ライフサイエンスコーパス: be reversed by

1 ramidal cells of rodents, and this reduction is reversed by 17beta-estradiol (E2) treatment in a mode

2 biodiversity trends from habitat conversion are reversed by 2050 for almost all of the models.

3 The dipole orientation can be reversed by a critical electric field, producing shar

4 Persistent FoxO activation can be reversed by a high-protein diet in adulthood, through

5 sion is dependent on DNA methylation and can be reversed by a methylation inhibitor.

6 inflammation and neuronal injury markers can be reversed by a single dose of PrP-lowering ASO adminis

7 P ribose polymerase-1 (PARP-1) cleavage) and was reversed by a pan-caspase inhibitor.

8 ranase, TF, TFPI, and TFPI-2, and the effect was reversed by a peptide-inhibiting heparanase/TF compl

9 ry effects of Delta9-THC in endotoxemic mice were reversed by a cannabinoid receptor type 1 (CB(1)R)

10 e effects of metformin to reduce body weight were reversed by a GFRAL-antagonist antibody.

11 All of these effects were reversed by a miR-204 inhibitor (miR-204 I) or with

12 , METH-induced changes to BLA spine dynamics were reversed by a single systemic injection of an NMII

13 wn increased cardiac damage after I/R, which was reversed by AAV9-mediated ectopic MANF expression.

14 es and increased Proteobacteria, which could be reversed by Abx.

15 Both outcomes can be reversed by activation of macrophages with pneumococc

16 ata that sepsis-induced mitochondrial damage is reversed by activation of mitochondrial biogenesis an

17 e cortical effects of threat-induced anxiety are reversed by acute anxiolytic treatment.

18 ell density increases, and these defects can be reversed by acute physical reduction of cell density.

19 tionally, inhibition of thrombin is shown to be reversed by addition of single-stranded DNA antidotes

20 The intestinal pathology of Fx-/- mice was reversed by addition of fucose to the diet, which re

21 These effects were reversed by addition of 10 mM 2,3-butanedione 2-mon

22 These effects were reversed by addition of TGF-beta signaling inhibito

23 These effects are reversed by administering a small FOXO1-derived phos

24 This effect could partly be reversed by administration of PGE2 to COX-2 mice.

25 lues, and hypoxic pulmonary vasoconstriction was reversed by administration of sildenafil (50 mg) to

26 While ADP-ribosylation can be reversed by ADP-ribosylhydrolases, this protein modif

27 es caused by developmental loss of NLG-1 can be reversed by adult expression.

28 and tumor-associated macrophages, which can be reversed by AHR inhibition.

29 whether past acidification effects persist, are reversed by alleviation of pCO2 stress, or are worse

30 indolence in two cancer types, and show this is reversed by allowing the stabilization of Hypoxia Ind

31 The OxPhos deficit in cINs could be reversed by Alpha Lipoic Acid/Acetyl-L-Carnitine (ALA

32 s in mitochondrial function and arborization were reversed by alpha lipoic acid and acetyl-L-carnitin

33 Treg cell accumulation and bone regeneration was reversed by AMD3100, an antagonist of the chemokine

34 on in cerebellar slice cultures, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor b

35 s due to ACE C-domain catalytic activity; it is reversed by an ACE inhibitor but not by an angiotensi

36 This activity was reversed by an AMPK inhibitor (compound C).

37 The enhancing effects were reversed by an mGluR2/3 antagonist or by activating

38 r the RvE1 receptor, and the actions of RvD1 were reversed by an RvD1 receptor inhibitor.

39 ed depletion of LSK cells in the bone marrow was reversed by ANG-(1-7).

40 ed the recovery of blood flow, both of which were reversed by ANG-(1-7) in both models of diabetes.

41 e and induction of browning in WAT and could be reversed by antagonism of beta3 adrenergic receptors.

42 d sucrose reinstatement by mGluR2/3 blockade was reversed by antagonizing mGluR5, but reinstated sucr

43 hn's disease in the AGLCD patient, which can be reversed by anti-TNFalpha therapy.

44 nts depended on NOTCH2 activation because it was reversed by anti-NOTCH2 negative regulatory region a

45 mpanied by depression-like behavior, and can be reversed by antidepressant treatment.

46 h adenylyl cyclase to produce cAMP, and this is reversed by antidepressant treatment.

47 rand breaks in epithelial cells, which could be reversed by antioxidant treatment.

48 tent to which these B cell abnormalities can be reversed by antiretroviral therapy (ART) are limited.

49 Notably, the magnetization of the sample can be reversed by applying a small direct current.

50 ng Aurora-B, an attachment destabiliser, but is reversed by artificially tethering PP1 near the C-ter

51 pressive resistance, and this resistance can be reversed by blockade of IL-1beta, IL-6, or STAT3.

52 mmatory cytokine impairment of BM that could be reversed by blocking IL-1R or IL-6R.

53 This could be reversed by blocking of NKR-P1A.

54 striatum and central thalamus that could not be reversed by blocking the dopamine transporter.

55 lactate's ability to stimulate neurogenesis is reversed by blocking MAPK.

56 ed following C. trachomatis infection, which was reversed by blocking LOS synthesis.

57 These impairments were reversed by blocking C1qBP, but not C3aR1 receptors

58 All of these changes were reversed by blocking TSP1 effects.

59 ic homolog (SMAD/P-SMAD)1 and 5, which could be reversed by BMP receptor inhibitors and ALK3 knockdow

60 Notably, these effects were reversed by both repeated and single-Reelin infusio

61 % CI, -0.47 to -0.07]; P<0.001), which could be reversed by cardiac-specific Lrg1 delivery mediated b

62 expression pattern of many EAE-induced genes was reversed by CBD treatment which was consistent with

63 Importantly, these effects were reversed by CBFA2T3 re-expression.

64 The effective magnetic field can be reversed by changing the direction of the applied ele

65 show cocaine-primed reinstatement which can be reversed by chemogenetic manipulation of excitatory c

66 ls had improvements in memory precision that were reversed by chemogenetic silencing of the transplan

67 ed TSLP levels were steroid resistant, which was reversed by clinically available inhibitors of MEK a

68 The addition reaction can be reversed by CO reduction of [Au(25)SR(19)](0), leadin

69 All of these effects were reversed by co-ablation of ATGL.

70 These enhancing effects were reversed by coapplication of a alpha4beta2-nAChR an

71 atient-derived xenograft (PDX) tumors, which was reversed by combination with SFX-01.

72 of MDA-MB-231 cells by HDAC5 overexpression was reversed by concurrent LSD1 depletion, indicating th

73 This effect on proliferation is reversed by COP1 knockdown and ectopic expression of

74 sorders, but whether established disease can be reversed by correcting these mutations is unclear.

75 polysis, HGP, and ketogenesis; these effects were reversed by corticosterone infusion.

76 reference in male C57BL/6 mice, effects that were reversed by cotreatment with JQ1.

77 Deficits in this task following seizures were reversed by COX-2 inhibition, which prevented sever

78 inflammatory transcriptional profile, which was reversed by CR.

79 e proinflammatory ligand-receptor interplay, were reversed by CR.

80 TRIMCyp shows anti-retroviral activity that is reversed by cyclosporine, but it does not activate Nf

81 These effects were reversed by DAU 5884 (M(3) receptor antagonist) but

82 All of the cellular immune abnormalities were reversed by day 360 in abstinent AH patients; howev

83 In some cases, the modification is reversed by deacylases of different types.

84 charomyces cerevisiae, dna2Delta inviability is reversed by deletion of the conserved helicase PIF1 a

85 The response to FG-4592 was reversed by deletion of HIF1A, demonstrating that EG

86 anti-tumour effects of autophagy inhibition are reversed by depleting CD8(+) T cells or reducing sur

87 bstituted 1,4-naphthoquinones is possible to be reversed by deprotonation and application of the resu

88 The WT Treg induction defect was reversed by DGAT1 inhibition.

89 ogenase activity and oxygen consumption rate were reversed by dichloroacetate (in RVfib and in vivo)

90 is increased in insulin-resistant states and is reversed by diet or the insulin sensitizer pioglitazo

91 cell-autonomous mechanisms, in a manner that was reversed by dietary ascorbate.

92 Drug sensitivity was reversed by dimedone treatment, indicating Drk1 resp

93 These effects were reversed by donepezil treatment in adulthood.

94 gmentation of OrxA-induced glutamate release was reversed by DynA.

95 cells mimicked shd-knockdown defects, which were reversed by ectopic expression of EcR.B2 but not by

96 incides with a reduction in MYC/MYCN and can be reversed by ectopically restoring MYC activity.

97 All effects were reversed by EE.

98 lling (including glutamate receptors), which was reversed by EHMT1/2 inhibition.

99 sion after isolation, and that this loss can be reversed by engrafting cells back into an intact CNS

100 dly inhibited by ethanol, an effect that can be reversed by enhancing norepinephrine release.

101 ated ACE2 expression in mice, an effect that was reversed by exogenous IFN-beta administration, and I

102 -/-) tracheal ring non-responsiveness to sHA was reversed by exogenous TSG-6 addition.

103 the therapeutic effects of BOLA3 expression were reversed by exogenous glycine supplementation.

104 ot tips of dark-grown seedlings, which could be reversed by exposing plants to light.

105 Moreover, the MET can be reversed by expression of the EMT transcription facto

106 a slow rate of mitochondrial dynamics, which was reversed by expression of wild-type or catalytic-dea

107 d by repeated cocaine-cue pairings, but this is reversed by extinction training or by optogenetic ind

108 This effect was reversed by farnesyl transferase inhibitors and by t

109 on in the presence of DENV antibodies, which was reversed by FcgammaR blocking antibodies.

110 membrane transporters in T. sanguinis, which is reversed by fluoxetine exposure.

111 and repeated ACC optogenetic stimulation and is reversed by fluoxetine.

112 te survival and differentiation, which could be reversed by folate intake.

113 adherin and up-regulation of vimentin, which were reversed by FPR2 knock-down, implying the involveme

114 it pain, produce pain during neuropathy that is reversed by gabapentin.

115 ted phenotype driven by Rap1a(G12V) or Radil is reversed by Galphai1(Q204L), but not by WT Galphai1 e

116 The increases in ROS and root hairs in tt4 are reversed by genetic or chemical complementation.

117 The tt4 root phenotype was reversed by genetic and chemical complementation.

118 ion of Bcl6 increased MLL mRNA levels, which was reversed by genetic deletion and pharmacological inh

119 ostsynaptic-current events in mutants, which was reversed by GSK3beta inhibition genetically and phar

120 The formation of ANKRD9/IMPDH2 rods is reversed by guanosine, which restores ANKRD9 associat

121 agonist of apelin receptor, and its activity is reversed by heparin.

122 Ongoing LMWH and A6 hyperalgesia are reversed by HMWH.

123 ADP-Ribosylation is reversed by hydrolases that cleave the glycosidic bon

124 II and III generated by PA and this increase was reversed by hypothermia.

125 PBP1B lysis was reversed by: (i) reintroducing wild-type uppS, (ii)

126 Reductions in CXCL10 and T cell accumulation were reversed by IDH-C35, a specific inhibitor of mutant

127 entation caused by IRF2 downregulation could be reversed by IFN-stimulated induction of the transcrip

128 The effects of the FMD are reversed by IGF-1 treatment and recapitulated by PKA

129 and activation of stress kinases, which can be reversed by IL-22 treatment via the induction of meta

130 ated polyfunctional Th22-cell expansion that was reversed by IL-22 deletion or IL-6R inhibition.

131 sis in human and mouse sepsis monocytes, can be reversed by increasing H2O2 and sulfenylating SIRT6.

132 a hysteretic loop in Raman spectra, and can be reversed by increasing or decreasing the gate voltage

133 over lower nicotine content cigarettes could be reversed by increasing the response cost necessary to

134 preparation, we found that each form of LTF is reversed by inhibiting distinct isoforms of protein k

135 utophagy gene that is polymorphic in humans, is reversed by inhibiting necroptosis.

136 astrocytes but not neurons, and this ability was reversed by inhibiting NQO1.

137 s, leading to a proadhesive state, which can be reversed by inhibition of glycolysis.

138 However, this can be reversed by inhibition of inflammatory cytokine produ

139 rrelated with a luminal cell fate that could be reversed by inhibition of PDGFR activity.

140 This is reversed by inhibition of nerve growth factor (NGF)-m

141 attenuation of HR protein expression, which was reversed by inhibition of IL6 or JAK signaling.

142 This reduction was reversed by inhibition of TLR4.

143 ts in synaptic density and arborization that were reversed by inhibitors of protein kinase C, a downs

144 organoids and GBM surgical specimens, which was reversed by integrin alpha(v)beta(5) inhibition.

145 c to the overexpression of FAAH because they were reversed by intra-BLA administration of an FAAH inh

146 This phenotype was reversed by intranasal delivery of recombinant r-IL-

147 ly impacts mitochondrial function, which can be reversed by iron supplementation.

148 tive oxygen species, whereas such phenotypes were reversed by its product lactate or antioxidant N-ac

149 pared nerve injury model of neuropathic pain was reversed by ivermectin treatment.

150 tase, a catalytic subunit of telomerase that was reversed by JNK inhibition.

151 5) protein, and SMC de-differentiation which was reversed by KLF5 siRNA.

152 resulting from delta-catenin knockdown could be reversed by knockdown of autophagy-related 7 (ATG7),

153 to a reduction in Akt activation, which can be reversed by knocking down paxillin.

154 cells (SMCs); however, this phenotype could be reversed by knocking-down of 5-HTT or endothelial cel

155 ated diastolic and microvascular dysfunction are reversed by late-life exercise training.

156 r amyloidogenesis, and that these could both be reversed by LBP.

157 The patient's cellular abnormalities were reversed by lentiviral-mediated restoration of IRP2

158 ent in MTO enzymatic activity; these effects were reversed by lentivirus-mediated expression of wild-

159 sed mechanical and thermal hyperalgesia that was reversed by LI-1.

160 ed suicidal neuronal cell death, which could be reversed by lithium.

161 2R-induced paradoxical ChI excitation, which was reversed by mAChR inhibition.

162 This metabolic imbalance was reversed by mammalian target of rapamycin complex 1

163 -associated stem cell functional decline can be reversed by manipulating epigenetic factors that beco

164 sm, depended on infection history, and could be reversed by manipulation of the microbiota.

165 al allele-specific expression of Igf2, which were reversed by metformin.

166 AGS, HGC-27, and SGC-7901 cells, which could be reversed by miR-596 and miR-3620-3p.

167 Calcium bursts and hypersecretion are reversed by mutations in the ryanodine receptor but

168 These phenomena can be reversed by NaHS supplementation.

169 1 dimerization and activation, both of which are reversed by NEK1 kinase-mediated S336 phosphorylatio

170 Hepatotoxicity in the absence of RelA could be reversed by neutralization of tumor necrosis factor a

171 ent, and leukocyte extravasation with stress were reversed by nIL-1R1(-/-).

172 This switch away from fatty acid oxidation was reversed by nitrate treatment in hypoxic WT but not

173 The psoriatic skin and joint phenotypes are reversed by normalization of skin KLK6 levels and at

174 sue hyperoxia and that disease pathology can be reversed by normalization of excess oxygen, suggestin

175 NF-alpha-induced NFkappaB pathway activation was reversed by NOSTRIN.

176 sitive foci in response to DNA damage, which is reversed by nuclear TRADD expression.

177 duction of PD-1(+)CD38(hi) CD8(+) cells that is reversed by optimal priming.

178 We found that this self-renewal can be reversed by oral administration of a small molecule (

179 a competitive advantage to cells, which can be reversed by over-expression of the JNK kinase kinase

180 nd loss of self-renewal ability, which could be reversed by overexpressing mutant KRAS, demonstrating

181 egulation of transcription-and that this can be reversed by overexpression of an acetylation-defectiv

182 Each of these outcomes could be reversed by overexpression of DUOX1 or enhanced by sh

183 including keratin 1, keratin 10, and DSC-1, is reversed by p63 blockade.

184 These effects were reversed by peripheral CB(1) R antagonist JD5037 in

185 disease pathway and that this phenotype can be reversed by pharmacologic inhibition.

186 These age-dependent declines were reversed by pharmacological gap junction activation

187 ce bias and establish that the crosslink can be reversed by phosphine reduction of azide trigger grou

188 Both effects of ATP addition are reversed by phosphorylation of the RLC.

189 ylated nonmuscle myosin IIs (NM2s), and this is reversed by phosphorylation of the regulatory light c

190 lopment under chronic Pi deprivation but can be reversed by Pi resupply.

191 ith S. aureus experienced lethal sepsis that was reversed by PMN expansion mediated by injection of w

192 d to aberrant chemotactic signaling that can be reversed by post-injury injections of Plerixafor (AMD

193 stress in ifosfamide-injured bladder, which are reversed by pretreatment with IPSE.

194 s of Ro 61-8048 in monkeys, but not in rats, were reversed by pretreatment with a positive allosteric

195 h CF-associated mutations; these differences were reversed by pretreatment with NLRP3 inflammasome in

196 This inhibition can be reversed by PTCSC2, which acts as a suppressor.

197 with poor prognosis features that could not be reversed by radiotherapy doses up to 86 Gy.

198 These effects were reversed by rapamycin treatment.

199 mTOR activation on hepatic cleaved caspase 3 were reversed by rapamycin, an inhibitor of mTOR signali

200 -induced reduction of TNF secretion from DCs is reversed by receptor antagonists for EP2 and EP4, ind

201 e reduced tumor growth upon EHMT2 deficiency was reversed by recombinant DKK1 or LGK974, which also i

202 nockout cell line is impaired, and that this is reversed by reconstituting GNPTAB expression.

203 Such toxicity can be reversed by reducing circulating glucose levels by fa

204 rmore, age-associated microbiota changes can be reversed by reducing TNF using anti-TNF therapy.

205 n episode of acute kidney injury at 7 months was reversed by reducing the tacrolimus dose to 14 mg tw

206 aring loss-induced behavioral deficits could be reversed by reinstating normal inhibitory strength.

207 otein significantly increased, both of which were reversed by reintroducing NAT1 into the knockout ce

208 Ca(2+) store content observed after exercise was reversed by repetitive high-frequency stimulation, c

209 decreased BCRP expression, and this decrease was reversed by rescuing AhR expression.

210 uced by diverse anti-cancer drugs that could be reversed by restoration of wild-type PD-L1, but not m

211 larly impaired resolution profile that could be reversed by restoring miR-223 levels using a miR-223

212 plays pronounced locomotion defects that can be reversed by restoring the expression levels of a volt

213 ogramming transcription factor SOX2, and can be reversed by restoring TP53 and RB1 function or by inh

214 size and inhibited tumor growth, which could be reversed by restoring Yki/Yap activity.

215 he antiviral effects of BPIFB3 depletion can be reversed by RETREG1 silencing, suggesting a specific

216 KCTD13/CUL3 ubiquitin ligase substrate, and is reversed by RhoA inhibition, suggesting increased Rho

217 revealed that many of the gene changes in AD are reversed by riluzole.

218 rt1/mTORC2/Akt signaling, and the inhibition was reversed by rimonabant or JD5037 in wild-type but no

219 administration increased Rac1 activity which was reversed by Robo4 and Paxillin siRNA.

220 This conformational change is reversed by S-peptide association, which also stabili

221 OA caused alphaS inclusion formation, which was reversed by SCD inhibition.

222 as depression-like behaviors, both of which are reversed by selective serotonin reuptake inhibitors

223 maging cardiac effects of hyperglycaemia can be reversed by selective PKC inhibition.

224 ErbB4 ICD undergoes SUMO modification, which was reversed by sentrin-specific proteases (SENPs) 1, 2,

225 the DHHC family of palmitoyltransferases and is reversed by several acyl protein thioesterases(1,2).

226 The effect of lithium was reversed by SGK1-inhibitor GSK650394 (24 h 10 uM).

227 bleeding time, and time to thrombosis, which are reversed by silencing hepatocyte Plat Conversely, he

228 ly, ethanol-induced beta-arrestin2 reduction was reversed by siRNA-mediated MDM2 knockdown or proteas

229 of RvE1 on LTB4-induced [Ca(2+)](i) increase were reversed by siRNA for the RvE1 receptor, and the ac

230 migration of VEGFR1(+) myeloid cells, which were reversed by siRNA or pharmacological inhibition of

231 The oncogenic effects of nutrients were reversed by SIRT3, which deacetylates lys(101) acet

232 and decreased amplitude of mAHP of NAcS MSNs were reversed by SK channel activator 1-EBIO and mimicke

233 tiapoptotic protein B-cell lymphoma 2, which were reversed by small-molecule inhibitors.

234 This phenotype can be reversed by Snapin-enhanced retrograde transport, whi

235 drives resistance to BRAF inhibitors, which is reversed by SRF/MRTF inhibitors.

236 preserved hippocampal BDNF content and could be reversed by stimulation of BDNF signaling, suggesting

237 neurons of several neocortical regions that is reversed by subsequent E2 treatment in ovariectomized

238 ly incubated in high-glucose, an effect that was reversed by subsequently switching to low glucose me

239 cis-amide bond is sterically driven and can be reversed by substituting glycine for alanine in posit

240 This linkage is reversed by SUMO proteases, of which there are two in

241 multifractionated irradiation and could not be reversed by suppressing excessive end resection.

242 long-term BAT grafts, this deterioration can be reversed by swimming exercise because of sympathetic

243 ractivity and SNc hypoactivity that can also be reversed by systemic 5-HT2C receptor antagonism.

244 SSRI-induced motor deficits can be reversed by systemic or SNr-localized 5-HT2C receptor

245 pothesized that antimicrobial resistance can be reversed by targeting chromosomal non-essential genes

246 at pre-existing cardiac aging phenotypes can be reversed by targeting mitochondrial dysfunction and i

247 ed whether BBS pathology in Bbs2-/- mice can be reversed by targeting the underlying ciliary defect v

248 s that retain the APC protein; these effects are reversed by TGFB inhibitor.

249 and clicks after sciatic nerve injury, which was reversed by THC, CBD, and morphine.

250 These effects are reversed by the anti-oxidant N-Acetyl Cysteine.

251 , shows elevated autophagy levels, which can be reversed by the Acc1 inhibitor soraphen A.

252 inhibitor with a kinetic profile that cannot be reversed by the accumulation of any enzyme substrates

253 in APPswe/PS1DeltaE9 male mice, which could be reversed by the actin-polymerizing agent jasplakinoli

254 probability of channel activation, which can be reversed by the binding of alpha7 selective positive

255 b resistance mediated by ACK1 inhibition can be reversed by the EGFR inhibitor gefitinib.

256 thesized that this effect may preferentially be reversed by the HMAs decitabine and azacitidine.

257 of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling.

258 ice are hypercontractile, and this phenotype is reversed by the addition of recombinant BPIFA1.

259 13 display accelerated leaf senescence which is reversed by the ore1 mutation.

260 duced growth or regression, in a manner that is reversed by the pharmacological inhibitor of ferropto

261 ears safe and can reduce uGAG, although this is reversed by the presence of inhibitory ADA.

262 eleterious for LS function, a condition that is reversed by the presence of the lipopeptide SP-C.

263 ssociated with impaired MSC recruitment that is reversed by the topical administration of recombinant

264 l in D. discoideum and macrophages, and this was reversed by the addition of extracellular polyphosph

265 ession of multiple autophagic proteins which was reversed by the addition of hydroxychloroquine.

266 Beneficial ACE10 phenotype was reversed by the angiotensin-converting enzyme inhibi

267 However, WIN55212 inhibition was reversed by the CB1 receptor antagonist rimonabant i

268 a, because the swelling induced by metformin was reversed by the inhibition of mitochondrial calcium

269 taAR antagonist propranolol, and this effect was reversed by the mGlu3-negative allosteric modulator

270 O also raised ONOO(-) levels, an effect that was reversed by the ONOO(-) scavenger, FeTPPS [5,10,15,2

271 Sigma-1-mediated antihyperalgesia was reversed by the opioid antagonists naloxone and nalo

272 the fluorescent strain TJ375 (hsp-16.2::GFP) was reversed by the presence of both natural and semi-sy

273 In the absence of LRAP, PPi inhibition was reversed by the presence of etched enamel surfaces a

274 d endothelial to mesenchymal transition that was reversed by the pretreatment with TGF-beta neutraliz

275 p1 knockout-associated metastasis repression was reversed by the reintroduction of either WISP1 or sn

276 cal, peripheral activity in this test, which was reversed by the sigma(1)R agonist PRE-084.

277 ion and secretion in neurons, an effect that was reversed by the sirtuin 1-specific inhibitor sirtino

278 eration in HTori3 cells, whereas the effects were reversed by the overexpression of HECW1.

279 eased disruption of airway epithelium, which was reversed by therapeutic blockade of IFN-gamma.

280 We found that some of the alterations were reversed by these therapeutic interventions.

281 2 recruitment to and signaling of PAR1 could be reversed by TM2.

282 The effects of STIM1 knockdown were reversed by transduction of MIN6 cells with an aden

283 asymmetry in a sensorimotor (cylinder) test is reversed by transplantation.

284 sked whether these behavioral deficits could be reversed by treating one of the central impairments:

285 phenotypes of GABAA receptor mutant mice can be reversed by treatment with conventional antidepressan

286 and some breast cancer cell lines, and could be reversed by treatment with DNA methyltransferase inhi

287 ficantly impaired by tau aggregation and can be reversed by treatment with small-molecule regulators

288 in basal bladder cancer cell lines, and this is reversed by treatment with DNA methyltransferase inhi

289 is in organotypic coculture assays, and this is reversed by treatment with human recombinant (rh)EGFL

290 ormally found in portacaval anastomosis rats were reversed by treatment with ammonia-lowering therapy

291 IFN-gamma and IFN-alpha gene signatures that were reversed by treatment with EZH2 inhibitors.

292 ate that the charge transport anisotropy can be reversed by tuning the degree of polymer backbone ali

293 nces, until the early 2000s, when this trend was reversed by unconstrained functionals sacrificing ph

294 ion and enhances tumorigenicity, which could be reversed by Usp9x knockdown or inhibition.

295 Appetite suppression was reversed by vagotomy, suggesting involvement of MGL

296 ia-like behaviors, including the sleep loss, were reversed by valproate, and re-emerged when treatmen

297 lane orthogonal to the applied field and can be reversed by varying frequency.

298 ver induced by HFD is highly dynamic and can be reversed by weight loss.

299 esistance to continuous use of letrozole can be reversed by withdrawal and reintroduction of letrozol

300 current by approximately 60%, and the effect was reversed by yohimbine, confirming that it was mediat