ライフサイエンスコーパス: lose the ability to

1 Most mutants lost the ability to accumulate in one or more of the mul

2 ts showing that highly malignant tumors have lost the ability to accumulate nCLU levels, thereby avoi

3 tonated, the resulting 1,2,3-triazolium ions lose the ability to act as H-bond acceptors, and the pol

4 Our results show that UASs lose the ability to activate normal transcription as the

5 a total or partial ligand binding domain but lose the ability to activate transcription through a fai

6 ins the ability to activate Ral proteins but loses the ability to activate Akt also fails to promote

7 All mutations resulted in arginine losing the ability to activate mouse NAGS, and inhibit X

8 region domains activated RhoA and Rac-1 but lost the ability to activate Cdc42.

9 Importantly, none of the mutants that lost the ability to activate Jak2 retained the ability t

10 show that the resultant CD26-depleted clones lose the ability to adhere to fibronectin and collagen I

11 ants defective for the interaction with Bop1 lose the ability to affect rRNA maturation and the cell

12 oth p53 and HIF-1alpha genes have completely lost the ability to alter the cell cycle in response to

13 k/light transitions, the CCA1-ox plants have lost the ability to anticipate this daily change in thei

14 late-embryonic development, retinal neurons lose the ability to attach and extend neurites on the ex

15 Retinal neurons lose the ability to attach to and extend neurites on sub

16 Accordingly, Cac0437 has apparently lost the ability to autophosphorylate in vitro; instead

17 prisingly, although the DGH177-179KLN mutant lost the ability to be a negative regulator in ABA signa

18 These mutant proteins lost the ability to be phosphorylated by MAP kinase both

19 uncation fragments shorter than 15 residues, lost the ability to be stabilized by metal ions.

20 lerate tumors in NIH 3T3 cells, whereas they lose the ability to bind DNA in vitro.

21 AX3 WS mutants with mutations in homeodomain lose the ability to bind mitotic chromosomes.

22 MgrA occurring in cell extracts caused it to lose the ability to bind norA promoter DNA.

23 tations cluster in the UBA domains of SCCRO, lose the ability to bind to polyubiquitinated proteins,

24 the mutant model after in silico mutagenesis loses the ability to bind bile acids.

25 Upon binding of Phe, the enzyme loses the ability to bind D-erythrose-4-phosphate and bi

26 on of Ras by ExoS, where ADP-ribosylated Ras loses the ability to bind guanine nucleotide exchange fa

27 ild-type apoptotic properties but completely loses the ability to bind microtubule-associated protein

28 ated Thy-1, in which RLD is replaced by RLE, loses the ability to bind the integrin.

29 ified L. monocytogenes sensor of bile, which loses the ability to bind to and repress the mdrT promot

30 A 54-kDa protein lost the ability to bind (125)I-plasminogen after treatm

31 C392A, C394A, and P393A lost the ability to bind a metal ion with high affinity

32 antly, CaV beta mutants were identified that lost the ability to bind AID but retained their associat

33 ed a mutant protein, TrfA-44Delta2, that had lost the ability to bind and load the DnaB helicase of P

34 A point mutation that lost the ability to bind Bak retained its ability to bin

35 ibit preferential binding of GDP, while D60K lost the ability to bind both GTP and GDP.

36 The N250A mutant receptor lost the ability to bind both radiolabeled agonist and a

37 Another mutant, T255A, lost the ability to bind E4orf6, but unexpectedly, viral

38 miR-30 variants that had lost the ability to bind Exp5 effectively were not effic

39 binding domain containing p.Q131E completely lost the ability to bind F-actin in C2C12 cells.

40 Some of the mutants that lost the ability to bind fH, iAb, or both had only a sin

41 er mutants retained stimulatory activity but lost the ability to bind folded ssDNA.

42 ass of P-loop GTPases and has evolutionarily lost the ability to bind GTP; instead, it uses ATP hydro

43 nished mannose-binding activity and had also lost the ability to bind human bladder cells.

44 The reason why ICA family members have lost the ability to bind iron is potentially related to

45 LOS isolated from this strain lost the ability to bind monoclonal antibody (MAb) 2-1-L

46 ectants expressing a Claudin-4(N149D) mutant lost the ability to bind or respond to CPE, while transf

47 eration of the Src homology 3 binding domain lost the ability to bind p85.

48 e localization of ERK2 and mutants that have lost the ability to bind PEA-15.

49 round pH 7, thus indicating that it may have lost the ability to bind phosphotyrosine.

50 observed that TRAP mutant proteins that had lost the ability to bind RNA were no longer recognized b

51 main mutant of HRas, HRasN17G37, selectively lost the ability to bind smgGDS.

52 S analysis showed that the mutant cells have lost the ability to bind the toxin, indicating that they

53 d for S1, approximately 50% of the molecules lost the ability to bind to ATP.

54 the intact CBD(CelK), W56A and W94A totally lost the ability to bind to cellulose, Y136A bound to bo

55 CV-1, CV-2, and CV-5, however, lost the ability to bind to IL-6R.

56 gulatory subunits, whereas PPP2R1A-mutations lost the ability to bind to most B56 subunits except B56

57 The MS11Deltaopa bacterium lost the ability to bind to purified lipooligosaccharide

58 5 was mutated to alanine, the mutant Insig-1 lost the ability to bind to Scap and, thus, was unable t

59 mutants in amino acids 1 to 350 of Sendai L lost the ability to bind to Sendai P, although they were

60 that lost the oligomerization capacity also lost the ability to bind to the HIV-1 core.

61 utant proteins were identified, all of which lost the ability to bind to the progesterone response el

62 utagenized library for 2B variants that have lost the ability to bind wild-type 2B.

63 nuated phenotype to wild-type SBV, as it has lost the ability to block the innate immune system of th

64 capture early folding intermediates, and it loses the ability to capture and reactivate rhodanese if

65 roximately 15 A in length, all three mutants lose the ability to catalyze lactose transport.

66 A 10 residue deletion lost the ability to catalyze ATP synthesis, but was stil

67 Primary hepatocytes quickly lose the ability to clear LDL during in vitro culture.

68 and mice deficient in both IL-17A and IL-17F lost the ability to clear S. aureus nasal colonization.

69 he virus and caused the RNase H of RSV RT to lose the ability to cleave the PPT specifically.

70 A truncated protein lost the ability to cleave the core protein precursors.

71 ture, the upper temperature at which insects lose the ability to cling to an inclined surface, in rep

72 k veins, encoding an essential dpp receptor, loses the ability to clonally populate a niche.

73 hasia (PNFA) is a syndrome in which patients lose the ability to communicate fluently in the context

74 ns for people with severe paralysis who have lost the ability to communicate orally are limited.

75 MLL fusion proteins of leukemia which would lose the ability to complex with C180 have their stabili

76 nt RyR1 channels carrying both substitutions lost the ability to conduct Ca2+.

77 e willing to participate in research if they lost the ability to consent.

78 Mouse STAP cells lose the ability to contribute to the placenta as well a

79 tants that lack PIPKIgamma or PIP(2) binding lose the ability to control directional cell migration.

80 letions at the C-terminal end of the protein loses the ability to control the spontaneous activation

81 fferentiation so that these effector T cells lost the ability to control virus but were still capable

82 interact with ELOB/C or CUL2, respectively, lost the ability to counteract bovine A3 proteins.

83 oprotease (MT1-MMP), and that DC transiently lose the ability to degrade the extracellular matrix aft

84 some carbon sources such as glucose, but had lost the ability to degrade cellulose.

85 nd evolved, in some cases, into species that lost the ability to degrade crystalline cellulose while

86 istent with the observation that the culture lost the ability to degrade DCM.

87 surface c-Kit expression, was found to have lost the ability to differentiate into dendritic cells a

88 ful dilator of most vascular beds, virtually lost the ability to dilate cerebral arteries and arterio

89 By mixing the two genomes, PCR loses the ability to discriminate among the different al

90 trast, NBF-1 carrying the DeltaF508 mutation loses the ability to discriminate between these two phos

91 ments show that these mutant terminases have lost the ability to discriminate between lambda and 21 d

92 In both cases, myeloid progenitor cells lose the ability to distinctly differentiate granulocyte

93 mma (IFN-gamma) knockout (IFN-gamma-KO) mice lost the ability to downregulate osteoclastogenesis.

94 Both WT and Y497F hIL-4Ralpha lose the ability to drive Th2 differentiation and cell e

95 ss this important issue for older adults who lose the ability to drive.

96 RGCs stimulated out of synchrony rapidly lost the ability to drive tectal postsynaptic partners w

97 g sequences from murine leukemia virus (MLV) loses the ability to efficiently infect nondividing cell

98 egion have reduced growth in rice leaves and lose the ability to elicit a hypersensitive response (HR

99 cells retain the capacity to proliferate but lose the ability to enter their final neurogenic divisio

100 BD-associated bacteria supplemented with QSI lost the ability to establish disease, while healthy cor

101 protected mice, at 5 days postinfection, had lost the ability to express EGFP and had deletions in th

102 arising variants of different PyVs that have lost the ability to express miRNAs.

103 181 traumatic brain injury patients who had lost the ability to fixate at ICU admission (phase 1) an

104 tion of flippase mutants that either gain or lose the ability to flip phosphatidylserine (PS) to dete

105 Importantly, ASAH1-null cells also lose the ability to form cancer-initiating cells and to

106 orrect addition of sialic acid and galactose loses the ability to form fibrils.

107 Methylation-defective HDAg lost the ability to form a speckled structure in the nuc

108 Cells released from the polyamine inhibition lost the ability to form colonies, failed to replicate t

109 Finally, CHO-H466D lost the ability to form complexes with glycine betaine

110 ical abnormalities at either pH; however, it lost the ability to form hyphae on medium 199 and on 10%

111 We demonstrate that null MEFs have lost the ability to form Smad-containing DNA binding com

112 e LacD.2-like levels of enzymatic efficiency lost the ability to function as regulators, suggesting t

113 ial cells with knockdown or knockout of Pkd2 lose the ability to generate nitric oxide (NO).

114 rch neural crest, is reduced in size and has lost the ability to generate neural crest cells.

115 hibitors, anaerobiosis, freezing or boiling) lost the ability to generate RG-II dimers.

116 Most of these mutants lost the ability to generate the high phosphorylation po

117 Mouse molars lose the ability to grow continuously, whereas incisors

118 r alanine dehydrogenase and alanine permease lost the ability to grow on either isomer of alanine, wh

119 The amyA::lacS mutant lost the ability to grow on starch, glycogen, or pullula

120 ratory strains of human cytomegalovirus have lost the ability to grow on vascular endothelial cells,

121 In HuPON1, variant H115W loses the ability to hydrolyze VR but has improved activ

122 The R210K dimeric motor has lost the ability to hydrolyze ATP; however, it has rescu

123 r critical asparaginase-active site residues lost the ability to hydrolyze glutamine and were unable

124 to immortalize T lymphocytes, the M22 mutant lost the ability to immortalize infected cells.

125 -inhibitory effects of D-amino acids without losing the ability to incorporate at least one noncanoni

126 E. coli treated with the pantothenamides lost the ability to incorporate [1-(14)C]acetate to its

127 s for all eight influenza virus RNAs, but it lost the ability to independently reassort its HA or NS

128 uppressor activity because monomeric mutants lose the ability to induce apoptosis after genotoxic str

129 with no endoderm, while vegetal blastomeres lose the ability to induce mesoderm.

130 Finally, we show that TVGR also loses the ability to induce expression of a reporter con

131 ncement on susceptible soybean varieties and lost the ability to induce a chlorotic response on the r

132 also have generated FGF19 variants that have lost the ability to induce hepatocyte proliferation but

133 e immunosuppressive activities of hIL-10 but lost the ability to induce immunostimulatory activities

134 duced endothelium-specific PIEZO1 deficiency lost the ability to induce NO formation and vasodilation

135 while peptide-pulsed, cytokine-activated EC lost the ability to induce T cell division.

136 However, the virus lost the ability to infect cells expressing only nectin-

137 dates by serial passage in fibroblasts, have lost the ability to infect epithelial and endothelial ce

138 ty to infect feline cells and simultaneously lost the ability to infect murine cells in tissue cultur

139 d that CD4(+)CD25(+) Tr cells exposed to PF4 lose the ability to inhibit the proliferative response o

140 A mutant of IRS-1 lacking the PTB domain loses the ability to inhibit the differentiation program

141 In contrast, AML1b(Del179-242) has lost the ability to inhibit both ovarian cell proliferat

142 hibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro.

143 t peptide insertions and selected those that lost the ability to inhibit cellular transcription and c

144 show that CRF-BP(R56A) and CRF-BP(D62A) have lost the ability to inhibit CRFR1-mediated responses to

145 find that the HH-associated mutant H41D has lost the ability to inhibit iron release despite binding

146 highly susceptible to human complement, had lost the ability to inhibit phagolysosomal fusion transi

147 by a competing peptide, parathyroid hormone lost the ability to inhibit phosphate transport.

148 Kalpha recruitment and RelA phosphorylation, lost the ability to inhibit Tax-mediated tumorigenesis.

149 ALF depleted by a coating of B. dermatitidis lost the ability to inhibit TNF-alpha production (P < 0.

150 repore) is acidified in solution, it rapidly loses the ability to insert into membranes.

151 ation-deficient mutants of p53 concomitantly lose the ability to interact with BclXL and promote cyto

152 to regulate E2F1-induced apoptosis, and E2F1 loses the ability to interact with this site following D

153 As a result, the mutant CARD8 protein lost the ability to interact with the NOD domain of NLRP

154 Interestingly, pHA-UL3825-331 lost the ability to interact with TSC2 but retained the

155 to express cell-surface bound Gal8 but also lose the ability to internalize FV.

156 Even spent merozoites, which had lost the ability to invade, retain the ability to adhere

157 The antiserum also lost the ability to kill the mutant strain in a bacteric

158 oplasm, and catalytic variants of the enzyme lost the ability to kill the yeast host, indicating that

159 The derived CTL-FDs have lost the ability to kill via the perforin/granule exocyt

160 MK is knocked down in MDA-MB-231 cells, they lose the ability to lead strands of collectively invadin

161 h neurogenesis ablated at the time of injury lost the ability to learn spatial memory tasks.

162 l and ventral prefrontal cortex, the monkeys lost the ability to learn these associations within a se

163 In DeltaCmNox1, CmSlt2-GFP fusion protein lost the ability to localize to the cell nucleus accurat

164 If an organism loses the ability to maintain a balance between quiescen

165 he mechanisms by which a stable diploid cell loses the ability to maintain genomic integrity are not

166 well as the zinc finger-like region quickly lost the ability to maintain episomal genomes.

167 xpression, decreased insulin production, and lost the ability to maintain glucose homeostasis.

168 ration of transformed mutant cells that have lost the ability to maintain tissue integrity.

169 enomic analyses show that Perkinsela sp. has lost the ability to make a flagellum but retains hallmar

170 expressed a variety of neurotransmitters but lost the ability to make certain subtypes of neurons tha

171 volved such extreme genome reduction that it lost the ability to make its own virions independent of

172 specialized for flight that they have almost lost the ability to manoeuvre on land at all.

173 encoded by the H2g7 MHC haplotype aberrantly lose the ability to mediate the thymic deletion of autor

174 we show that mitochondria in senescent cells lose the ability to metabolize fatty acids efficiently.

175 e residues, only C145S and C195S derivatives lost the ability to methylate As(III) and MAs(III).

176 ndogenous overexpressing PEDF melanoma cells lost the ability to migrate and form tubes in vitro.

177 Interestingly, Trps1-deficient cells lost the ability to mineralize and demonstrated decrease

178 fragment of cIAP1 that failed to bind TRAF2 lost the ability to modulate NF-kappaB activity, demonst

179 Instead, PSGL-1-deficient Tregs lost the ability to modulate T cell movement and failed

180 n congenital disease centronuclear myopathy, lost the ability to negatively regulate autophagy.

181 y heparin chains lacking the N-sulfate group lost the ability to neutralize infection, confirming tha

182 deleted (based upon the subcloning results) lost the ability to oxidize either phosphite or hypophos

183 66D formed a stable complex with choline but lost the ability to oxidize the substrate.

184 Three additional species have lost the ability to parasitize insects and do not disper

185 ace to the bottom' as members of a community lose the ability to perform functions whose products are

186 pecialized to perform specific functions and lose the ability to perform others.

187 Losing the ability to perform such functions can be adva

188 B was disrupted moved unusually rapidly, but lost the ability to perform macropinocytosis and therefo

189 ach that selectively targets cells that have lost the ability to perform MMR.

190 They almost completely lost the ability to phagocytose zymosan beads.

191 arasites harbor a secondary plastid that has lost the ability to photosynthesize yet is essential for

192 roduction in developing Th2 cells; (b) OX40L lost the ability to polarize Th2 cells in the presence o

193 abled-2 (Dab2), the primitive endoderm cells lose the ability to position on the surface, resulting i

194 which could not be phosphorylated by HIPK3, lost the ability to potentiate SF-1 activity for Cyp11a1

195 Losing the ability to present neoantigens through human

196 ative LL-37, the modified peptide completely lost the ability to prevent morbidity and mortality in a

197 Specifically, day 7 DC lost the ability to prime CD8(+) T cells but preferentia

198 n the same throughout the disease course and lose the ability to produce IFN-alpha in late-stage lupu

199 entiated virus-specific CD8+ T cells notably lose the ability to produce IL-2 but also lose expressio

200 diabetic (NOD) fetal pancreas organ cultures lose the ability to produce insulin when maintained in c

201 A transition zone where cells lose the ability to produce light and beyond which >50%

202 Differentiated embryonic carcinoma cells lose the ability to produce the E1A-like activity.

203 nsertional inactivation of the luxS gene and lost the ability to produce AI-2.

204 iltrated prostate tumors, where they rapidly lost the ability to produce effector cytokines.

205 gous recombination, and the resultant mutant lost the ability to produce fumonisins.

206 or knockout mice significantly or completely lost the ability to produce inositol phosphate or diacyl

207 Isogenic mtp mutants lost the ability to produce Mtp in vitro and demonstrate

208 ted kpsM, kpsS and kpsC mutants of C. jejuni lost the ability to produce O-antigen.

209 cells activated solely through TCR ligation lose the ability to proliferate as a result of autocrine

210 Mammalian cardiomyocytes lose the ability to proliferate shortly after birth, and

211 Terminally differentiated myocytes have lost the ability to proliferate, indicating the existenc

212 In contrast, both pendrin mutants lose the ability to promote iodide efflux.

213 A1 astrocytes lose the ability to promote neuronal survival, outgrowth

214 The cleaved MDM2 loses the ability to promote p53 degradation and may pot

215 ke yellow stripe3-like (ysl1ysl3), which has lost the ability to properly regulate iron deficiency-in

216 However, we show that the E163K mutant loses the ability to protect against oxidative stress wh

217 nal produced long nicked double-stranded DNA loses the ability to protect AgNPs from salt-induced agg

218 nd an EBNA2 mutant unable to bind Nur77 also lost the ability to protect cells from SV-induced apopto

219 SPP loses the ability to proteolytically remove the transit

220 itutions at any of the other three positions lost the ability to provoke LSHR but induced SHR instead

221 that evolve in pathogenic infections do not lose the ability to recognize CCR5 or Bob/GPR15.

222 nd or as antagonist attractant, the nematode loses the ability to recognize a second attractant.

223 ve temperature, and that melanoblasts die or lose the ability to recover after being held at the rest

224 inone levels comparable to those of MR-1, it lost the ability to reduce iron(III), manganese(IV), and

225 ith washed cells showed that this mutant had lost the ability to reduce U(VI) or Cr(VI), providing an

226 Following depletion of NAD by >95%, cells lose the ability to regenerate ATP.

227 Maturing neurons gradually lose the ability to regenerate axons.

228 Axons of the mammalian CNS lose the ability to regenerate soon after development du

229 The central nervous system (CNS) loses the ability to regenerate early during development

230 can be switched between SLN and PLB without losing the ability to regulate SERCA activity; however,

231 We found that R175H lost the ability to regulate centrosome duplication, whi

232 These "hypercyst" mutants have lost the ability to regulate cyst cell formation in resp

233 eterostrophus MAT genes shows that they have lost the ability to regulate sexual reproduction in U. b

234 However, memory CD4 T cells lose the ability to reject skin grafts when transiently

235 replication and amount of variation without losing the ability to replicate because of excessive mut

236 ture-sensitive lactose repressor mutant that loses the ability to repress its target promoter at high

237 us, E1A mutants that failed to bind p300/CBP lost the ability to repress FER-1, whereas mutants of E1

238 ively older, asynchronous cells that rapidly lose the ability to reproduce.

239 ations fixed for PI Wolbachia infection have lost the ability to reproduce sexually, even when cured

240 Furthermore, mutant FMRP loses the ability to rescue presynaptic action potential

241 tant to human biology; when it is mutated it loses the ability to respond properly to bacterial cell

242 However, the cells lost the ability to respond to dilauroyl phosphatidyleth

243 These betagamma complex-deficient cells lost the ability to respond to G protein-mediated signal

244 o or more changes in H7.59, E7.63, and R7.67 lost the ability to respond to OT in a dose-dependent ma

245 These lal(-/-) T cells lost the ability to respond to T cell receptor stimulati

246 rnal self-fertilization, hermaphrodites have lost the ability to respond to the male soporific-induci

247 titutively active) mutant of CFP-TM-GalphaoA lost the ability to restrict Gbeta1gamma2-YFP mobility,

248 ctivation is the commitment point when cells lose the ability to return to quiescence and decide to p

249 nocytes differentiate into macrophages, they lose the ability to secrete proinflammatory cytokines in

250 neutrophil retains its granule contents and loses the ability to secrete them in response to secreta

251 sal polarity, but they were disorganized and lost the ability to secrete SMGC.

252 beta-cells become metabolically inflexible, losing the ability to select between carbohydrates and l

253 r cells were believed until recently to have lost the ability to senesce.

254 between the OM and the peptidoglycan, cells lost the ability to sense defects in envelope integrity.

255 cumulated larger amounts of Ca2+ before they lost the ability to sequester Ca2+.

256 become resistant to suppression by IL-4 and lose the ability to signal through IL-4R.

257 oplast SRP (cpSRP) RNA binds cpSRP54 but has lost the ability to significantly stimulate the GTPase c

258 e Paul Broca, described two patients who had lost the ability to speak after injury to the posterior

259 Many group II introns have lost the ability to splice autonomously as the result of

260 rge near the FAD N(1) locus, choline oxidase lost the ability to stabilize negative charges in the ac

261 uence was deleted, the resulting RbfADelta25 lost the abilities to stably associate with the 30S subu

262 f ATPase and helicase activity, but that has lost the ability to stably associate with DNA.

263 MPEP loses the ability to stimulate locomotion in conditional

264 IL-15 retained their cytolytic capacity but lost the ability to stimulate naive T cells.

265 with glutamine produced mutant proteins that lost the ability to stop cellular growth upon overexpres

266 a2-3Gal, its original substrate in ducks, it lost the ability to support viral growth in the duck int

267 fails to accumulate at R loops in cells, and loses the ability to suppress R loops and associated gen

268 When the EPCR was blocked, F. tularensis lost the ability to suppress activation of HUVECs.

269 its full metabolic activity, apelin-36(L28A) lost the ability to suppress blood pressure in spontaneo

270 ntrosome-binding(-) mutant almost completely lost the ability to suppress centrosome duplication.

271 ssage pathways are attenuated, and they have lost the ability to suppress lateral pseudopod formation

272 In the absence of NOX2 activity, MDSC lost the ability to suppress T cell responses and quickl

273 ver millions of years, these mutualists have lost the ability to survive outside the sheltered enviro

274 -viscosity medium, CatSper2-null spermatozoa lost the ability to swim forward, whereas wild-type cell

275 elective attention so that listeners with HL lose the ability to switch attention rapidly (a skill th

276 The last variant (K1B6me) lost the ability to switch to the TK+ phenotype, althoug

277 wever, pol II preinitiation complexes (PICs) lose the ability to synthesize RNA very rapidly upon exp

278 to identify candidate strains that may have lost the ability to synthesize a translocated substrate

279 Although humans have lost the ability to synthesize ASC, our mouse models sug

280 the mutant did not sporulate, and the strain lost the ability to synthesize cytochrome aa3.

281 ions in both plants and animals, humans have lost the ability to synthesize it.

282 yme is active under these conditions, it has lost the ability to synthesize primers of defined length

283 oduced by conspecifics, even after they have lost the ability to synthesize siderophores.

284 Cultured macrophages lost the ability to take up the recombinant protein when

285 erminally differentiated Th2 cells that have lost the ability to transcribe the IL-2 gene.

286 The phosphorylated autokinase lost the ability to transfer its phosphoryl group to ADP

287 methylcobalamin holoenzymes have completely lost the ability to transfer the methyl group from methy

288 in activity of EntF C-A formed seryl-AMP but lost the ability to transfer the seryl moiety to the cog

289 How did the animal-adapted strains lose the ability to transmit between humans?

290 fast input fluctuations over few layers, but lose the ability to transmit slower, population-wide inp

291 erate transport velocity, and had completely lost the ability to transport hexoses.

292 s undergo a switch in myogenic potential and lose the ability to undergo mitosis.

293 ant with Csf1r downregulation, 32D/WT1 cells lost the ability to undergo myeloid differentiation in r

294 e of deletion of SK residues 1-59, SKDelta59 loses the ability to unfold Glu-Pg during complex format

295 bind blunt dsDNA, the RecB-mutant enzyme has lost the ability to unwind DNA unless the substrate cont

296 karyotes including parasites and most yeasts lost the ability to use this metal.

297 have undergone this recombination event have lost the ability to utilize either N-acetylgalactosamine

298 ement selenium is variable as many organisms lost the ability to utilize Sec.

299 Remarkably, 30% of the lineages had lost the ability to utilize xylose as a carbon source.

300 SPG5 patients lost the ability to walk independently after a median di