ライフサイエンスコーパス: be reversed by

1 bly, the epigenetic repression of PDLIM2 can be reversed by 5-aza-2-deoxycytidine and vitamin D to su

2 rate that both pain and markers of ER stress are reversed by a chemical chaperone.

3 US$140 million (US$640 per household), could be reversed by a 71% reduction in phosphorus loading.

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

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

6 tivator of PKA, 8-bromo cAMP; (4) failure to be reversed by a protein translation inhibitor; (5) prim

7 tory avoidance training or reactivation, can be reversed by a reminder, including re-administration o

8 nce was only approximately 10 fold and could be reversed by a single point mutation, indicating that

9 or lipoylation of the target protein and can be reversed by a sirtuin-associated macrodomain protein.

10 stress invariably lead to pain behavior that is reversed by a chemical chaperone and an inhibitor of

11 ch affects numerous biological processes and is reversed by a class of enzymes known as deubiquitinas

12 ernal mitochondrial fusion delays PME, which is reversed by a fission defect in maternal mitochondria

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

14 ion and the associated drop in Arf6 activity were reversed by a knockdown of BRAG2.

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

16 In rat vessels, these effects were reversed by a phosphodiesterase type 5 inhibitor.

17 the medial prefrontal cortex; these changes were reversed by a single injection of ketamine (5 mg/kg

18 also occurred in Rag1(-/-) DeltaLC mice but was reversed by Ab-mediated ablation of NK cells.

19 ively impaired MSO task performance and this was reversed by ABT-418.

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

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

22 nhibition of PV interneurons in brain slices was reversed by activation of alpha4beta2 nAChRs.

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

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

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

26 nsive necrosis of ischemic skin flaps, which was reversed by adenoviral expression of ANKRD1, and del

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

28 The defect in the mucosal response was reversed by administering exogenous properdin to P(K

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

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

31 Cs and impaired vascular repair, which could be reversed by alpha4-integrin mutation.

32 the proneural gene Mash1, and such reduction was reversed by an RBM4-induced Numb isoform containing

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

34 e PI3K/AKT pathway and the expression of CSC were reversed by an miR-21 inhibitor.

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

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

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

38 t not late stages of adipogenesis, which can be reversed by antagonism of RA receptors or knockdown o

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

40 mmatory TH17 cell functionalities, which can be reversed by anti-IL-1beta treatment.

41 s in the rodent social defeat model that can be reversed by anti-inflammatory treatment with minocycl

42 thrombelastometric clotting patterns, which was reversed by antifibrinolytics and heparinase.

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

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

45 age, affects IgG opsonizing activity and can be reversed by antiviral therapy.

46 toantibodies in ApoE/LXR-beta-deficient mice was reversed by ApoA-I expression.

47 However, this can largely be reversed by appropriately controlling for expected li

48 effects of innate immune activation on CD36 were reversed by at least 50% by an EP2 antagonist, and

49 oration and PARP inhibitor resistance, which is reversed by ATM kinase inhibition.

50 d expression of proinflammatory genes, which was reversed by blockade of AMPK or ablation of adiponec

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

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

53 These effects can be reversed by blocking PD1 and TIM3, which increase the

54 myeloid cells present in blood, which could be reversed by blocking the CD39/CD73 and PD-1/PD-L1 axe

55 ultured with MDSCs against tumor cells could be reversed by blocking TIGIT or ROS production.

56 These effects were reversed by blocking TIGIT on NK cells or by inhibi

57 both PPAR-gamma and catalase activity, which are reversed by both ACEA and troglitazone.

58 oked GABA-mediated excitation of AVP neurons was reversed by bumetanide, and furosemide blocked AVP r

59 tophagosome accumulation in JNCL cells could be reversed by Ca(2+) chelation.

60 This effect was reversed by caffeine, whereby velocity was increased

61 n oxidative stress-induced DNA damage, which was reversed by catalase.

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

63 es against APAP hepatotoxicity, effects that were reversed by chloroquine to disrupt autophagy.

64 iated with increased autophagy, effects that were reversed by chloroquine treatment.

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

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

67 stase-induced emphysema, and this resistance was reversed by coadministration of a beta-catenin inhib

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

69 emale germlines and somatic cells, which can be reversed by codepleting Nup155.

70 turnover and the resulting thrombocytopenia were reversed by concomitant deletion of the gene encodi

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

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

73 These GMFG knockdown impaired effects could be reversed by cotransfection of GFP-tagged full-length

74 te injury in vivo and that this effect could be reversed by cotreatment with the OAT6 inhibitor probe

75 These effects were reversed by cotreatment with the Akt inhibitors per

76 late and sinusoidal endothelial cells, which was reversed by CPA and GCS21680.

77 ction of Cut7-driven microtubule sliding can be reversed by crowding it with non-Cut7 proteins.

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

79 mice with upregulated D2Rs (D2R-OEdev mice) are reversed by decreasing function of the striatopallid

80 nuation of Her2/Her3 signaling, and this can be reversed by deinduction of PIK3CA(H1047R) expression.

81 d by the m(6)A methylation "writers" and can be reversed by demethylases that serve as "erasers." In

82 This migratory inhibitory effect was reversed by depleting EPOR expression on HSPC.

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

84 lled and excessive alcohol drinking that can be reversed by directly activating the BDNF receptor, tr

85 xpressing iPLA2gamma, and the cytoprotection was reversed by dominant-negative ATF6.

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

87 ut the expected stimulation of Ca(2+) efflux is reversed by E2-stimulated tyrosine phosphorylation of

88 g for reduced CD4 T-cell survival, which can be reversed by early treatment initiation in HIV-1 infec

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

90 ecapitulated in bcl11ba-deficient zebrafish, were reversed by ectopic expression of functionally inta

91 brotic gene induction and growth arrest that were reversed by ectopic PPM1A expression.

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

93 The latter was reversed by ectopically transfecting the miRs, which

94 in presence of calcium (KD~2 pM), which can be reversed by EDTA allowing controlled "capture and rel

95 was synergistic, and their antiviral effect was reversed by either AAK1 or GAK overexpression.

96 sant bupropion, and this effect of bupropion was reversed by either D1 or D2 family antagonism.

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

98 escent phase of the pyl8-1pyl9 double mutant was reversed by exogenous IAA.

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

100 These effects of ASNS silencing were reversed by exogenous supplementation with asparagi

101 to Cyfip1's role in actin polymerization and are reversed by expression of a Cyfip1 mutant protein re

102 esistance in K. pneumoniae clinical isolates is reversed by expression of Gam.

103 orced renal cancer cell proliferation, which was reversed by expression of 3'UTR-less IGF-1R and cons

104 he development of certain illnesses that can be reversed by favorable alterations by probiotics.

105 e mice exhibit depressive-like behavior that is reversed by FGF2 administration.

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

107 ontraction when HLMCs were present, but this was reversed by fluticasone.

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

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

110 activity because of deletion of this region is reversed by further deletion of specific sequences in

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

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

113 Glutathionylation was reversed by glutaredoxin 1 (Grx1), and GSH plus Grx1

114 messenger RNA (mRNA) translation, which can be reversed by GSK3 protein kinase via phosphorylation o

115 These effects were reversed by GW-9662, an irreversible peroxisome pro

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

117 lete loss of the epithelial phenotype, which was reversed by Her2 or Wnt inhibition.

118 Ongoing LMWH and A6 hyperalgesia are reversed by HMWH.

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

120 The wecE shape defects were reversed by: (i) preventing initiation of ECA biosy

121 mbin time and tail-vein bleeding time, which were reversed by idarucizumab.

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

123 ions followed by Foxp3 downregulation, which was reversed by IFN-gamma deficiency.

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

125 erified in patient keratinocytes, where they were reversed by IL-36 blockade.

126 the Talpid3-binding protein, Rab8, which can be reversed by inactivating Mib1.

127 ely, some of the effects mediated by Ox-PAPC were reversed by increased NOTCH1 signaling, suggesting

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

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

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

131 f phosphofructokinase 1 (PFK-1), which could be reversed by inhibiting O-GlcNAcylation.

132 This therapeutic effect is reversed by inhibiting actin polymerization in the CD

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

134 Moreover, injury-induced tactile allodynia was reversed by inhibiting and exacerbated by exciting i

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

136 This is reversed by inhibition of Akt, mTOR or glucose metabo

137 d transdifferentiation, an effect that could be reversed by iNOS overexpression.

138 and progressed to blindness 8 mo after birth was reversed by intraocular injection of MTS-AAV express

139 These effects were reversed by introducing GIV but not a GIV mutant th

140 emodynamic and pulmonary vascular remodeling were reversed by iron replacement (ferric carboxymaltose

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

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

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

144 in IS and in diestrus female rats could not be reversed by ketamine.

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

146 -independent conditions, outcomes that could be reversed by knocking down focal adhesion kinase and d

147 glycolysis state, and that this binding can be reversed by knocking down GAPDH expression or by incr

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

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

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

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

152 t adipocyte-conditioned medium on BrCA cells was reversed by Lcn2 deletion.

153 e of twist and snail genes in TS Huh-7 cells were reversed by LDE225, a potent Smoothened antagonist.

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

155 ortening by difopein in G2019S-LRRK2 neurons was reversed by LRRK2 kinase inhibitors.

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

157 ation-driven sensitization to venetoclax can be reversed by metabolic supplementation with TCA cycle

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

159 Hyperlocomotion and impulsive behavior were reversed by methylphenidate, a psychostimulant comm

160 The effects of fluvastatin were reversed by mevalonic acid or geranylgeranyl pyroph

161 HHcy/HG-induced eNOS-pThr497/495 was reversed by micro-calpsiRNA and adenoviral transduce

162 triking, 60% increase in infarct size, which is reversed by microglial repopulation.

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

164 P14 proteolysis by the 26S proteasome, which was reversed by mutation in CULLIN1 (CUL1), suggesting a

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

166 nsity and NS1619-mediated relaxations, which were reversed by N-acetylcysteine.

167 ucose levels inhibited epicardial EMT, which was reversed by NAC treatment.

168 These effects were reversed by neutralization of stem cell factor (SCF

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

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

171 significant decrease in intraluminal pH that was reversed by omeprazole in fundic organoids and indic

172 ") from inflammatory or neuropathic pain can be reversed by opioid antagonists.

173 mary porcine alveolar macrophages could also be reversed by overexpression of miR-24-3p.

174 Importantly, compulsive alcohol intake was reversed by overexpression of the wild-type valine68

175 the sGCbeta1 proximal promoter, which could be reversed by panobinostat (LBH-589) treatment.

176 We found that SCA1 phenotypes could be reversed by partial suppression of human mutant ATXN1

177 d by mechanical silencing, an induction that is reversed by passive mechanical loading.

178 Inhibition was reversed by pertussis toxin (PTX), which blocks Galp

179 gp-dependent potentiated cytotoxicity, which was reversed by Pgp inhibition.

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

181 ociated with pathological endothelium, which is reversed by pharmacological inhibition of these nanos

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

183 berrant functional phenotype, and this could be reversed by phosphoinositide 3-kinase inhibitors.

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

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

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

187 The inhibitory effect of MQC was reversed by pretreatment with pertussis toxin, indic

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

189 These beneficial effects of gAD were reversed by pretreatment with AdipoR1 siRNA.

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

191 hibited PTH-stimulated cAMP responses, which was reversed by PTX.

192 esicle (SV) size, and that these alterations are reversed by Rab11 overexpression.

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

194 These effects were reversed by rapamycin treatment.

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

196 m growth factor deprivation; this effect can be reversed by re-expression of wild-type elafin but not

197 a on Deltaf(R) was not arousal-dependent but was reversed by reacidifying the blood (acetazolamide; 3

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

199 ssion of type 2 cytokine signaling, and they are reversed by recolonization of the antibiotic-treated

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

201 nsiveness because of excess nitric oxide can be reversed by reducing nitric oxide.

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

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

204 implying that the climate transition cannot be reversed by removing the additional forcing.

205 crements in kidney function, and this effect is reversed by renal transplantation.

206 e norovirus (MNoV) infection, an effect that was reversed by replenishment of the bacterial microbiot

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

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

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

210 tly, the direction of the voltage change can be reversed by reversing the direction of current, and t

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

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

213 These alterations induced by CUS were reversed by RNA interference (RNAi)-mediated prefro

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

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

216 The effect of SKF 81297 was reversed by SCH 23390 (an antagonist at D1/D5 recept

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

218 his so-called multidrug resistance (MDR) may be reversed by selective, potent, and nontoxic inhibitor

219 n allogeneic transplant recipients, where it was reversed by selective depletion of NKR-P1B(hi) NK ce

220 The beneficial effects were reversed by selective adenosine A1 agonist N6-cyclo

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

222 inhibitory effect of WNK4(Y1143F) could not be reversed by SGK1.

223 Cell adhesion was reversed by shedding of endothelial E-selectin, P-se

224 1 (UCP1) in primary human adipocytes, which was reversed by silencing of C/EBP homologous protein (C

225 cell leukemia sequence 1 (MCL-1), and could be reversed by simultaneous inhibition of MCL-1.

226 ls through ERK1/2 phosphorylation, which can be reversed by siRNA-mediated knockdown of uPA.

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

228 al fat and Th2 responses in Chi3l1 null mice were reversed by Sirt1 inhibition.

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

230 -dependent manner and that this effect could be reversed by small interfering RNA-mediated knockdown

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

232 These changes were reversed by soft matrix via extracellular signal-re

233 The TAPBPR/MHC-I interaction is reversed by specific peptides, related to their affin

234 ggerated hypoxic pulmonary hypertension that is reversed by subsequent iron administration.

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

236 imulation during allosensitization and could be reversed by sustained rapamycin treatment.

237 Avoiders exhibited thermal hyperalgesia that was reversed by systemic or intra-CeA injection of a CRF

238 hypothesized that this drug-drug interaction is reversed by taking erlotinib with the acidic beverage

239 severely reduced growth of the fungus, which was reversed by targeted deletion of the Dicer2-encoding

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

241 de of the energy supply, cytotoxic edema may be reversed by temporary blockade of Na(+) channels.

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

243 ted Ca(2+) entry in DeltakatG-infected cells are reversed by the Ca(2+) channel inhibitors 2-aminoeth

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

245 Protein methionine oxidation can be reversed by the action of stereospecific enzymes know

246 y of cells the increased threshold could not be reversed by the application of the reducing agent dit

247 ntly, TLR4-dependent Th17 polarization could be reversed by the enteral administration of retinoic ac

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

249 MbtA acetylation can be reversed by the NAD(+)-dependent DAc (deacetyltransfe

250 Importantly, these effects can be reversed by the PP2A activators FTY720 and AAL(s), or

251 ncing of DNA damage repair gene, Ogg1, could be reversed by the use of demethylating agents.

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

253 More notably, this high bone mass phenotype is reversed by the deletion of Oxtr in Oxtr(-/-):Avpr1al

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

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

256 Moreover, this modification is reversed by the sirtuin CobB.

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

258 ot rescue the phenotype, which, in contrast, is reversed by the upregulation of NRF2 by rosiglitazone

259 in B. distachyon leaf blades, an effect that was reversed by the addition of the FA biosynthesis inhi

260 irway surface liquid volume hyper-absorption was reversed by the BK opener mallotoxin and the clinica

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

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

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

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

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

266 tion of alkaline phosphatase, which in turn, was reversed by the phosphatase inhibitor vanadate.

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

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

269 e of IFN was dependent on circulating Ab and was reversed by the transgenic expression of the activat

270 aine-mediated reductions in synaptic contact were reversed by the beta-lactam antibiotic ceftriaxone.

271 The effects of DEX on human primary T cells were reversed by the GC receptor antagonist mifepristone

272 All these effects were reversed by the inhibition of oxidative stress usin

273 These effects were reversed by the recoupling agent 6-ketocholestanol

274 Notably, these effects were reversed by Tomo1 rescue and overexpression.

275 Only Ca-sensitising leak can be reversed by traditional RyR inhibitors such as tetrac

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

277 on/survival signals in FL-fibroblasts, which were reversed by transduction with Ad-PAI-1.

278 T-cell defects in tumors can be reversed by treating tumor-bearing mice with multival

279 The transformed phenotypes are reversed by treatment with the theilericidal drug bu

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

281 xiety and depressive-like behaviors that can be reversed by treatment with MAO inhibitors, as well as

282 y of mMDSC isolated from cancer patients can be reversed by treatment with TLR7/8 agonists, which ind

283 This potentiated adhesion was reversed by treatment with a PKA inhibitor, overexpr

284 The platelet overproduction phenotype was reversed by treatment with cyclin-dependent kinase 4

285 ased OC numbers and activity, an effect that was reversed by treatment with NB-DNJ.

286 This was reversed by treatment with the Itpkb product and PI3

287 ndle misorientation and NuMA mislocalization were reversed by treatment with a low dose of the microt

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

289 uced oxidative stress and insulin resistance were reversed by treatment with antioxidants.

290 guingly, aging-induced unfavorable responses were reversed by treatment with the autophagy inducer ra

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

292 sts from human venous leg ulcer patients can be reversed by ultrasound, demonstrating that the approa

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

294 Additionally, this effect was reversed by using inhibitory anti-MIP antibodies.

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

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

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

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

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

300 the major EMT inducer ZEB1, as these effects are reversed by ZEB1 knock-down by means of RNA interfer