ライフサイエンスコーパス: be restored by

1 th defect of the DeltatofI strain, LSUPB145, was restored by 1 microM N-octanoyl homoserine lactone (

2 ed impaired prohealing functions, which also were restored by 14S,21R-diHDHA treatment.

3 hed in a murine knock-out of SIGN-R1 and can be restored by a knock-in with human DC-SIGN.

4 a degraded working memory representation can be restored by a later cue.

5 cally destabilizing, but stability can often be restored by a second mutation that replaces the origi

6 tionality of the ZIF-8-protected biochip can be restored by a simple water-rinsing step, making it hi

7 nd the initial isolated Mo oxide species can be restored by a treatment with gas-phase oxygen.

8 Nonetheless, replicative fitness is restored by a compensatory mutation that restores par

9 Plasticity onset was restored by a homeoprotein Otx2, which binds the maj

10 H3 knockdown (KD) cells, and the suppression was restored by a re-introduction of the GOLPH3 gene.

11 lock host gene expression, but this activity was restored by a single amino acid substitution (K186E)

12 Such ability was restored by a single amino acid substitution in posi

13 her an N-terminal or a C-terminal truncation were restored by a methionine mutation at the putative g

14 nnot be counterbalanced by glutamine but can be restored by acetate.

15 t while ovariectomy abolished pLTF, it could be restored by acute systemic E2, or by intraspinal appl

16 modest loss in relaxation activity that can be restored by adding back Ca(2+).

17 A binding affinities but full activity could be restored by adding back Zn(2+).

18 ecute fusion; however, fusion function could be restored by adding known hyperfusogenic mutations to

19 Importantly, B cell function was restored by adding anti-TNF-alpha Ab to cultured B c

20 of SABRE at low substrate concentrations can be restored by addition of a suitable coordinating ligan

21 aphy and metal chelators, its activity could be restored by addition of excess ZnCl2 .

22 the proliferative defect of the cells could be restored by addition of exogenous IL-2 or blockade of

23 Spindle bipolarity is restored by addition of purified, recombinant Nup98 C

24 nd inhibition of aggrecan release by rhFGF18 was restored by addition of an antibody to Timp1.

25 Furthermore, the abnormal CUX1 expression was restored by addition of TGF-beta via the p38 mitogen

26 However, performance was restored by additional reversal training.

27 s at transcriptional level, and most of them were restored by ADMA.

28 defects in HO-1-deficient murine macrophages were restored by administration of CO.

29 These defects were restored by administration of the lung ILC product

30 Rag1(-/-) mice reduced pulmonary injury that was restored by adoptive transfer of 10(6) purified iNKT

31 n decreased food allergy symptoms that could be restored by adoptively transferred MMC9s.

32 ut also subsequent T-cell alterations, could be restored by adoptively transferring CCR8-expressing m

33 However, translocation could be restored by alpha-helical domains in a position- and

34 ral life cycle; however, replicative fitness was restored by an additional change (V403A) within the

35 ted Th2-mediated lung inflammation, and this was restored by antagonizing miR-1.

36 nnel protein in SZ neocortex, a deficit that is restored by APDs.

37 ltured myotubes from Stac3 mutant mice could be restored by application of 4-chloro-m-cresol, a ryano

38 ur in the absence of maturing leaves but can be restored by application of C(19)-GAs, identifying the

39 GABA is more depolarized in mutant mice, but is restored by application of the NKCC1 inhibitor bumeta

40 The assembly of all three substrates can be restored by artificially tethering a region of the su

41 mpletely eliminates localized silencing, but is restored by artificially targeting Fob1 or Sir2 as Ga

42 ference between placebo and nonsmoker groups were restored (by at least 50%) toward nonsmoker levels

43 e dopaminergic therapy), but this connection was restored by atomoxetine.

44 ty was strongly reduced under -DIF but could be restored by auxin application in an ACC Synthase-depe

45 CC Synthase was reduced under -DIF but could be restored by auxin application.

46 TORC2-Ypk2 interaction was reduced and could be restored by AVO1 overexpression, highlighting the imp

47 d context-dependent sensitization, could not be restored by blocking Ca(2+)-permeable AMPARs.

48 nd IFN-gamma production that could partially be restored by blocking GITR on NK cells, thus indicatin

49 This could be restored by blocking inhibitory pathways and, in part

50 xhibit reduced migratory capacity, which can be restored by blocking netrin-1.

51 n the basal part of the hypocotyl under -DIF was restored by both 1-aminocyclopropane-1-carboxylic ac

52 Normal kidney size was restored by breeding the hypomorphic mutant with a r

53 the expression of a set of SPCH target genes was restored by BRs.

54 c butyrate and HIF expression, both of which are restored by butyrate supplementation.

55 wer; these changes in mitochondrial function were restored by CaMKIIdelta deletion.

56 n expression in a hypomorphic lau allele can be restored by cAMP agonists.

57 Both trimer and tetramer formations were restored by cardiolipin.

58 of pancreatic cancer cells, which could not be restored by caveolin-1-rescue construct.

59 Moreover, this methylribosylation defect was restored by cellular complementation with normal tRN

60 ed in a propeptide-deletion mutant but could be restored by co-expression of the propeptide in trans

61 t1 function abrogated by Ssn6 overexpression is restored by co-overexpression of Mth1.

62 as also impaired in the pain model but could be restored by coapplication of VU0360172 and ACEA.

63 ably, synaptic activity in these neurons can be restored by coculturing them with normal rat hippocam

64 ice had a very low degree of sialitis, which was restored by colonization with select microbial linea

65 he activities of the mutated HCV IRESs could be restored by compensatory mutations in the 18S rRNA.

66 These phenotypes are restored by complementation with a plasmid expressin

67 fection; log rank test), and virulence could be restored by complementation of the wecA gene in trans

68 utant S. exfoliatus DeltapenR ZD27 but could be restored by complementation with either penR or pntR.

69 iptional regulation of the flagellins, which was restored by complementation with wild type pseB or F

70 When alpha3 receptors were restored by complementation using domains with and

71 ly transcribed genes in the luxS mutant, 209 were restored by complementation with a gene encoding th

72 ase in glycosylinositolphosphoceramides that were restored by complementation with a wild-type copy o

73 roduction of flagellin and swarming motility were restored by complementation with znuCB in trans.

74 Shape defects were restored by complementation.

75 Defective NKT development was restored by compound deficiency of MALT1, a key down

76 hematopoietic stem cell self-renewal, which is restored by concomitant deletion of Tet2, a gene comm

77 henocopied by HSC70 RNAi depletion and could be restored by conditionally increasing HSC70 abundance.

78 d ESX-1 component, substrate gene expression was restored by constitutive, but not native, expression

79 educed the half-life of COX-2 protein, which was restored by COX-2 enzyme inhibitors but not by prote

80 n as HCRTR2), but normal OX2R expression can be restored by Cre recombinase.

81 release function of impaired primary clones was restored by creating a G76W substitution.

82 gic responsiveness in dyssynchronous HF that are restored by CRT.

83 However, selectivity was restored by crude cell lysate or purified G-actin, w

84 are defective in pre-miRNA processing which is restored by cyclin D1a rescue.

85 After mitochondrial MEND blockade, MEND is restored by cytoplasmic acyl CoA or CoA.

86 Fusion could be restored by decreasing the activation energy of refol

87 ed a dramatic loss of acetylation that could be restored by deleting the enzyme that degrades acetyl

88 n (RFP) expression from mutated T-strand can be restored by delivery of synthetic DNA and RNA oligonu

89 The efficacy of MPL monotherapy was restored by depletion of T regulatory cells, whereas

90 se reduces serum cholesterol levels that can be restored by dietary cholesterol.

91 d emission of QDs through the FRET mechanism is restored by displacing the dextran from Con A.

92 TRIM27 protein levels were restored by disrupting the RING domain of ICP0 or b

93 ions 92 and 99, the function of which cannot be restored by disulfide bond reduction after cysteine m

94 stem functions, and the source of income can be restored by diversification with nitrogen-fixing tree

95 Consistent with this, spectral fidelity was restored by dividing the mass scan range (initially

96 at normal excitability and NMDA currents had been restored by early adolescence.

97 of ASCIZ, and normal B cell development can be restored by ectopic Dynll1 expression.

98 The adherence of the ctpA mutant could be restored by ectopic expression of the paralogous pilA

99 defects and loss of proliferation that could be restored by ectopic expression of the yeast NADH dehy

100 in Zbtb24 homozygous mutant mESCs, which can be restored by ectopic ZBTB24 expression.

101 abrogated by genetic deletion of TRIM21 and was restored by ectopic expression of TRIM21.

102 ession in D1:0900 h ovaries, but the decline was restored by either FSH or LH replacement on D4 after

103 iation of Itch(-/-) T cells into T(FH) cells was restored by enforced expression of Bcl-6.

104 ir capacity for functional activation, which is restored by enhancing structural support of the ECM.

105 Levels of these esters, however, were restored by ethylene treatment (100ppm, 24h) before

106 had reduced functional capacity, which could be restored by exogenous IL-10.

107 th in vivo and in vitro, which could largely be restored by exogenous ORM1.

108 IL-1Ra secretion is restored by exogenous antioxidants that oppose oxidat

109 exhibited impaired chemotaxis to CCL19 that was restored by exogenous leukotriene C4 .

110 monary inflammation in SM22-Adam17(-/-) mice was restored by exogenous TGFalpha application, confirmi

111 The site specificity of 9NL27 may be restored by expanding its "recognition site" from ATG

112 Fructification and stalk formation were restored by exposing DgcA-null slugs to wild-type s

113 Defective platelet matrix interaction can be restored by exposure to WT plasma or to purified VWF

114 oxylated LAO surface; interface conductivity is restored by exposure to light, which induces reproton

115 Normal growth characteristics can be restored by expressing the genes for OLE and OAP from

116 us to oxidative stresses, and the resistance was restored by expressing a C25S mutant copy of cymR.

117 d by c-di-AMP, and high aspartate levels can be restored by expression of a c-di-AMP-insensitive LlPC

118 This growth-retarded phenotype was restored by expression of either wildtype PSI1 or PS

119 Leukemogenesis was restored by expression of GAB2 but not by GAB2 mutan

120 d independent of the ammonium conditions and was restored by expression of the wild-type 65 kDa encod

121 ing observed in stable PREX1 knockdown cells was restored by expression of wild-type but not GEF-dead

122 a chemical inhibitor of PNKP, but resistance was restored by expression of wild-type SHP-1 in these c

123 LTP was restored by expression of wild-type Syt7 but not of

124 r abnormalities in patient dermal fibroblast were restored by expression of WT NSMCE2, but not a muta

125 pment is deficient in germ-free mice and can be restored by feeding TLR2 agonists that activate T cel

126 Interestingly, flavivirus replication was restored by folinic acid, a thymidine precursor, in

127 NDRs can be restored by forced expression of OCT4 in somatic cell

128 biologic function in cells, even when levels were restored by forced overexpression.

129 esponse in human HD neural stem cells, which was restored by genetic correction of the disease-causin

130 c mice, sparse granule cell activation could be restored by glutamine application, implicating compro

131 er a severe dopamine depletion and could not be restored by grafted serotonergic neurons.

132 ces its electron-donating ability, which can be restored by halide binding.

133 Growth of the DeltaluxS(Hp) mutant was restored by homocysteine or cystathionine and growth

134 In addition, NOV expression is restored by hormone-deprivation therapies in mice and

135 on, colony formation and invasiveness, which were restored by human PINK1 overexpression.

136 surface expression of the misfolded mutants was restored by (i) introducing second site suppressor m

137 increased CRF mRNA expression induced by ARS were restored by icv-injection of OXT.

138 nked pathological conditions in CGD that can be restored by IL-1 receptor blockade.

139 passive anaphylaxis in IL-10(-/-) mice could be restored by IL-10 administration.

140 ed metabolic switch to glycolysis, which can be restored by IL-2.

141 also impaired in mouse Il2(-/-) T cells but was restored by IL-12Rbeta2 expression.

142 0% deficit in (18)F-FDG concentration, which was restored by iMAR processing, indicating that metal a

143 during translation itself as GFP expression is restored by increased tRNA levels or by non-native tR

144 ng rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitme

145 LTP in adult NCAM-deficient (NCAM(-/-)) mice is restored by increasing the activity of the NMDA subty

146 Bacterial adherence was restored by incubation of postextracted cells with P

147 31.3% reduction in phagocytic capacity that was restored by inducing HO-1 activity or supplementing

148 A1 mutant is attenuated for virulence, which is restored by infection in gp91Phox(-/-) mice.

149 played reduced proliferative capacity, which was restored by inhibiting TGF-beta signaling.

150 kinetochore-MTs and that stable attachments are restored by inhibition of Aurora A kinase at spindle

151 bits insulin-induced vasodilation, which can be restored by inhibition of JNK.

152 g a reduction in PSaV replication that could be restored by inhibition of nitric oxide synthase via t

153 These changes were restored by inhibition of gamma-secretase or promot

154 T cell dysfunction, and proper function can be restored by inhibitory therapies to enhance parasite

155 istamine-induced venular permeability, which was restored by injecting anti-P-selectin mAb to prevent

156 Seizures were restored by injecting either glucose (metabolic rev

157 tating single conserved amino acids, but can be restored by insertion of the corresponding motif of A

158 e Th1 differentiation in an aged environment is restored by interleukin (IL)-6 blockade or IL-6 defic

159 The behavioural response to stress can be restored by intra-amygdala injection of neuropsin int

160 utrophil recruitment and bacterial clearance were restored by intranasal administration of recombinan

161 ost in plasminogen-deficient mice, but could be restored by intravenous injection of plasminogen.

162 low amounts of surface TG2, but binding can be restored by introduction of TG2 expressed on a plasmi

163 ance to sensitive cells and that sensitivity was restored by introduction of a WDR85 cDNA into resist

164 intracellular redox dysregulation, which can be restored by Keap1 inhibition.

165 nfirmed deficient Golgi glycosylation, which was restored by lentiviral transduction with wild-type T

166 function of NK cells from patients with pDGS were restored by lentiviral transduction of CrkL.

167 due to a lack of proper leptin signaling and was restored by leptin treatment.

168 and slower growth velocities, both of which were restored by low concentrations of the microtubule-d

169 The downregulated miR-188-3p expression was restored by MAGL inhibition.

170 efficient actomyosin complex, and (ii) could be restored by manipulating myosin expression.

171 as a nonfunctional lectin pathway, which can be restored by MASP-1, implying that this component is c

172 Both glycosylation of gB and viral growth were restored by medium supplementation with either UDP-

173 sion of thiourea-appended naphthalimides can be restored by metal binding and that metal affinity and

174 Has2) was elevated by a loss of Smpd3, which was restored by MK2206.

175 attenuated by knocking out WNT5A, but could be restored by MMP7 overexpression.

176 tion of wild type (WT) GFP-NM II, but cannot be restored by motor mutant NM II.

177 e decreased in the absence of Rac1, and both were restored by mutation of NF2/merlin.

178 levels of ER genes in ibm1 and edm2 mutants are restored by mutations in the genes encoding the hist

179 sed AMPK phosphorylation and activity, which was restored by NaHS.

180 atory cytokine production that can, in part, be restored by neutralizing proinflammatory cytokines.

181 We show that the Esx-1 function was restored by nonsense suppression.

182 significantly reduced in DM patients, which was restored by ONOO(-) scavenger, iron-(III)-tetrakis(N

183 tion and long-term humoral immunity can also be restored by OSGE treatment of CD4 T cells prior to ad

184 ration and invasion, and this inhibition can be restored by overexpressing the short interference RNA

185 and baseline expression of ECM targets could be restored by overexpression of miR-29.

186 also occurs in Msx2 null mutant mice, which is restored by overexpression of the receptor activator

187 ble to undergo electrotaxis, and this defect is restored by overexpression of wild-type kindlin-1 but

188 Production of infectious HCV was restored by overexpression of an shRNA-resistant DCI

189 Swarming in the waaL mutant was restored by overexpression of flhDC in trans or by a

190 nst the GPA, we show that resistance in adf3 was restored by overexpression of the related ADF4 and t

191 tient induced pluripotent stem cells (iPSCs) was restored by partial ASM inhibition.

192 Sensorimotor functions are restored by peripheral nerve regeneration with great

193 y reduced in the Cln3(Deltaex7/8) brain, and were restored by PF-06266047.

194 icacy, and antitumor CD8(+) T cell responses were restored by pharmacologic inhibition of IDO.

195 Spinous and granular differentiation were restored by pharmacologic inhibition of MAPK/ERK ki

196 he inflammatory chemokines CXCL9-12 that can be restored by pharmacological blockade of the enzymatic

197 tion activity of CMS rats, and this decrease is restored by pharmacologically attenuating the activit

198 substitutions at multiple residues and could be restored by phosphomimetic Asp substitutions at these

199 Wild-type levels are restored by photoreceptor-specific expression of Car

200 differentiation along the gammadelta-lineage was restored by pre-TCR coexpression, which induced grea

201 -3p and Rad51 expression in response to LDIR was restored by pretreatment with N-acetyl-cyctein.

202 e inductive interaction, MS-derived BWMs can be restored by preventing zygotic MOM-2 expression, whic

203 ess relative to wild-type cells, which could be restored by proline or the corresponding genetic comp

204 of the alpha(V)beta(3)-integrin to OPN could be restored by proteolytic removal of the C terminus by

205 GF-induced VEGFR2 phosphorylation, which can be restored by PTP1B siRNA.

206 scission in these hammerhead ribozymes could be restored by putative t2M/t4M refolding of stem second

207 mpared with wild type, and this defect could be restored by putrescine in a PlaP-dependent manner.

208 N3A1 abolished stimulation by IPP that could be restored by re-expression of BTN3A1 but not by BTN3A2

209 al adhesion kinase and paxillin, which could be restored by re-expression of GIT1.

210 e found that H3K4me1, but not H3K27ac, could be restored by re-expression of MyoD1 in MyoD1(-/-) myob

211 cantly in all of these cell models and could be restored by re-expression of WT c-Abl.

212 In Tpcn1/2(-/-) cells, NAADP sensitivity was restored by re-expressing wild-type TPCs, but not by

213 (2+)]mito uptake capacity of Bcl-xL-KO cells was restored by re-expression of mitochondrially targete

214 This survival was restored by re-expression of wild-type Ufm1 with con

215 However, activity could be restored by reacting aqueous OXA-24 with a large exce

216 limb regenerative capacity of failed stumps was restored by reamputation once endogenous macrophage

217 s approach assumes that organ physiology can be restored by rebalancing mitochondrial dynamics, but t

218 Serum resistance could be restored by recombinant PKF, which was shown to reduc

219 Normal levels of autophosphorylation are restored by reconstituting wild type IQGAP1 and enha

220 etion of the empABC operon, a phenotype that was restored by reconstituting in situ the empA gene.

221 ood allergy and anaphylaxis, and Th2 priming was restored by reconstitution with il4(+/+) or il4(-/-)

222 However, chemo-taxis can be restored by reducing adhesion.

223 Hindlimb locomotion was restored by reestablished integrity of submidbrain c

224 MRLC) diphosphorylation in HeLa cells, which was restored by reexpression of small interfering RNA-re

225 growth and developmental defects that cannot be restored by reintroducing lsp.

226 Activation could be restored by reintroducing multiple repeats of the 12-

227 m formation and host colonization that could be restored by reintroducing the SE sequence into its na

228 The hypoxia escape response was restored by reintroducing either Gyc-89Da or Gyc-89D

229 use pHFD abolishes NMDA-LTD, a function that is restored by RELN overexpression.

230 Here, we report that these deficits are restored by repeated, systemic administration of AMP

231 microglial necroptosis), and neuronal death was restored by rescue of microglia with necrostatin-1.

232 the degranulation defect in patient T cells were restored by retroviral reconstitution.

233 We next showed that scale invariance can be restored by returning the running wheels.

234 ity was lost in L-NAME-treated arteries, but was restored by Rho kinase inhibition or statin treatmen

235 ippocampal respiration-coupled rhythm, which was restored by rhythmic delivery of air puffs into the

236 Completion of meiosis I could be restored by ROS scavengers, showing this is the prima

237 ecreased isolated myocyte contraction, which was restored by rottlerin treatment.

238 protein unstable, but the protein stability was restored by SaeQ, suggesting a possible SaeQ-SaeS in

239 NOS, neuronal NOS, and VEGF, an effect that was restored by seeding ADCSs on the SIS graft.

240 A binding activity of full-length SaeR could be restored by sensor kinase SaeS-induced phosphorylatio

241 die during embryogenesis, although viability is restored by simultaneous deletion of the IRP2, but no

242 (LMO4 KO) was severely compromised but could be restored by single-cell overexpression of LMO4.

243 potentials was absent in SK2-S only mice and was restored by SK2-L re-expression.

244 pamine signaling only in the dorsal striatum was restored by subjecting the mice to instrumental trai

245 activity, but their enzymatic function could be restored by subsequent incubation at 37 degrees C.

246 The disturbed eating behavior can be restored by substitution with the leptin analog metre

247 induced recessive mutant tup5-1, root growth was restored by supplementation with arginine and its me

248 nding Chlamydomonas reinhardtii mutant cgld1 was restored by supplementation with Mn(2+), but not Ca(

249 er, Mga2p processing and BMV RNA replication are restored by supplementing free ubiquitin, which is d

250 evels of cytotoxic-mediator genes, which can be restored by supplying recombinant IL-17A in vitro and

251 ing starvation-induced GSC loss, GSC numbers are restored by symmetric renewals.

252 circulating AM levels in Adm(AM+/Delta) mice were restored by systemic peptide delivery.

253 of TIM-3 and regulatory cytokines, and this is restored by T-cell-specific CEACAM1 expression.

254 observed in FIH-1-overexpressing HCEKs could be restored by the addition of c-kit ligand.

255 owed impaired antifungal activity that could be restored by the addition of extracellular S1P.

256 s not required, because memory formation can be restored by the addition of short-lived, Ag-pulsed AP

257 the cytostatic activity of gemcitabine could be restored by the co-administration of tetrahydrouridin

258 It would be restored by the development of antibiotics to which b

259 Signaling via GS domain ALK2 mutants could be restored by the expression of either BMP type II rece

260 pressive function of Itk deficient cells can be restored by the expression of the transcription facto

261 ses chemotherapy-induced cell death that can be restored by the inhibition of ABCG2.

262 VZV-CMI declines greatly with aging, but can be restored by the licensed zoster vaccine.

263 n these cells DFF40/CAD cytosolic levels can be restored by the overexpression of their own endonucle

264 ratory function in hem15Delta cells can also be restored by the presence of a heterologous plasma mem

265 bit markedly reduced growth rates, which can be restored by the selective application of protein synt

266 tyrosine kinase-induced WASP activation, and is restored by the activation of SH2 domain-containing i

267 ation of TFIIB E62K with the PMA1 terminator is restored by the Ssl2 H508R suppressor.

268 decrease of breast cancer cell invasion that was restored by the addition of non-cleavable proNGF.

269 As mitochondrial ATP production was restored by the addition of reductants, these findin

270 ermal strips of des1 mutants, an effect that was restored by the application of exogenous H2S.

271 liver induced by a model of high-fat feeding was restored by the hepatic lipid control of CNS glycine

272 gradation of a ubiquitin-dependent substrate was restored by the rpt2(E301K) mutation, indicating tha

273 in cells nor Ca(2+)-triggered SUV-GUV fusion was restored by the Syt1 mutants.

274 In each mutant strain, biofilm formation was restored by trans complementation of the aspA deleti

275 Function of DCs could be restored by transfer of Ig irrespective of antigen sp

276 cells, and ALDH activity in CRBPII(-/-) DCs was restored by transfer to a wild-type recipient.

277 Protection against infection was restored by transferring ILCs into Raggammac(-/-) mi

278 he l-Glu sensitivity of the mekk1/2/3 mutant was restored by transformation with a construct carrying

279 is and reduction of proliferation rates that are restored by transient expression of miR-155.

280 128 cells at the early symptomatic stage but was restored by treating the slices with tetrabenazine.

281 hy control levels of synaptic activity could be restored by treatment of ChAc neurons with the F-acti

282 Bulk chromatin acetylation can be restored by treatment of NMC cells with histone deace

283 e functionality of beta1 and beta2 integrins was restored by treatment of CF monocytes with the CFTR-

284 ependent signaling to promote lipolysis, and was restored by treatment with purified human ANGPTL4.

285 The dynamics of autophagy was restored by treatment with the PLD product, phosphat

286 NPY exhibited impaired HSPC trafficking that was restored by treatment with truncated NPY.

287 Wild-type rates of 2-AG oxygenation were restored by treatment of H388YmPGHS-2 with hydroper

288 d that kidney genes deregulated after injury were restored by treatment with mesenchymal stromal cell

289 d with impairment of angiogenic response and were restored by treatment with the peroxynitrite scaven

290 ial hypoxia and Salmonella restriction could be restored by tributyrin treatment.

291 rogated myofibroblast differentiation, which was restored by TRPV4 reintroduction.

292 RILP expression was restored by up-regulation of the transcription facto

293 idneys after hemorrhagic shock/resuscitation was restored by valproic acid treatment.

294 Interestingly, sensitization could also be restored by virus-mediated inactivation of NR1 in all

295 and extinction learning in ASIC1a null mice were restored by virus-mediated expression of wild-type

296 ciency driven by procalcific stressors could be restored by vitamin D receptor activators, in vitro a

297 ed inhibition of 3' processing, all of which is restored by wild-type-p53 expression.

298 to FLT3-ITD inhibition by crenolanib, which was restored by wild-type (WT)-LC3, but not mutants of L

299 ipid raft-associated inhibitor of Src, which was restored by wild-type GRIM-19.

300 Normal function was restored by wild-type TTC7A expression or addition o