ライフサイエンスコーパス: growth inhibition

1 80% vs. 40% survival rate; 75% vs. 34% tumor growth inhibition).

2 in Ewing sarcoma cells produced significant growth inhibition.

3 e effects and produce cell and proliferation growth inhibition.

4 correlation between BRC1 expression and bud growth inhibition.

5 r models, resulting in tumour regression and growth inhibition.

6 that low pH strongly potentiates VPA-induced growth inhibition.

7 nted with ribose, which led to chlorosis and growth inhibition.

8 and provides insight into the origins of ice-growth inhibition.

9 ession in cells refractory to RUNX1-mediated growth inhibition.

10 hours and custom software measured bacterial growth inhibition.

11 t of cells' response to chemotherapy-induced growth inhibition.

12 degrees is absent and slow H2 efflux causes growth inhibition.

13 rganisms is usually evaluated by determining growth inhibition.

14 ized NSCLC cells to c-MET inhibitor-mediated growth inhibition.

15 cells largely insensitive to auxin-dependent growth inhibition.

16 astuzumab resulted in significant but modest growth inhibition.

17 of ovarian cancer cells to TGF-beta-induced growth inhibition.

18 ely impaired resistance to TGF-beta-mediated growth inhibition.

19 ry and sufficient for mediating TLR4-induced growth inhibition.

20 osolic Ca(2+) changes are required for rapid growth inhibition.

21 sulted in inactivation of EGFR signaling and growth inhibition.

22 s correlated with reduced ethylene-dependent growth inhibition.

23 l inhibition of DOT1L target genes and tumor growth inhibition.

24 by MEF2C was responsible for MEF2C-mediated growth inhibition.

25 assical mechanisms of layer-by-layer crystal growth inhibition.

26 prostate cancer cells for IFN-gamma-mediated growth inhibition.

27 esulted in SPARC downregulation and leukemia growth inhibition.

28 ne regulator (agr) alleles in the absence of growth inhibition.

29 ownregulation of EGFR protein and tumor cell growth inhibition.

30 specific antibodies led to significant tumor growth inhibition.

31 del-dependent tumor cell apoptosis and tumor growth inhibition.

32 d-type p53, leading to cell cycle arrest and growth inhibition.

33 more activated, cytotoxic, and resistant to growth inhibition.

34 de MEK/ERK activity can paradoxically induce growth inhibition.

35 ative breast cancer (TNBC) resulted in tumor growth inhibition.

36 athogens is often accompanied by significant growth inhibition.

37 actate production in vitro, followed by cell growth inhibition.

38 , p53/LKB1 and p73/LKB1 axes in breast tumor growth-inhibition.

39 ts potent cytostatic properties (mean of 50% growth inhibition = 0.2 mum) in almost all cell lines of

40 in the latter case, in addition to microbial growth inhibition, a microbial inactivation effect.

41 This pathway induces rapid growth inhibition, a novel fluorescence burst, cell wall

42 The peptide showed a 16-fold greater growth inhibition activity against S. aureus (4 muM) tha

43 llective behavior that is independent of its growth-inhibition activity.

44 Regarding ZOL, we found a powerful growth inhibition after enforced miR-34a expression, whi

45 train overproducing EsaD elicits significant growth inhibition against a sensitive strain.

46 neomycin, and tetracycline show synergistic growth inhibition against the Salmonella bacteria when c

47 bitor Ex527 greatly enhances MK-1775-induced growth inhibition and apoptosis in human lung cancer cel

48 4 downregulation results in significant cell growth inhibition and apoptosis in response to TGF-beta1

49 Whereas TM-2-51 selectively induced cell growth inhibition and apoptosis in SH-SY5Y cells, it sho

50 We found that GA induced growth inhibition and apoptosis of both GCB- and ABC-DLB

51 CDK7 inhibitor THZ1 synergized in producing growth inhibition and apoptosis of human TNBC cells.

52 thin 1 hour of exposure, resulting in robust growth inhibition and apoptosis.

53 circulatory networks, requiring coordinated growth inhibition and arterial-venous specification.

54 olved in programmed cell death or reversible growth inhibition and bacterial persistence is a matter

55 Ezh2-specific drug, GSK126 through increased growth inhibition and cell death.

56 1 using siRNA significantly suppresses cell growth inhibition and death induced by phycocyanin, wher

57 d (C62S) partially abolished PL-induced cell growth inhibition and decreased the enhanced expression

58 enhancer restored EVI1 silencing and led to growth inhibition and differentiation of AML cells, whic

59 ation or pharmacological inhibition leads to growth inhibition and differentiation of MLL-driven leuk

60 mulation in tumours had significantly better growth inhibition and enhanced survival.

61 Apple replant disease (ARD) leads to growth inhibition and fruit yield reduction in replanted

62 These analyses revealed that auxin-induced growth inhibition and gravitropic bending are significan

63 sights into the molecular mechanisms of axon growth inhibition and identify PARP1 as an effective tar

64 mma deficiency also caused a loss of contact growth inhibition and increased anchorage-independent gr

65 8 partially rescued SHMT1 loss-induced tumor growth inhibition and migration.

66 ted within the intestinal lining, leading to growth inhibition and mortality.

67 eficiencies of Trx f1 and NTRC led to severe growth inhibition and perturbed light acclimation, accom

68 pression of membrane proteins often leads to growth inhibition and perturbs central metabolism and th

69 -mediated knockdown of Lat1 results in tumor growth inhibition and points to Lat1 as a potential ther

70 This results in tumour growth inhibition and radiosensitization despite the use

71 y and CDK4/6 inhibitors induces irreversible growth inhibition and senescence in vitro, and diminishe

72 the ability of 1,25D to induce irreversible growth inhibition and slow the progression of AML in mou

73 lon cancer cells, enhancing TGFbeta-mediated growth inhibition and stress-induced apoptosis.

74 f p38-p53 signaling, thereby contributing to growth inhibition and suppression of stress-induced apop

75 esults show a link between the observed leaf growth inhibition and the expression of specific cell cy

76 -galactosidase expression, autofluorescence, growth inhibition, and ATM pathway activation.

77 (LAZ1H1), causes vacuole morphology defects, growth inhibition, and constitutive activation of BR sig

78 in that binds AtRALF1, is essential for root growth inhibition, and has no role in AtRALF1 alkaliniza

79 emonstrate targeted mRNA suppression, larval growth inhibition, and mortality.

80 ion reduced foci formation, alleviated yeast growth inhibition, and partially rescued autophagic alph

81 d region (3'UTR) and 5'UTR, leading to tumor growth inhibition, and sensitizes NPC tumors to radiatio

82 ed growth of CC, whereas SC was resistant to growth inhibition, and this was coupled to increased tyr

83 h a reduction of IFN-induced apoptosis, cell growth inhibition, antiviral defense, and chemotaxis.

84 mesenchymal markers and consequently induce growth inhibition, apoptosis and prevent spheroid format

85 of cancer cell in a quiescent state, such as growth inhibition, apoptosis, G0/G1 arrest and chemoresi

86 MMAE-based NDC doubled the duration of tumor growth inhibition as compared to cisplatin.

87 in that its activation results in prolonged growth inhibition as well as reduced clonogenic survival

88 iple regression analysis of dose versus root growth inhibition, as well as saturation binding kinetic

89 parasites as judged by an in vitro parasite Growth Inhibition Assay (GIA).

90 nterest in functional in vitro mycobacterial growth inhibition assays (MGIAs), which provide a measur

91 Multicolor flow cytometry, cell sorting and growth inhibition assays were employed to compare the fr

92 in Tanzania, Senegal, and Mali were used in growth inhibition assays with transgenic parasite lines.

93 ial compound was demonstrated using in vitro growth inhibition assays.

94 teractions between jazQ and phyB reveal that growth inhibition associated with enhanced anti-insect r

95 S-12 BM) of multiple myeloma, with 93% tumor growth inhibition at 50 mg/kg QD upon oral dosing.

96 s fitted to the data on bacterial population growth inhibition at different enrofloxacin concentratio

97 ffect" has been described as the reversal of growth inhibition at high doses of echinocandins, most u

98 We modelled the 50% growth inhibition bioassay end-point (GI50) of 17,142 co

99 active Akt construct partially relieved cell growth inhibition but was less effective than inhibition

100 1) required for abscisic acid (ABA) mediated growth inhibition, but not for stomatal closure.

101 s by a Utp22-independent mechanism following growth inhibition, but that its long-term dissociation r

102 dopsis mutants with increased sensitivity to growth inhibition by ABA.

103 NEDD4 knockdown sensitized cancer cells for growth inhibition by an anti-HER3 antibody.

104 3)H]PMX and [(3)H]C2 transport and decreased growth inhibition by C1 and C2, and to a lesser extent b

105 expression of IL-9, were resistant to tumor growth inhibition by DTA-1.

106 s ACC deaminase activity protect plants from growth inhibition by flooding and anoxia, drought, high

107 inuous logistic equation modified to include growth inhibition by metal accumulation to intracellular

108 ed tumor growth in vivo, and prevented tumor growth inhibition by PMPs.

109 Bacterial growth inhibition by PRP occurred in the first 24 hours

110 in cleavage by Lrig2 is required for neurite growth inhibition by RGMa in vitro and for cortical neur

111 Not only subjected to growth inhibition by spermine, the pauA2 mutant became m

112 beta-dependent P-body formation and promoted growth inhibition by TGF-beta.

113 ty points to a mechanistic difference in ice growth inhibition by the different classes of AFPs: bloc

114 oli) between experimental and predicted cell growth inhibition by using DNA DeltaTm and UPPS IC50 exp

115 e growth at a level on par with the level of growth inhibition by vancomycin.

116 Further investigation revealed that the growth inhibition caused by DDX24 depletion is independe

117 Contact-dependent growth inhibition (CDI) is a mechanism by which bacteria

118 Contact-dependent growth inhibition (CDI) is a mechanism of inter-cellular

119 Contact-dependent growth inhibition (CDI) is a phenomenon defined by the d

120 Contact-dependent growth inhibition (CDI) is a wide-spread mechanism of in

121 Contact-dependent growth inhibition (CDI) is a widespread form of inter-ba

122 Contact-dependent growth inhibition (CDI) is a widespread mechanism of bac

123 Contact-dependent growth inhibition (CDI) is a widespread mechanism of int

124 Contact-dependent growth inhibition (CDI) is a widespread mechanism of int

125 Contact-dependent growth inhibition (CDI) is an important mechanism of int

126 uction that is mediated by contact-dependent growth inhibition (CDI) system proteins.

127 Contact-dependent growth inhibition (CDI) systems function to deliver toxi

128 r-bacterial competition is contact-dependent growth inhibition (CDI), in which Gram-negative bacteria

129 tition in a process termed contact-dependent growth inhibition (CDI).

130 In CME and growth inhibition cell-based assays, the data obtained w

131 Measures of growth inhibition, cell cycle analysis, morphologic asse

132 d inhibition of gene expression resulting in growth inhibition, changes in susceptibility to small mo

133 s to DNA damage and results in p53-dependent growth inhibition compared with corresponding NEDD4-1-pr

134 INOX experienced significantly greater tumor growth inhibition compared with i.v. FOLFIRINOX.

135 duration was achieved displayed more robust growth inhibition compared with tumors with lower SN-38

136 The values of PD parameters such as maximal growth inhibition, concentration achieving a half of the

137 tion within tumors, driving correlated tumor growth inhibition, decreased metastasis, and increased c

138 nhibitor to a BRAF inhibitor enhances tumour growth inhibition, delays acquired resistance, and abrog

139 However, alleviating growth inhibition does not invariably result in increase

140 Growth inhibition due to ULK2 induced high levels of aut

141 r, N-methylprotoporphyrin, produced a potent growth inhibition effect against cultures of P falciparu

142 The most pronounced cell growth inhibition effect was obtained in the breast aden

143 al suppression of SlFRK2 induced significant growth-inhibition effects, including the wilting of matu

144 K studies and demonstrated significant tumor growth inhibition efficacy in mouse flank xenograft mode

145 This rebound is suppressed and tumor growth inhibition enhanced with combined inhibition of P

146 s (RLR) signaling represses TGF-beta-induced growth inhibition, epithelial-mesenchyme transition (EMT

147 Further, a correlation of growth inhibition (EWS-FLI1 expressing TC32 cells) and t

148 We performed extensive growth inhibition experiments, and we discovered that ce

149 umor cells and is able to drive potent tumor growth inhibition following intratumoral or intravenous

150 umor xenograft model with evidence for tumor growth inhibition following oral dosing.

151 ycans (CSPGs) are major contributors to axon growth inhibition following spinal cord injury and limit

152 ed in 1alpha,25(OH)2D3 and MART-10 meditated growth inhibition for CCA as knockdown of NGAL decreased

153 cell screening approach measuring effects on growth inhibition for human cells containing EWS-FLI1 (T

154 owth sites may be a general mode of hemozoin growth inhibition for the quinoline antimalarials.

155 Growth inhibition from bacteriostatic antibiotics was as

156 Prostate cancer cells escape growth inhibition from transforming growth factor beta (

157 ate products 7b, 7c, and 7f exhibited potent growth inhibition (GI50 = 0.16-0.99 muM) against the maj

158 ing the early stages of melanoma, poor tumor growth inhibition has been observed in more advanced mel

159 D4(+) or CD8(+) T lymphocytes abolished this growth inhibition, identifying it as an immune-mediated

160 ET phosphorylation in mice, and robust tumor growth inhibition in a MET-dependent mouse efficacy mode

161 Two compounds demonstrated significant tumor growth inhibition in a mouse xenograft model of head and

162 ell cycle and its genetic depletion leads to growth inhibition in a subset of high MELK-expressing ba

163 ynamic biomarker of CDK8 activity, and tumor growth inhibition in an APC mutant SW620 human colorecta

164 est phase of auxin-induced ion signaling and growth inhibition in Arabidopsis roots.

165 cromolar range, whereas measurable bacterial growth inhibition in broth medium required >10-fold high

166 Growth inhibition in cAS cells was closely related to th

167 wth inhibition) of 90% without any mortality growth inhibition in comparison to reported leads.

168 optosis, which resulted in significant tumor growth inhibition in CRC mouse models that express high

169 of caspase-1 and caspase-11 are required for growth inhibition in different cell types.

170 d p16(INK4a) promoter repression and induced growth inhibition in HCT116 cells.

171 ally, RT53-killed B16F10 cells induced tumor growth inhibition in immunocompetent mice following a re

172 The nanovaccine led to potent tumour growth inhibition in melanoma, colon cancer and human pa

173 t inhibitor causes apoptosis and synergistic growth inhibition in multiple EGFR tyrosine kinase inhib

174 the adaptive transition and led to prolonged growth inhibition in multiple patient-derived cell lines

175 azole 4-carboxamide ribonucleotide (ZMP) and growth inhibition in NCI-H460 and MDA-MB-231met2 cancer

176 SCLC lines and primary samples that undergo growth inhibition in response to GSK2879552 exhibit DNA

177 iabetes, but the mechanism of metformin's PC growth inhibition in the context of a prediabetic state

178 gs for compounds that induced cold sensitive growth inhibition in the model bacterium Escherichia col

179 he new compounds (2d, 2j, 2k, and 2n) showed growth inhibition in the XTT dye assay.

180 g large amounts of siderophore suffered less growth inhibition in toxic copper.

181 istently correlated with the extent of tumor growth inhibition in tumor xenograft models.

182 in massive synergistic tumor cell death and growth inhibition in tumor-bearing mice.

183 ehydrogenase complex, caused a profound cell growth inhibition in tumour cells harbouring KRAS mutati

184 ith AKT inhibitors causes synergistic tumour growth inhibition in vitro and in vivo.

185 d photodynamic therapy demonstrated complete growth inhibition in vitro of 2 multidrug-resistant MRSA

186 ession of PUMA and BIM, led to apoptosis and growth inhibition in vitro, and tumor regression in vivo

187 impact in vitro but results in a remarkable growth inhibition in vivo.

188 was synergistic with chemotherapy for tumor growth inhibition in vivo.

189 in different models, and also leads to tumor growth inhibition in vivo.

190 prodrug molecules and shows effective tumor growth inhibition in vivo.

191 ivo effecting c-Myc downregulation and tumor growth inhibition in xenograft studies.

192 Changes in Cd toxicity (growth inhibition) in the presence of different essentia

193 , resulting in mitochondrial dysfunction and growth inhibition, in an miR-24-dependent manner.

194 ombination immunotherapy that enhanced tumor growth inhibition, increasing the rates and durability o

195 ctivation reduced premature catagen and hair growth inhibition induced by oxidative stress (H2O2 or m

196 ibition exhibited the most potent effects on growth inhibition, induction of apoptosis, and delay of

197 owth inhibition of tumor cell lines and that growth inhibition is associated with cytoplasmic retenti

198 rtually irreversible, and we confirm the ice growth inhibition is consistent with the Gibbs-Thomson l

199 ium smegmatis, suggesting that V-58-mediated growth inhibition is due to interference with specific M

200 Further growth inhibition is obtained when DZNep is combined wit

201 stress triggers various responses, including growth inhibition, mediated by the plant hormone abscisi

202 y events toward the adverse outcome on algae growth inhibition, might discriminate between different

203 cells could infiltrate tumors and that tumor growth inhibition occurred without an enrichment of sCSC

204 In vitro studies demonstrate that Ct growth inhibition occurs by interferon-gamma (IFN-gamma)

205 pin RNAs (shRNAs) against MCT4, resulting in growth inhibition of 50-80% under hypoxia in two lines.

206 ation, this extended to an enhanced relative growth inhibition of a heterologous parasite line, altho

207 1B molecules are sufficient to induce strong growth inhibition of a microtubule plus end in vitro.

208 of tankyrase, revealing the compound induced growth inhibition of a number of tumor derived cell line

209 tivity and on its ability to rescue the cold-growth inhibition of a Saccharomyces cerevisiae tgs1Delt

210 with POS and ITC, C14 exhibited synergistic growth inhibition of all C. albicans strains, except C.

211 mouse xenograft tumor models with a complete growth inhibition of AsPC1 human pancreatic tumors and i

212 while aged Ti3C2Tx membrane showed over 99% growth inhibition of both bacteria under same conditions

213 The growth inhibition of both drugs were mediated by inducti

214 ilic molecule in the series showing the best growth inhibition of both leukemia and solid tumor cell

215 Complete growth inhibition of both MRSA strains was demonstrated

216 llular cholesterol levels correlate with the growth inhibition of cancer cell lines upon statin treat

217 hanced LSD1 inhibitor-induced senescence and growth inhibition of cancer cells in vitro and in mice.

218 arrest induction, and anchorage-independent growth inhibition of cancer cells.

219 act as transmembrane receptors that mediate growth inhibition of chondroitin sulfate proteoglycans (

220 ctural scaffolds for MTAN inhibition and for growth inhibition of cultured H. pylori.

221 contact- and Esx secretion pathway-dependent growth inhibition of diverse Firmicute species.

222 the S. cattleya toxin RelE2sca caused severe growth inhibition of E. coli and S. lividans, but RelE1s

223 nversely, overexpression of FabI rescued the growth inhibition of Escherichia coli by 6-OH-BDE-47, va

224 Here, we show that growth inhibition of Escherichia coli during allicin exp

225 a library of 309,989 chemical compounds for growth inhibition of Ewing sarcoma cells to provide the

226 the half-life of MYC to achieve substantial growth inhibition of high CD25-expressing AML cells.

227 geneic orthotopic animal models, and induces growth inhibition of low-passage human PDAC cells in a s

228 ly member inhibitors resulted in synergistic growth inhibition of MDA-MB453 cells, implicating Src as

229 ated doses, compound 28 leads to significant growth inhibition of MOLM13 xenografts in nude mice, and

230 Functional analyses encompassing in vitro growth inhibition of MRSA, and in vivo protection studie

231 or NSAH is within twofold of gemcitabine for growth inhibition of multiple cancer cell lines, while d

232 e novel AKT3 variant resulted in significant growth inhibition of multiple head and neck cell lines,

233 In cell-based assays, the compounds show growth inhibition of Plasmodium falciparum 3D7 with IC50

234 est antimicrobial potential, having revealed growth inhibition of Pseudomonas aeruginosa.

235 An adenovirus expressing ORCTL3 leads to growth inhibition of renal tumours in vivo and to substa

236 D complex of the HIPPO pathway, resulting in growth inhibition of several neoplasias.

237 produce functioning CDI systems that mediate growth inhibition of sister cells lacking the cognate im

238 +) near the bacteria cell wall that leads to growth inhibition of the bacteria.

239 cell lines and was able to induce 60% tumor growth inhibition of the CW22Rv1 in vivo xenograft model

240 Root toxicity assays revealed increased root growth inhibition of the mutants if cultivated in the pr

241 iazoles and leucine linker to obtain maximal growth inhibition of the parasite.

242 Growth inhibition of the small intestinal mucosa by fast

243 of p27(Kip1)) are critical for CCN5-induced growth inhibition of TNBC cells.

244 Lastly, blocking CDKN1B and CDKN1C reversed growth inhibition of TOX knockdown.

245 racellular and non-cell-autonomous apoptotic growth inhibition of tumor cell lines and that growth in

246 f SDT with IR-780 revealed significant tumor growth inhibition of xenografts of 4T1 cancer cells; it

247 ing sensitivities to Cu (72-h 50% population growth inhibitions of 8-47 mug Cu/L).

248 hich were screened for effects on tumor cell growth, inhibition of tubulin polymerization, and induct

249 port inhibitors produced strong, synergistic growth-inhibition of several fungi.

250 er (TNBC) syngeneic models with a TGI (tumor growth inhibition) of 90% without any mortality growth i

251 >/=25 muM As, reflected in stronger seedling growth inhibition on agar plates.

252 d, which resulted in significant increase in growth inhibition on various cancer cell lines with mini

253 acteria upon cell-cell contact, resulting in growth inhibition or death unless a specific immunity pr

254 asm of a neighboring bacterium, resulting in growth inhibition or death unless the recipient bacteriu

255 2-ADC treatment leads to a significant tumor growth inhibition or tumor regression of cell line-based

256 using both sorafenib and MEAN enhanced tumor growth inhibition over monotherapy with either agent.

257 igh specific activity induced superior tumor growth inhibition (P = 0.021, n = 5/group) without subac

258 ELP brachytherapy (n=6) induced significant growth inhibition (p=0.001, ANOVA) and enhanced median s

259 the predicted drug-pathway associations and growth inhibition patterns are mostly consistent with th

260 The growth inhibition potentials of both 0.06%w La(NO3)3 and

261 SYK, or LCK showed additive effects on cell growth inhibition, providing a rationale for combination

262 s to varying degrees, with the most profound growth inhibition recorded for miR-182-5p.

263 c stress and apoptosis associated with tumor growth inhibition related to an interference with hypoxi

264 he "overflow hypothesis." According to this, growth inhibition results in the rate of photosynthetic

265 e affinity of cell binding and ensuing tumor growth inhibition reveal the linker length to be a bidir

266 To corroborate the growth inhibition role of SVP2 in kiwifruit development

267 ty-related readouts, including flg22-induced growth inhibition, ROS production and callose deposition

268 Analysis of SOG1's role in Al-dependent root growth inhibition shows that sog1-7 prevents Al-dependen

269 ranscriptional regulation, contact-dependent growth inhibition, swarming motility, and induction of a

270 rtemisinin family anti-malarials, we observe growth inhibition synergism with low doses of this beta2

271 X-loaded vesicles demonstrated greater tumor growth inhibition than free DOX without causing signific

272 showed low levels of free cAMP and exhibited growth inhibition that was not proportional to the cAMP

273 he suppression of APY1 and APY2 is linked to growth inhibition, the gene expression changes that occu

274 e of wild-type allele expression resulted in growth inhibition, the loss of approximately 20S editoso

275 K-562 cell line) did not result in selective growth inhibition; this is similar to the findings repor

276 s and in stress by antagonizing SA-dependent growth inhibition through UPR modulation.

277 We conclude by arguing that auxin-mediated growth inhibition under abiotic stress conditions is one

278 type of TTK RNAi, demonstrated in vivo tumor growth inhibition upon oral dosing, and was selected for

279 sor p53 plays an important role in mediating growth inhibition upon telomere dysfunction.

280 logy studies showed that the observed tumour growth inhibition was accompanied by increased presence

281 Growth inhibition was accompanied by perturbed Krebs cyc

282 Growth inhibition was associated with increased numbers

283 ivity of g6pd6 mutant plants to PAMP-induced growth inhibition was complemented by a phosphomimetic b

284 Kidney growth inhibition was manifested by a decrease in the si

285 Significant tumor growth inhibition was observed as low as 0.5 mg/kg dose

286 Growth inhibition was observed following treatment with

287 Similar growth inhibition was observed in syngeneic GL261 GBM (p

288 In lindane-exposed daphnids, a significant growth inhibition was observed, with concomitant increas

289 a significantly lower nitrogen content and a growth inhibition were observed, with a concomitant incr

290 Phagocytosis and intracellular growth inhibition were significantly enhanced when BCG w

291 over, both cell types manifested synergistic growth inhibition when treated with chloroquine plus the

292 icit the greatest sensitivity to NO-mediated growth inhibition, whereas all but the periplasmic nitri

293 overexpression improved fulvestrant-mediated growth inhibition, whereas cells expressing the LRIG1 mu

294 ibitor, triggered even greater apoptosis and growth inhibition, whereas normal hematopoietic stem/pro

295 ain inhibitor I-BET151 resulted in selective growth inhibition, whereas treatment of leukaemia cells

296 Setdb1 ablated ES cells exhibit severe growth inhibition, which is not rescued by exogenous Nan

297 e SOX2 repression and long-term breast tumor growth inhibition, which lasted for >100 days post impla

298 Significant tumor growth inhibition with brontictuzumab was observed exclu

299 sed targeting approach to long-lasting tumor growth inhibition with potential applicability to many o

300 ing kiwifruit development SVP2 has a role in growth inhibition, with high-chill kiwifruit Actinidia d