ライフサイエンスコーパス: growth advantage

1 s and NKTL cell lines leads to a significant growth advantage.

2 ions are passengers that confer no selective growth advantage.

3 ssage, suggesting it conferred a significant growth advantage.

4 rred an approximately 3.0-fold intracellular growth advantage.

5 nd FBN2 resulted in an anchorage-independent growth advantage.

6 nary phase and the presence of Rsr confers a growth advantage.

7 death, but in cycling cells, the result is a growth advantage.

8 y require genomic re-stabilization to gain a growth advantage.

9 d mTOR signaling provides tumors a selective growth advantage.

10 when the transgene might impart an intrinsic growth advantage.

11 selection, suggesting that it may provide a growth advantage.

12 o mutations in a subset of genes that confer growth advantage.

13 inhibition ameliorates the Nf1-/- astrocyte growth advantage.

14 red unless a mutation provides a survival or growth advantage.

15 onment, p53 mutant cells exhibit a selective growth advantage.

16 selective pressure, providing mutants with a growth advantage.

17 while simultaneously using this cytokine for growth advantage.

18 dampen the p53 response to gain a selective growth advantage.

19 apable of conferring upon the cell an actual growth advantage.

20 s some of the mutant clones with a selective growth advantage.

21 s how FH inactivation can endow cells with a growth advantage.

22 beta phosphorylation and rescued the EC cell growth advantage.

23 e deregulated with microvascular invasion or growth advantage.

24 ed editing event does not confer a selective growth advantage.

25 es two distinct metabolic strategies to gain growth advantage.

26 events that give the cells with a selective growth advantage.

27 netic mechanisms confer equivalent selective growth advantages.

28 corresponding to cancer drivers with strong growth advantages.

29 by premalignant cells to gain a competitive growth advantage(18).

30 tion-defective counterpart, fully mimics the growth advantages afforded by EGF to these cancer cells.

31 tness and provides Enterobacteriaceae with a growth advantage against competitors in the inflamed gut

32 stem cells (KSC), which confers a selective growth advantage allowing clonal expansion during tumor

33 cyte cultures did not show a cell-autonomous growth advantage, anchorage-independent growth, increase

34 on related; they have mutations conferring a growth advantage and are enriched during the propagation

35 s, termed driver mutations, confer selective growth advantage and are implicated in cancer developmen

36 model, repaired hepatocytes have a selective growth advantage and are thus able to proliferate to eff

37 ronment where the glycolytic phenotype has a growth advantage and consequently is most likely to appe

38 Primary Runx2-null osteoblasts have a growth advantage and exhibit loss of p21(WAF1/CIP1) and

39 We show that Alk expression leads to a growth advantage and induces cell death in surrounding c

40 he growth factor/receptor family that confer growth advantage and metastasis.

41 kinase), H-Ras-transformed cells lose their growth advantage and no longer form colonies.

42 dow of opportunity for PFI to bind provide a growth advantage and possibly a predisposition to resist

43 ltransferase activity is also able to confer growth advantage and rescue growth inhibition on endogen

44 ned expression of CBX7 in EC cells confers a growth advantage and resistance to retinoic acid-induced

45 iver, up-regulation of MAT2A also provides a growth advantage and SAMe and MTA can block mitogenic si

46 ty of latent pathways consistently offers no growth advantage and tends, in fact, to inhibit growth a

47 creatic ductal epithelial cells had a slight growth advantage and were resistant to premature senesce

48 onfer producing organisms with a competitive growth advantage, and also are thought to be virulence f

49 nce to apoptotic stimuli, enhanced survival, growth advantage, and differentiation arrest of CD34+ pr

50 ancer genes, where they can confer selective growth advantage, and over fragile sites, where they are

51 ed an increase in MIPS activity, conferred a growth advantage, and partially rescued sensitivity to v

52 at developmental pathways giving a selective growth advantage are often recapitulated in tumors, we i

53 that have been provided with a survival and growth advantage as a consequence of overexpression of t

54 hat loss of caveolin-1 confers a significant growth advantage, as measured via cellular proliferation

55 on for alterations that promote survival and growth advantage, as well as by the particular dysfuncti

56 lls in vivo and demonstrate that a selective growth advantage at a level distal to HSC can result in

57 n the other hand, RUNX1 conferred no obvious growth advantage at low cell density and actually delaye

58 nduced metabolosome formation and provided a growth advantage at the physiological levels found in ur

59 Alternative models of upward growth advantage based on redox/resource gradients fail,

60 expression confers thyroid cells with little growth advantage because of concomitant activation of DN

61 these genes serve dual functions, providing growth advantages both in the primary tumour and in the

62 o provide the mutant clone with an extrinsic growth advantage, but some features of PNH argue that th

63 ells harboring activated ras could provide a growth advantage by conferring resistance to apoptosis.

64 Cancer cells often gains a growth advantage by taking up glucose at a high rate and

65 Hematologic maligancies exhibit a growth advantage by up-regulation of components within t

66 , in addition to the mutations that confer a growth advantage, cancer genomes accumulate a large numb

67 elevation provided human cancer cells with a growth advantage, caused chromosomal instability in vitr

68 mal rearrangements in trisomic cells provide growth advantage compared to cells without rearrangement

69 n to bone marrow stromal cells; overcome the growth advantage conferred by antiapoptotic protein Bcl-

70 y, expression of miR-9 antagonizes the tumor growth advantage conferred by DeltaEGFR.

71 genes confirmed that they accounted for the growth advantage conferred by pMB2 in iron-depleted medi

72 ith their parental clones, we quantified the growth advantage conferred by putative CLL drivers in vi

73 ageous mutations rather than from an initial growth advantage conferred by the polymerase variant its

74 ot rapamycin alone, was able to overcome the growth advantage conferred on MM cells by interleukin-6

75 nase (ERK) activation and also overcomes the growth advantages conferred by interleukin-6, insulin-li

76 defined regions during clonal selection for growth advantage define the minimally lost regions as th

77 ation of mutations that conveyed a selective growth advantage during adaptation to a glycerol-based g

78 beta-Catenin overexpression offers growth advantage during liver regeneration.

79 a) initiated, pre-malignant cells can have a growth advantage during repopulation, not just during th

80 n or class of mutations that confers a large growth advantage during the respiratory phase of yeast c

81 ikely responsible for conferring a selective growth advantage during tumour evolution and outgrowth.

82 in a solid tumor, Mtss1 does not confer any growth advantage, either in basal conditions or followin

83 ty modalities give P. aeruginosa a selective growth advantage, enabling it to self-segregate from oth

84 controlling properties that confer selective growth advantages even in the presence of a high backgro

85 hese larger placentas did not confer a fetal growth advantage; fetal size was normal in Ipl nulls wit

86 elial cells confers them with a survival and growth advantage, following exposure to DNA-damaging age

87 Mutations in the AR likely confer a growth advantage for a subset of progressive prostate ca

88 rozygosity may provide a non-cell-autonomous growth advantage for astrocytes that may involve p27-Kip

89 of Tsc1 in mice provides a context-dependent growth advantage for astrocytes that results in abnormal

90 of the bacterial food source, resulting in a growth advantage for both organisms, similar to that ach

91 ve no abnormalities and offer a considerable growth advantage for future exploitation.

92 e also observe a significant and competitive growth advantage for KITD816V in Tet2-nullizygous compar

93 tion of the JmjC domain of dUTX results in a growth advantage for mutant cells over adjacent wild-typ

94 hese results suggest that Melk may provide a growth advantage for neoplastic cells and, therefore, in

95 ch leads to its killing, thereby providing a growth advantage for P. aeruginosa in bacterial competit

96 rathionate as an electron acceptor produce a growth advantage for S. Typhimurium over the competing m

97 rdinated surface modifications may provide a growth advantage for Salmonella in host tissues by limit

98 plication, and that human STAT2 can confer a growth advantage for SV5 in the murine host.

99 These increases are not caused by a growth advantage for the revertants and are restricted t

100 e mutation confers a host factor-independent growth advantage for the survival of HBV variants in gra

101 These trade-offs add up to a significant growth advantage for the two natural isoforms.

102 L. pneumophila feoB gene conferred a modest growth advantage for the wild type over the mutant in a

103 or patient prognosis, thus likely conferring growth advantage for tumor progression.

104 his metabolic phenotype provides a selective growth advantage for tumour cells in vivo.

105 ort a novel function of PCGEM1 that provides growth advantages for cancer cells by regulating tumor m

106 overexpression of putative oncogenes confer growth advantages for tumor development.

107 monacha-lucida likewise obtains an intrinsic growth advantage from reduced investment in male gametes

108 also show that it detects growth-defect and growth-advantage genes previously shown to impair or enh

109 resource-poor, bacteria may gain significant growth advantages if they can exploit the ephemeral nutr

110 o the wild-type parent strain and also had a growth advantage in a continuous flow biofilm system.

111 Evidence is provided that S. Typhimurium's growth advantage in an inflamed gut is because of its ab

112 EC strains to utilize ethanolamine to gain a growth advantage in AUM, suggesting that ethanolamine is

113 rgeted role in hTERT regulation leading to a growth advantage in cells expressing HPV16 E6.

114 ht to endow P. aeruginosa with a competitive growth advantage in colonized tissue and is also thought

115 oma formation, but can provide a cooperative growth advantage in concert with genetic alterations in

116 gnaling in Nf1-/- astrocytes abrogated their growth advantage in culture, restoring normal proliferat

117 cells from the transgenic tumors exhibited a growth advantage in culture.

118 r variants that provide mutated cells with a growth advantage in culture.

119 One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic ce

120 n conventionally raised mice, but provide no growth advantage in germ-free mice.

121 gnificant proliferative stimulation and/or a growth advantage in hepatocarcinogenesis of woodchucks w

122 mutant GNAO1(R243D) conferred a significant growth advantage in human mammary epithelial cells, conf

123 A mechanism for clonal growth advantage in isolated del(5q) disease remains elu

124 ement by CCL22 in ATLL cells and conferred a growth advantage in long-term in vitro cultures.

125 Y705 (Y705F/S727E) resulted in a remarkable growth advantage in low-serum, enhanced anchorage-indepe

126 at increased STAT5A/B copy numbers conferred growth advantage in PCa cells in vitro and as xenograft

127 ive genomic changes that provide a selective growth advantage in pluripotent stem cells is of concern

128 LA-deficient DC subsets displayed a specific growth advantage in repopulating the spleen in competiti

129 Lckpr-hTCL1Atg T cells gained a leukemogenic growth advantage in scenarios of receptor stimulation.

130 t interact cooperatively to gain a selective growth advantage in some cases.

131 Despite having no growth advantage in standard laboratory conditions, near

132 evolved under prolonged stress often have a growth advantage in stationary phase (GASP); we expect G

133 ted single nucleotide polymorphisms in known growth advantage in stationary phase alleles and produce

134 These mutants also fail to express the "growth advantage in stationary phase" phenotype as do wi

135 tead expressing two additional new types of "growth advantage in stationary phase" phenotype.

136 play an increased fitness referred to as the growth advantage in stationary phase, or GASP, phenotype

137 The quadruple mutant displayed a growth advantage in the amoebal host Dictyostelium disco

138 r emerging neoplastic cells with a selective growth advantage in the hostile tumor microenvironment.

139 Presence of HtrA resulted in bacterial growth advantage in the IAV-infected LRT and protection

140 umor/host estrogen production and acquired a growth advantage in the presence of host bone marrow cel

141 tes with the PBP2a E246G substitution have a growth advantage in the presence of penicillin but the a

142 and selecting for transformants exhibiting a growth advantage in the presence of the anti-microbial a

143 in one gene, ponA1, demonstrated an in vitro growth advantage in the presence of the drug rifampicin.

144 ETC-impaired cells display a marked growth advantage in the presence or absence of oncogenic

145 suggests that d-serine catabolism provides a growth advantage in the urinary tract.

146 these systems provide B. pseudomallei with a growth advantage in vitro and in vivo, but relatively li

147 -MMP, confers tumor cells with a distinct 3D growth advantage in vitro and in vivo.

148 We report that p12 conferred a selective growth advantage in vitro and increased the colony forma

149 se mice do not demonstrate a cell-autonomous growth advantage in vitro and lack properties of transfo

150 NOS2(-/-) and wild-type C57BL/6 mice, and a growth advantage in vitro in liquid culture.

151 r cdk4 overexpression provides a cooperative growth advantage in vitro, CDK4-overexpressing C6 glioma

152 ugh TWEAK-overexpressing cells do not have a growth advantage in vitro, they form larger and more hig

153 ve mutant, in a glioma cell line conferred a growth advantage in vitro.

154 ing to external stimuli are likely to gain a growth advantage in vivo.

155 es, greater maximum culture densities, and a growth advantages in pairwise competition relative to th

156 roperties in PDA cells by enabling them with growth advantages in stressful tumor microenvironment ni

157 MAOA provides tumor cell growth advantages in the bone microenvironment by stimul

158 Cancer cells gain growth advantages in the microenvironment by shifting ce

159 ins, losses, and mutations, some providing a growth advantage, including alterations in MLL2, EPHA7,

160 The IL-15-mediated growth advantage is abolished by mitogen-activated prote

161 This growth advantage is diminished if cells with only oncoge

162 using IL-15-responsive SD-1 cells shows this growth advantage is maximal under low-serum conditions,

163 by which these LMW forms give tumor cells a growth advantage is not known and is the subject of this

164 lysis and is suggested to bestow a selective growth advantage, is a promising target.

165 for in oncogenesis because it confers clonal growth advantage, may also provide an important mechanis

166 ll cell population experiences a significant growth advantage, much greater than with cooperation or

167 ygen suggesting that ESR1 mutations confer a growth advantage not only during estrogen deprivation bu

168 such strains endow host cells with a general growth advantage, not only on cefotaxime but also on sev

169 n of PRL-3 confers cytokine independence and growth advantage of AML cells.

170 es and the EBV LMP-1 gene, which mediate the growth advantage of B cells infected with type 1 EBV.

171 The growth advantage of dUTX mutant tissue is caused, at lea

172 stoma (Rbf in Drosophila) contributes to the growth advantage of dUTX mutant tissue.

173 The selective growth advantage of gene-modified cells in patients with

174 ecause of a second mutation or a conditional growth advantage of GPI(-) cells in the presence of an i

175 hus by functional loss may contribute to the growth advantage of neoplasia.

176 s and could be dictated by either selection (growth advantage of one phase) or signaling (preferentia

177 death, whereas its overexpression leads to a growth advantage of prostate cancer cells.

178 e in SI growth rate results in a significant growth advantage of SI over NSI when the immune system i

179 rgely normalizes oxygen consumption, and the growth advantage of these cells can be suppressed by inh

180 with eGFP-transposons revealed no selective growth advantage of transposon-harboring cells.

181 Rapamycin also reverts a growth advantage of Tsc2(-/-)TP53(-/-) cells.

182 tumor progression by allowing for selective growth advantage of tumor cells.

183 w the PPP is regulated to confer a selective growth advantage on cancer cells is not well understood.

184 hate pathway, thereby conferring a selective growth advantage on cancer cells.

185 c pathway is predicted to confer a selective growth advantage on cells.

186 ens and identified genes conferring a clonal growth advantage on normal and neoplastic (cutaneous squ

187 The circadian clock confers a growth advantage on plants and uses environmental inform

188 fic nutrient (ethanolamine) confers a marked growth advantage on Salmonella enterica serovar Typhimur

189 pressing stroma, which confers a competitive growth advantage on the cancer cells.

190 that the recombinant protein does not confer growth advantages on l-Arg as a nitrogen source.

191 od for ascertaining whether a gene confers a growth advantage or disadvantage in skin tumorigenesis.

192 , certain cell populations might have gained growth advantage or metastatic potential, as a result of

193 of epigenetic marks that confer a selective growth advantage or through a specific pathway initiated

194 tor system, the wild-type strain exhibited a growth advantage over 042PicS258A in a culture of cecal

195 that a pyelonephritis clinical isolate had a growth advantage over a laboratory strain of E. faecalis

196 lancin gives B. subtilis a major competitive growth advantage over a range of other bacteria thriving

197 death upon growth factor deprivation, and a growth advantage over control cells under suboptimal gro

198 ssion of Wnt3a in H929 MM cells conferred no growth advantage over empty vector-transfected cells in

199 However, P18 had a growth advantage over ISP794 at all temperatures, sugges

200 ed hepatocytes (Fah(-/-)/Hpd(-/-)) display a growth advantage over non-edited hepatocytes (Fah(-/-)/H

201 G1 arrest, which may account for a selective growth advantage over normal cells.

202 he Philadelphia chromosome (Ph+) clone has a growth advantage over normal hematopoiesis.

203 to regenerate it, with diploidy providing a growth advantage over polyploidy.

204 Each phenotype was designed to confer a growth advantage over the other phenotype in a certain e

205 38 Ile) virus had a slight, but reproducible growth advantage over the wild-type s55 (nsP1 538 Thr) v

206 pression may provide the transformed cells a growth advantage over their normal counterpart.

207 Here we show that trr mutant cells have a growth advantage over their wild-type neighbors and disp

208 onal lymphoid cells that possess a selective growth advantage over those carrying disruptive IL2RG mu

209 ahymena, the Stx-encoding bacteria display a growth advantage over those that do not produce Stx.

210 fective mutant killer virus with a selective growth advantage over those with WT killer virus.

211 hl(2B/2B) teratomas additionally displayed a growth advantage over Vhl(-/-)-derived teratomas, sugges

212 ne, overexpression of EGFR-T790M displayed a growth advantage over wild-type (WT) EGFR.

213 DeltaHmga2-derived BM cells had a growth advantage over wild-type cells in competitive rep

214 degradation-resistant HOXB4 that conferred a growth advantage over wild-type HOXB4 in myeloid progeni

215 virus growth kinetics and conferred a robust growth advantage over wild-type rVSV-MAK-GP on Vero E6 c

216 defining viral characteristics that confer a growth advantage, pathogenicity, or cell adaptability in

217 owing for the detection of growth-defect and growth-advantage regions.

218 pressed GAL gene expression and had a robust growth advantage relative to S. bayanus; transgenesis of

219 lar signaling, if and how fumarate confers a growth advantage remain unclear.

220 sistant to herbicides, providing them with a growth advantage so that they can outcompete weeds.

221 t defects in AR corepressor function yield a growth advantage specifically in AR-dependent cells.

222 age-encoded "anti-sRNA" provided EHEC with a growth advantage specifically in bovine rectal mucus rec

223 e allelic fraction of variants that confer a growth advantage, specifically gain-of-function variants

224 ls on antioxidants for redox homeostasis and growth advantage; targeting TXNRD1 resulted in dramatic

225 te fold representation is more predictive of growth advantage than a host of other potential growth-l

226 taneous immortalization and confers an early growth advantage that is resistant to stress-induced gro

227 associated with this QTL confer competitive growth advantages that depend on ascaroside secretion, i

228 show that IRAK1 overexpression confers TNBC growth advantage through NF-kappaB-related cytokine secr

229 Cancer cells gain a growth advantage through the so-called Warburg effect by

230 A in stromal fibroblasts provides tumor cell growth advantages through paracrine IL-6/STAT3 signaling

231 ect or aerobic glycolysis provides selective growth advantage to aggressive cancers.

232 s suggest that TGFBR1*6A confers a selective growth advantage to both normal appearing and cancerous

233 at a major hTERT splice variant can confer a growth advantage to cancer cells independent of telomere

234 hermore, enforced TFRC1 expression confers a growth advantage to cells and significantly enhances the

235 of the TSC2 tumor suppressor gene confers a growth advantage to cells by repressing hypoxic mTOR inh

236 xpressed by other tumors and could provide a growth advantage to cells that express it.

237 ion of GAL1 transcripts provides a transient growth advantage to cells upon addition of glucose.

238 Genes that provide growth advantage to cells via loss-of-function mutations

239 the contribution of a number of genes giving growth advantage to cells when transformed.

240 ed by IFN plus retinoic acid and conferred a growth advantage to cells.

241 timulatory loops and is believed to convey a growth advantage to cells.

242 urs, variants in the genome give a selective growth advantage to certain cells.

243 tive impairment of normal LTHSC growth and a growth advantage to CML LTHSC.

244 owth to energy storage could have provided a growth advantage to early cells, once the membrane compo

245 of estrogen receptor activity and provides a growth advantage to estrogen-dependent cells.

246 is a promising agent capable of providing a growth advantage to genetically modified hematopoietic s

247 reased levels of C18-ceramide might impart a growth advantage to HNSCC cells and that increased gener

248 Furthermore, GPR84 conferred a growth advantage to Hoxa9/Meis1a-transduced stem cells.

249 /-) mice, indicating that TdmhMtb provides a growth advantage to intracellular Mtb in an immunocompro

250 ld inhibit growth, PhtC and PhtD conferred a growth advantage to L. pneumophila thyA(+) strains.

251 FR-DNR approach suggests that EGFR confers a growth advantage to NuTu-19 cells in vivo.

252 allosteric stimulation of Sos and confers a growth advantage to oncogenic K-Ras harbouring cancer ce

253 nstream of Smad7 in a pathway that confers a growth advantage to pancreatic cancer cells and that inc

254 uiding modification on H69 provided a slight growth advantage to PCF parasites at 30 degrees C.

255 lung carcinogenesis may provide a selective growth advantage to premalignant cells.

256 es the AR pathway and confers a survival and growth advantage to prostate cancer cells in an androgen

257 f a gene(s) located in this region confers a growth advantage to some primary human lymphomas.

258 burgdorferi mouse infectivity and provide a growth advantage to spirochetes in the tick.

259 e cotraveling stromal cells provide an early growth advantage to the accompanying metastatic cancer c

260 The enzyme confers a growth advantage to the bacterium, providing essential a

261 down-regulation of either molecule confers a growth advantage to the cells.

262 uct of the inflammatory response conferred a growth advantage to the commensal bacterium Escherichia

263 tion, they steadily proliferate and confer a growth advantage to the entire population.

264 nslation to specific times of day provides a growth advantage to the organism.

265 tain iron via haem and vibriobactin confer a growth advantage to the pathogen only when CTX is produc

266 19) reveal that budding yeast cells confer a growth advantage to their daughters using a novel mechan

267 ls, suggesting that this mutation provides a growth advantage to this subset of MSI colon tumors.

268 with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK c

269 Oncogene amplification confers a growth advantage to tumor cells for clonal expansion.

270 lation of STRAP in human cancers may provide growth advantage to tumor cells via TGF-beta-dependent a

271 that although Gab2 overexpression may confer growth advantage to tumor cells, the functional requirem

272 Typically, mutations that do not confer growth advantage to tumors - passenger mutations - domin

273 sary for aerobic glycolysis and to provide a growth advantage to tumors.

274 poptotic sensitization by Pfn1 and confers a growth advantage to tumors.

275 ctly regulates the PPP to confer a selective growth advantage to tumours.

276 -regulated pilus) that confers a significant growth advantage to V. cholerae on a chitin surface; (ii

277 ses transcription of these genes, conferring growth advantages to cancer cells.

278 conjunction with cofactors, confers several growth advantages to cancer cells.

279 ion that ectopically expressed hTERT conveys growth advantages to cells, without having to postulate

280 on, some haplotypes confer proliferative and growth advantages to cells.

281 ges that lead to filopodia formation, confer growth advantages to fibroblasts under low serum conditi

282 mitochondrial biogenesis, affording distinct growth advantages to the prostate cancer cells.

283 an lead to alterations that confer selective growth advantages to the tumor, some of which play a rol

284 identify clonal genetic hits associated with growth advantage, tracking the evolution of bladder canc

285 bearing a functional EfeUOB displays a major growth advantage under aerobic, low-pH, low-iron conditi

286 ells suppress this signaling pathway to gain growth advantage under conditions of energy stress is la

287 lls from ferroptotic cell death, providing a growth advantage under conditions of oxidative stress an

288 h and that Atg1 mutant cells have a relative growth advantage under conditions of reduced TOR signali

289 hift to glycolytic metabolism and provides a growth advantage under hypoxic conditions, and HIF-1 kno

290 of YlxM conferred a significant competitive growth advantage under nonstress and acid stress conditi

291 sitive LNCaP cells with RGS2 silencing had a growth advantage under steroid-reduced conditions.

292 Multiple variants provided growth advantages under individual conditions; however,

293 rmal and malignant cells, thereby conferring growth advantages under stress as well as resistance to

294 with an EBV miRNA mutant conveyed a cellular growth advantage upon IFN treatment, and relevant miRNAs

295 a perineural location acquire a survival and growth advantage using a NFkappaB survival pathway.

296 n growth, and a defined lasR mutant showed a growth advantage when cocultured with the parent strain.

297 in IKKalpha expression provided a selective growth advantage, which cooperated with H-Ras mutations

298 ction mutations in these strains conferred a growth advantage with particular carbon and nitrogen sou

299 ve stress, MtbFHb-expressing cells exhibited growth advantage with reduced levels of lipid peroxidati

300 ay provide select prostate phenotypes with a growth advantage within the bone microenvironment.