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

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

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

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

6 The original 3D layered structure can be restored by a solvothermal process with pyridine, so

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

8 erations are reverted when membrane fluidity is restored by a chemical fluidizer.

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

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

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

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

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

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

15 n airway smooth muscle cell migration, which was restored by Abi1 rescue.

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

17 Current through these channels could not be restored by activators of TASK-1 channels.

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

19 ology, one mechanistic pathway to plasticity was restored by acute, adult anti-inflammatory treatment

20 , impaired in vitro serum control of KP that was restored by adding healthy serum.

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

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

23 ell lines of affected individuals that could be restored by addition of heparin, a GAG similar to hep

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

25 med Delta68-87) in primary human fibroblasts was restored by addition of ferric nitrate.

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 CL22 levels in lymphoid organs, and this can be restored by adoptive transfer of wild-type T cells or

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

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

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

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

34 colonic ACE2 expression in active CD and UC were restored by anti-cytokine therapy, most notably in

35 uman IEC or mouse enteroid monolayers, which were restored by anti-IL6.

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 , the 22q11DS calcium abnormality could also be restored by application of antipsychotics.

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

40 BMPRII expression was restored by Arf6 siRNA, Arf inhibitor Sec7 inhibitor

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

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

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

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

45 e-like structures from which native proteins are restored by ATP-dependent chaperones such as Hsp70 f

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

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

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

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

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

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

52 progenitor cell population of the retina can be restored by blocking the MAPK signaling pathway throu

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

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

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

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

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

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

59 Both trimer and tetramer formations were restored by cardiolipin.

60 impaired ciliogenesis in RPE-1 cells, which was restored by catalytically active ADAMTS9 or ADAMTS20

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

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

63 The reduced adhesion could be restored by chromosomal complementation.

64 ase (FBP1), epigenetically repressed in HCC, was restored by CM-272.

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

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

67 ated cell surface expression, but expression was restored by co-expression with the beta1-subunit.

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

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

70 lymphocytes in germ-free (GF) neonatal mice is restored by colonization with a human commensal, Bact

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

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

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

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

75 Shape defects were restored by complementation.

76 ATPSc methylation was restored by complementing the KO cells with enzymati

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

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

79 n of reconsolidation blockers, both of which were restored by concomitant theta burst stimulation of

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

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

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

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

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

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

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

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

88 emorrhage were observed at 1 and 7 days, and were restored by day 28 post-blast.

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

90 ve advantage of TLR-TRAF6-primed HSPCs could be restored by deletion of A20 or inhibition of the nonc

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

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

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

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

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

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

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

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

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

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

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

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

103 activation, and myocyte growth, all of which were restored by ectopic RHEB expression.

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

105 the trans-Golgi and generated less T3, which was restored by eliminating ER stress with the chemical

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

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

108 Virulence of the LdHSP78+/- strain was restored by episomal addition of the LdHSP78 gene.

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

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

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

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

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

114 ector of cytosolic phospholipase A(2), which was restored by exogenous PGH(2), implying that the effe

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

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

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

118 Virulence was restored by expressing atxA from an alternative, PTS

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

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

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

122 In contrast, ACh-mediated vasoconstriction was restored by expression of RGS2 WT, D40Y, and R44H bu

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

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

125 PM cholesterol was restored by expression of wild-type ORP1S or a phosp

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

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

128 n had lower density and reduced fitness that were restored by fecal microbiota transplantation.

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

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

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

132 tion into particles, yet incorporation could be restored by further truncating the CT or by using a c

133 d with a thymidine-kinase promoter but could be restored by fusion with the 100 bp minimum transcript

134 of systemic lupus erythematosus patients can be restored by GA stimulation.

135 in reduced axonal mitochondrial content that is restored by genetic inhibition of AMPK and autophagy.

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

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

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

139 scarce in germ-free mice, but their presence was restored by gut re-colonization.

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

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

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

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

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

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

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

147 0% deficit in (18)F-FDG concentration, which was restored by iMAR processing, indicating that metal a

148 overed and resistance to acute infection can be restored by immunization with highly attenuated vacci

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

150 ly compromised in a cdkg1-1 mutant, they can be restored by increasing the number of recombination in

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

152 31.3% reduction in phagocytic capacity that was restored by inducing HO-1 activity or supplementing

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

154 The 5-HT(2A) -induced Q pathway was restored by inhibiting PKA activity (Rp-8-Br-cAMPS).

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

156 NIH 3T3 fibroblasts expressing progerin, but were restored by inhibiting protein farnesylation.

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

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

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

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

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

162 Replication of the NS2/C113S mutant was restored by inserting an encephalomyocarditis virus

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

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

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

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

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

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

169 Capsid stability was restored by introduction of specific changes to the

170 f VZV IE62 and ORF63 suppressed by IFN-gamma was restored by JAK1 inhibitor treatment, indicating tha

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

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

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

174 ocked cytokine-induced FBGC formation, which was restored by lentivirus-mediated TRPV4 reintroduction

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

176 Importantly, these phenotypes can be restored by LINC00346 re-expression in KO cells (i.e.

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

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

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

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

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

182 TX decreases cortical Bdnf expression, which is restored by microglial depletion.

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

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

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

186 l replication and that the activity of UBE2N is restored by MvcA, an ortholog of MavC (50% identity)

187 spiration rhythms, and late evening activity are restored by NAD(+) repletion to youthful levels with

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

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

190 MP-triggered immunity (PTI) responses, which are restored by NIK1 reintroduction.

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

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

193 Remarkably, working memory deficits were restored by optogenetic stimulation of astrocytes w

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

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

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

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

198 etration and melanin production in DeltaSho1 were restored by overexpression of Vst50, suggesting tha

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

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

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

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

203 K1- and PARK2-linked Parkinson's disease and was restored by phosphomimetic ubiquitin in cells with r

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

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

206 -3p and Rad51 expression in response to LDIR was restored by pretreatment with N-acetyl-cyctein.

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

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

209 Replication of the mutant virus was restored by pseudoreversion (A287V) or adaptive muta

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

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

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

213 as not stimulated by DMB supplementation but was restored by raising pH to neutral.

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

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

216 sed BH3-only BIM and BIK proteins that could be restored by re-expression of PD-L1; re-introduction o

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

218 his structure-mediated regulation, which can be restored by re-introducing base-paired structures of

219 ncreased ICSA at high doses of nicotine that is restored by re-expression of beta4*nAChRs in the MHb-

220 d in a loss of antibacterial activity, which was restored by re-addition of GML.

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

222 (2+)]mito uptake capacity of Bcl-xL-KO cells was restored by re-expression of mitochondrially targete

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

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

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

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

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

228 Hindlimb locomotion was restored by reestablished integrity of submidbrain c

229 l TLR responses in PI4KIIalpha-deficient DCs are restored by reexpression of wild-type PI4KIIalpha, b

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

231 Myelin can be restored by regenerating oligodendrocytes from reside

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

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

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

235 deficient JGTA-S1 had reduced fitness, which was restored by reintroducing P. stutzeri JGTA-S1 coloni

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

237 re recombination-defective, but activity can be restored by replacing patches of Tn3 resolvase R inte

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

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

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

241 educed in the presence of I(47,) which could be restored by rhgalectin-3.

242 uction in cell migration and invasion, which was restored by rhgalectin-3.

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

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

245 1 gene expression, and both regulatory modes are restored by Sfh (HppH) in the absence of H-NS.

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

247 High replication origin density can be restored by somatic nuclear reprogramming.

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

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

250 Normal seedling growth of the OE lines was restored by sucrose supplementation to the growth me

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

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

253 AN-I patient PBMCs and Sptlc2-deficient mice were restored by supplementing with sphingolipids and ph

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

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

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

257 Intestinal ILC2 numbers in Itk(-/-) mice are restored by the administration of IL-2 complexes, al

258 y fluorescent; we show that fluorescence can be restored by the action of porcine liver esterase both

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

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

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

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

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

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

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

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

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

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

269 iated membrane protein 1 and 2 (LAMP1/2) and is restored by the combined use of mTORC1 and Akt pharma

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

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

272 ficit in long-term object recognition memory was restored by the administration of a selective Kv7 ch

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

274 ced cytokine response in Iqgap1(-/-) T cells was restored by the expression of the C-terminal IQGAP1.

275 (ii) the loss of a single SIM(362-364) motif was restored by the presence of four consecutive SIMs fr

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

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

278 HBV transcriptional silencing by Smc5/6 can be restored by therapeutic targeting of HBx.IMPORTANCE H

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

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

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

282 ion of HIF-1alpha/claudin-1 signaling, which was restored by transgenic expression of esophageal epit

283 ction, and susceptibility to infection could be restored by transient expression of CAR.

284 y glands decreased following irradiation but were restored by transient Hedgehog activation.

285 Cs from aging flies, and we show that it can be restored by treating flies with an Nrf2 activator, or

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

287 PRRSV-induced STAT2 degradation could be restored by treatment with the proteasome inhibitor M

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

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

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

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

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

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

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

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

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

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

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