 ults in a male-to-female conversion, whereas loss of a single suppressor of female development drives

7 The loss of a single transporter did not affect S. aureus Ho

8 The SGC plants showed a loss of ability to open stomata in anticipation of daily

9 key role in regulating myofiber length, as a loss of Abl2 leads to excessively long myofibers in the

10 ss of sub-bandgap photons and thermalization loss of above-bandgap photons as demonstrated by the Sho

11 Although there was loss of abundance relative to uncrowded myoglobin analyz

12 primary deactivation process consists of the loss of active sites through the agglomeration and possi

13 dified ASOs in the liver as evidenced by the loss of activity of GalNAc conjugated and unconjugated A

14 latively stable at 77 degrees C, with 59.93% loss of activity.

15 e tissue, exhibited a striking age-dependent loss of adipose tissue accompanied by evidence of adipoc

16 Furthermore, loss of AIBP increased vascular density and facilitated

17 Tln2 in preserving heart function, but that loss of all Tln forms from the heart-muscle cell leads t

18 Loss of alpha-amino trimethylation causes a reduction in

19 y studies of adducted human Hb that revealed loss of alpha-helical content and deoxygenation.

20 teroids, like prednisone, are known to delay loss of ambulation in patients with Duchenne muscular dy

21 , the absence of alphaXbeta2 resulted in the loss of antifungal activity by tissue Mvarphi and inhibi

22 This resulted in a selective loss of approximately 60% of layer VI A1-MGBv neurons.

23 motes both tumor initiation and progression; loss of Arf promotes tumor progression but not initiatio

24 a, is induced upon obesity, and silencing or loss of ARG2 markedly suppresses PDA.

25 oma cells using CRISPR/Cas9 showed a similar loss of Asc expression.

26 glutamate and potassium buffering capacity, loss of astrocyte coupling, and changes in cell morpholo

27 Loss of Atad3a caused accumulation of Pink1 and activate

28 r proteostasis occurring very early on after loss of ATM in order to counter protein damage originati

29 of DC autophagy slowed disease, the combined loss of autophagy in both cell types resulted in a letha

30 inantly protective or deleterious effects on loss of B cell self-tolerance in vivo, we depleted neutr

31 Surprisingly, loss of babA by phase variation or gene conversion is no

32 : 0=no impaired permeability to 100=complete loss of barrier function).

33 SK3beta), followed by phosphorylation of and loss of beta-catenin from the nucleus, thereby reducing

34 f its growth contribute substantially to the loss of biological diversity.

35 Loss of Bmp6 in ECs recapitulated the hemochromatosis ph

36 protoporphyrin IX significantly reduces the loss of body weight due to hRSV-induced disease.

37 uses its time-dependent dissociation and the loss of both DHO and ATC activities.

38 c gene deletion in trophoblasts reveals that loss of both GATA genes, but not either alone, leads to

39 s (SSBs) as indicated by the requirement for loss of both proteins to greatly reduce or ablate XRCC1

40 Loss of both RECQL5 and WRN severely compromises DNA rep

41 We report extensive, global loss of c-Fos and Arc/Arg3.1 immunoreactive neurons in t

42 Loss of Cadm1 protected mice from obesity, and tract-tra

43 rogates binding to DNA and leads to complete loss of canonical TH action.

44 ing support to a causal relationship between loss of CB1 in adipocytes and systemic metabolic changes

45 Loss of cell-cycle control is a hallmark of human cancer

46 ce between cell death and survival following loss of cell-matrix contact.

47 st, dihydro-beta-erythroidine, suggests that loss of cholinergic efficacy may also be the result of a

48 lowing infarction, which was associated with loss of chromatin accessibility around cell cycle genes

49 Loss of circular fibres led to a bifurcated anterior-pos

50 tibility to TB disease could be related to a loss of circulating Th1* CD4(+) T cells rather than majo

51 Loss of claudin-18 was sufficient to impair epithelial b

52 Loss of ClpC repression in MD mutants causes constitutiv

53 ed microbiota destruction and the consequent loss of colonization resistance can result in intestinal

54 mination of cardiac activity associated with loss of consciousness, of spontaneous breathing, and of

55 ergic pallido-STN inputs in PD mice, reduced loss of cortico-STN transmission and patterning and impr

56 In contrast, loss of CTRP6 enhanced insulin-stimulated Akt activation

57 Loss of CXCR7 expression by CRISPR-Cas9 gene editing res

58 To better understand how loss of D2-family dopamine receptors can ameliorate tau

59 Although a loss of DC autophagy slowed disease, the combined loss o

60 maging chemotherapy, consistent with a local loss of DDR, and identify a potential therapeutic strate

61 Taken together, these data indicate that loss of DDRGK1 decreases SOX9 expression and causes a hu

62 Further, the severe loss of dendritic cells in the draining lymph node had n

63 of PERK-K618A in primary neurons rescues the loss of dendritic outgrowth and number of synapses after

64 vation of PERK using GSK2656157 prevents the loss of dendritic spines and rescues memory deficits aft

65 We also found that loss of dnaA caused a decrease in the development of gen

66 Loss of DONSON leads to severe replication-associated DN

67 cued parkin mutant phenotypes, in particular loss of dopaminergic neurons, mitochondrial network stru

68 Genetic loss of DUSP5 exacerbated TNFalpha-mediated ERK 1/2 sign

69 el mutant mouse, dys-1A(-/-), with selective loss of dysbindin-1A and investigated schizophrenia-rela

70 Loss of dysbindin-1A resulted in heightened initial expl

71 l apoptotic enterocytes promote divisions by loss of E-cadherin, which releases cadherin-associated b

72 e a burst of reactive oxygen species induces loss of E-cadherin-mediated cell contact, followed by a

73 hat result in lack of glycosylation and thus loss of effector function, we demonstrate that the N297G

74 ex of 8-oxoG:dA extension results in further loss of efficiency when compared to 8-oxoG:dC extension.

75 ies, exactly as predicted by the alternative loss of either of the internal introns at the DNA level

76 Loss of either RNase H1 or Top1 caused R-loop accumulati

77 Loss of either the Exo1 or Sgs1 long-range resection pat

78 tric amount (0.25 equiv) without significant loss of enantioselectivity.

79 to the etiology of human disorders linked to loss of endosomal NHE function.

80 Conditional loss of endothelin receptor A in granulosa cells also de

81 elalgia could similarly be associated with a loss of epidermal nerve fiber density (ENFD).

82 Nanog promoter methylation and phenocopying loss of Eprn or Lin28a.

83 main for DNA binding, can compensate for the loss of ETS1 binding at adjacent sites.

84 tent Opera imaging identified 53 genes whose loss of expression led to a decrease in NB cell prolifer

85 t constructed in the impetigo strain Alab49, loss of FbaA resulted in a slight but significant decrea

86 a Fdxr-deficient mouse model and found that loss of Fdxr led to embryonic lethality potentially due

87 embryonic lethality) or results in profound loss of fitness.

88 ve chloride secretion, with the accompanying loss of fluid, is not normally stimulated by intestinal

89 monogenic cause of autism, results from the loss of FMR1, a conserved, ubiquitously expressed RNA-bi

90 tment use among patients with 0, 1, or 2 FLG loss of function (LOF) alleles was compared as well as t

91 iched in known driver genes.Variants causing loss of function (LoF) of human genes have clinical impl

92 ify and characterise a mouse line carrying a loss of function allele in Katnal1.

93 Here, we conditionally induce beta-catenin loss of function in resident cardiac fibroblasts using T

94 xcitability in the brain, where pathological loss of function leads to such disorders as epilepsy, Al

95 mutants in Caki2 cells (ccRCC cells with the loss of function mutation in PBRM1).

96 ing GPI anchor protein pathway genes induced loss of function mutations in human and mouse cell lines

97 mutations included five de novo heterozygous loss of function mutations/deletions in the PBX homeobox

98 The loss of function of MKK4/MKK5 also results in the same p

99 Pathogenic mutations cause a loss of function of the encoded protein Parkin.

100 Loss of function of the Rho-GAP oligophrenin-1 is associ

101 dence suggesting that LRRK2 G2019S and SYNJ1 loss of function share a similar pathogenic pathway in d

102 PCSK9 loss-of-function (LOF) variants allow for the examinatio

103 By using both gain-of-function and loss-of-function approaches, we demonstrate that HIPK2 c

104 on-induced cleavage were abolished in a TEP1 loss-of-function background.

105 Severe loss-of-function cases were incompatible with life, wher

106 acellular domain resulted in either gain- or loss-of-function changes, part of which was attributable

107 Basal lineage-specific profiling and genetic loss-of-function experiments revealed a critical role fo

108 , we investigate protein features underlying loss-of-function genetic variation and develop a machine

109 rol motivated behaviours and that VLS D2-MSN loss-of-function is a possible cause of motivation defic

110 wide DNA methylation in partial and complete loss-of-function met1 mutants.

111 In the tissue model, loss-of-function mutations facilitated breakdown of exci

112 Significantly, both RhoA GTPase gain- and loss-of-function mutations have been discovered in prima

113 SHP2 loss-of-function mutations in chondroid cells are linked

114 In contrast, loss-of-function mutations in GLI1 have remained elusive

115 Loss-of-function mutations in KCC2 are a known cause of

116 fection by Salmonella Typhimurium because of loss-of-function mutations in Nramp1 (SLC11A1), a phagos

117 Loss-of-function mutations in ORGANELLE RNA RECOGNITION

118 Loss-of-function mutations in SLC30A10, a cell-surface-l

119 This finding is in contrast to the loss-of-function mutations in SMCHD1 that have been asso

120 Specifically, loss-of-function mutations in the gene encoding LegC4 re

121 Loss-of-function mutations in the MCOLN1 gene, which enc

122 rcent of patients have compound heterozygous loss-of-function mutations in the Shwachman-Bodian-Diamo

123 ide a model for human patients with germline loss-of-function mutations in Wnt pathway genes, includi

124 2, DDX3X, KDM5C, KDM6A, and MAGEC3) harbored loss-of-function mutations more frequently in males (bas

125 nked CNM, is caused by myotubularin 1 (MTM1) loss-of-function mutations, while the main autosomal dom

126 Loss-of-function of FRS7 and FRS12 results in early flow

127 ominant diseases that feature both gain- and loss-of-function pathologies or have a heterogeneous gen

128 MicroRNAs (miRNAs) loss-of-function phenotypes are mainly induced by chemic

129 Loss-of-function point mutations in a component of this

130 Loss-of-function studies showed that autophagy in NP cel

131 te that Dicer1 can function as a traditional loss-of-function tumor suppressor gene, and they provide

132 symptoms seen in patients with a missense or loss-of-function variant in KCNB1 and how these symptoms

133 s in >6500 cancer exomes shows that putative loss-of-function variants predicted to be deleterious by

134 and their dysfunction may contribute to the loss of functional beta cell mass in diabetes.

135 Fragile X syndrome (FXS), caused by the loss of functional FMRP, is a leading cause of autism.

136 In humans and FVB/N mice, loss of functional tetraspanin CD151 is associated with

137 Genetic loss of Gcn2 intensified hepatic PERK activation to aspa

138 Loss of Gfi1 resulted in premature induction of effector

139 plants, and gene editing was accompanied by loss of GFP expression.

140 As a result, loss of GIRK function can enhance neuron excitability, w

141 ge-dependent responsiveness does not reflect loss of GLP-1R signaling in adult islets, since Ex-4 tre

142 istic target of rapamycin (mTOR) activation, loss of glutamate and potassium buffering capacity, loss

143 d to the extent that net oxidation occurs by loss of H2.

144 Despite a major loss of H3K27me3, PRC2 activity is still detected in DIP

145 These data support a role for loss of HBEGF in the neuroblastoma tumor microenvironmen

146 A mutation or high percentage of genome-wide loss of heterozygosity.

147 Many cancers are initiated by loss-of-heterozygosity (LOH) events that lead to the rep

148 different number of copies and copy-neutral loss-of-heterozygosity (LOH).

149 Loss of Hippo switches Ras activation from promoting cel

150 cape the host's immuno-surveillance, e.g. by loss of HLA class-I expression.

151 t during embryonic stem cell differentiation loss of HMGNs leads to down regulation of genes involved

152 Recent high annual losses of honey bee colonies are associated with many fa

153 ly through resorption, we show that an acute loss of IFT-B through cilia decapitation precedes resorp

154 Loss of IKBKE inhibits the initiation and progression of

155 n of CD4 Th cells most likely contributes to loss of immune control of LTBI in HIV-infected individua

156 etion causes severe defects in karyokinesis, loss of individual chromosomes, and gross defects in spi

157 d in curve-fitting, leading to a significant loss of information from experiments.

158 by establishing MOB1 variants with selective loss-of-interaction.

159 ry, people with dementia may also experience loss of interest in sexuality and intimacy.

160 mpairment of mitochondrial morphology with a loss of internal cristae.

161 reatment, changes in NOM consistent with the loss of iron-complexing carboxylate ligands were observe

162 Amitosis is also induced by the functional loss of ISCs coupled with tissue demand and in aging fli

163 ne with this, Foxp2-null mutants also show a loss of ITCs at postnatal time points, suggesting that F

164 A gene can be defined as essential when loss of its function compromises viability of the indivi

165 Additionally, loss of JMJ27 function leads to early flowering.

166 Loss of KinG function results in a decrease in the inter

167 Loss of KRIT1 leads to decreased microvessel barrier fun

168 We also demonstrate loss of LAT expression and lack of TCR signaling restora

169 the first 8 years after pEFS24, the average loss of lifetime was 0.31 mo/y (95% CI, 0.11 to 0.50 mo/

170 ty of stillbirth data to avoid this needless loss of lives.

171 Western blot analyses showed that the loss of LKB1 and phosphatase and tensin homolog deleted

172 However, the consequences of loss of Lpd in the CNS on behaviour are unknown.

173 of the Rasa1 gene in adult mice resulted in loss of LV endothelial cells (LECs) specifically from th

174 To better understand how loss of maternal UBE3A function derails brain developmen

175 Delayed self-righting can result in loss of mating opportunities or death.

176 he whole basin apparently reflected variable losses of MeHg exported from upstream wetlands due to de

177 right to others that proposed that with the loss of memory, people with dementia may also experience

178 reduced invasion, which is accompanied by a loss of mesenchymal phenotype and an increase in cell-ce

179 n CNTs can obviously enhance the penetration losses of microwaves in foams, leading to a greatly impr

180 the mitochondrial unfolded protein response, loss of mitochondrial membrane potential and sensitivity

181 In contrast, loss of Mll3/4 proteins leads to strong depletion of enh

182 apitulate the human disease-with progressive loss of motor neurons in heterozygous animals.

183 inal muscular atrophy (SMA) is caused by the loss of motor neurons, but astrocyte dysfunction also co

184 s in centrosome integrity do not result from loss of mRNA export.

185 Loss of mTORC1 signaling by removal of Raptor in tendons

186 Loss of MYO10 expression in osteoclast precursors inhibi

187 Loss of myristoylation abolished the tumorigenic potenti

188 pathogenic SIV infection is characterized by loss of naive B cells, loss of resting memory B cells du

189 r Ca(2+) transport, could be affected by the loss of nBMP2.

190 had increased LH pulse frequency, indicating loss of negative feedback.

191 As loss of neighbouring housekeeping genes can confer colla

192 is correlated with and probably results from loss of NELF association and function.

193 Loss of Neu5Gc in Homo likely had complex effects on imm

194 n undefined, but postulated pathways include loss of neuronal progenitor cells, damage to the develop

195 The neuropathological hallmark of HD is the loss of neurons in the striatum and, to a lesser extent,

196 phosphorylation and cell integrity, whereas loss of NLRX1 results in increased oxygen consumption, o

197 loid deposition is associated with premature loss of normal Abeta42 day/night patterns in older adult

198 Parkinson's disease (PD) patients experience loss of normal motor function (hypokinesia), but can dev

199 Moreover, the rapid losses of nucleobases to pond seepage during wet periods

200 In humans, tolerance of the loss of one or both functional copies of a gene is relat

201 o) from stromal cells is associated with the loss of osteoblastoid markers.

202 attributed to attenuation of the reflection loss of p-polarized light and multiple reflections withi

203 In this study, we investigate the effect of loss of P2X7 receptor function on retinal structure and

204 loss and p53 loss produce differing outcomes-loss of p53 promotes both tumor initiation and progressi

205 We demonstrate that partial loss of p85alpha increases the amount of p110alpha-p85 h

206 A relapse was defined as loss of partial response.

207 In this study, we find that loss of Pdcd4 increases the activity of mammalian target

208 Importantly, we have found here that loss of PDHK4, a key regulator of the pyruvate dehydroge

209 Accompanying this loss of performance was reduced response to rule-critica

210 t and periodontal homeostasis and during the loss of periodontal tissue integrity as a result of peri

211 ) with night blindness, and 56% (14/25) with loss of peripheral vision.

212 rtex identified either reduced expression or loss of phosphorylation at critical residues of differen

213 s (EAE), to evaluate the hypothesis that the loss of plasminogen would exacerbate neuroinflammatory d

214 nexpectedly, PI(4,5)P2 depletion also caused loss of pre-assembled Gag lattices from the PM.

215 lation of markers of non-mast cell lineages, loss of proliferative control, chromatin remodeling as w

216 , which led to a less-diverse microbiome and loss of protective gut commensal strains (of the family

217 istribution of ceramic result in much slower loss of protective oxide layers formed during ablation t

218 lineages, lower reconstitution potential and loss of protein polarity.

219 e antibodies are efficiently cleaved without loss of protein target antigenicity.

220 Loss of proteostasis underlies ageing and neurodegenerat

221 h cancer recurrence associated with combined loss of PTEN and FOXP1-SHQ1 genes.

222 n of the distal CTCF-binding site results in loss of Ramp3 expression in non-mammary tissues.

223 es manipulating small sample volumes without loss of rare disease-causing cells.

224 e largest effect on pseudogene formation and loss of regulatory regions.

225 Furthermore, loss of release did not disrupt the morphogenesis of pre

226 We show that loss of RER in B. subtilis causes strand- and sequence-c

227 n is characterized by loss of naive B cells, loss of resting memory B cells due to their redistributi

228 Loss of rfaH affected LPS synthesis in both species, res

229 lpha:RGS proteins was proposed to enable the loss of RGS in monocots.

230 Loss of RNF146 stabilized its substrate AXIN1, leading t

231 Interestingly, loss of RP-MDM2 binding significantly accelerated colore

232 We now show that the loss of S100A4 produces two mechanistically distinct phe

233 Loss of Sav1 induced Stat3 activation and a senescence-a

234 mature stop codon and led to small seeds and loss of seed shattering during African rice domesticatio

235 en leads to devastating consequences such as loss of senses or locomotion.

236 Moreover, loss of SEP4 severely impaired mutant conidiation, melan

237 Loss of sexual-lineage-specific RdDM causes mis-splicing

238 Loss of Sin3a in mouse early foregut endoderm led to a s

239 S) is a congenital disorder characterized by loss of smooth muscle contraction in the bladder and int

240 We demonstrate that neither loss of spatially coordinated apical constriction nor it

241 which is evident even in cells with partial loss of SPCA1.

242 ntagonism after experimental stroke prevents loss of splenic MZ B cells, preserves IgM levels, and re

243 Preceding RGC loss in the Ndufs4 KO is the loss of starburst amacrine cells, which may be an import

244 We demonstrate that loss of STIM2 results in decreased SOCE, particularly at

245 In vivo loss of STIM2 results in lower cytokine levels and prote

246 cause of a better balance between absorption loss of sub-bandgap photons and thermalization loss of a

247 sultines was kinetically preferred over the loss of sulfur dioxide leading to o-quinodimethane, whic

248 tin signaling pathway mediates Abeta-induced loss of surface AMPARs is unknown.

249 2), thereby alleviating amyloid-beta-induced loss of synapses and cognitive decline in Alzheimer's di

250 Loss of synapses or alteration of synaptic activity is a

251 The loss of synaptic GluA2 is caused by rapid trafficking of

252 aptic function and inhibiting both underlies loss of synaptic transmission via massive vesicle releas

253 Preferential loss of T-cell reactivity to Mtb epitopes that are homol

254 l ablation of neuronal Shh expression causes loss of taste receptor cells (TRCs).

255 abstraction is likely to further exacerbate loss of taxa and ecosystem alteration, especially in dry

256 glutamine catabolism, there is near complete loss of TCA intermediates, with no compensation from glu

257 Werner syndrome protein (WRN) suppresses the loss of telomeres replicated by lagging-strand synthesis

258 To identify pathways affected by loss of Tgif function during embryogenesis, we performed

259 Loss of THAP1 function disrupts a core set of OL maturat

260 enic factors, such as activation of ErbB2 or loss of the betasubunit of casein kinase 2, shifted the

261 Loss of the C. elegans DDC gene, bas-1, ameliorated the

262 ogether, these findings demonstrate that the loss of the Ca(2+) channel alpha2delta-1 subunit functio

263 This induces a high risk of sample loss of the collected rare cells.

264 tent state without inducing pathology due to loss of the Golgi GDP mannose transporter.

265 rain Apmu4 was derived, in which the rate of loss of the integration plasmid was much lower after ind

266 The WhiB1 structure suggests that loss of the iron-sulfur cluster (by nitrosylation) permi

267 al lethality, we sought to determine whether loss of the metabolic gene malic enzyme 2 (ME2) in the S

268 y of platelet mRNAs is slowed by the natural loss of the mRNA surveillance and ribosome rescue factor

269 dissatisfaction, use of second opinions, or loss of the patient to a second surgeon.

270 nd palate and tongue agenesis, following the loss of the primary cilia in the CNC-derived palatal mes

271 Surprisingly, the ubiquitous loss of the protein uniquely affects the formation of th

272 ions, no effect on organismal growth rate or loss of the reddish colony phenotype due to mutations in

273 differentiation defects that are mimicked by loss of the transcription factor KLF4.

274 Loss of the tumor suppressor p53 (encoded by TP53) provi

275 es is a common practice in order to preserve loss of the volatile profile.

276 es into account the radiation and scattering losses of the nano-sized probe neglected in previous mod

277 distribution of MENPs inside the cell and no loss of their elemental and crystalline characteristics.

278 ructure of F-actin and in protein transport, loss of this function might be the trigger for the resul

279 necessary for its interaction with Nba1, and loss of this interaction results in premature delocaliza

280 Since injury induces loss of this interaction, we hypothesized that strengthe

281 Loss of this organization underlies disturbed insulin se

282 nse to a high-fructose diet in mice and that loss of this transcription factor leads to hepatic infla

283 high sequence and structural similarity, and loss of Tim10 is accelerated by the disruption of conser

284 and ascorbic acid were reduced; retarded the loss of titratable acidity during 96h after treatment.

285 the role of regulatory T (Treg) cells in the loss of tolerance to gluten remains poorly understood.

286 IV-associated B cell dysfunction (defined by loss of total and memory B cells, increased B regulatory

287 beta4-containing nAChRs, in addition to the loss of total nAChR number.

288 We show here that loss of Trp53 activates canonical WNT signaling in these

289 Additional loss of Trp53 causes resistance to antiandrogen therapy.

290 Mechanistically, loss of UNC-45A results in increased levels of NMII acti

291 Loss of underlying permafrost with associated hydrologic

292 Urinary incontinence, the involuntary loss of urine, is a common health condition that may dec

293 i) needed for chamber SOA mass yields due to losses of vapors to walls as a function of species volat

294 c1, suggesting that this deletion caused the loss of vernalization response.

295 l-depleted cells for up to 30 d with minimal loss of viability, for longitudinal studies.

296 s, MEK inhibitors did not cause irreversible loss of vision or serious eye damage.

297 rs characterized by slow growth, progressive loss of vision, and limited therapeutic options.

298 We demonstrate that loss of Wnt5a results in cerebellar hypoplasia and deple

299 In females, erasure follows loss of X inactivation, causing X dosage excess.

300 and 95th percentiles for the time until the loss of ZIKV RNA detection were 14 days (95% confidence