ライフサイエンスコーパス: be defective for

1 om that observed in a ulp1(ts) strain, which is defective for a distantly related Smt3-specific prote

2 re also maintained in an suvh6 mutant, which is defective for a gene closely related to SUVH4.

3 spa2delta cells, like ssk2delta cells, were defective for actin recovery from osmotic stress.

4 nable to transform cells, suggesting that it is defective for action on an unknown cellular target es

5 rupt specific recognition of the UEE hairpin are defective for activation of lytic replication.

6 ation function of Dpb11 but that this domain is defective for activation of the principal checkpoint

7 kinase-deficient Bcr-Abl mutant (p210K1172R) was defective for activation of Jak2 in 32D cells and im

8 e intracellularly, the pilF and pilT mutants were defective for adherence to macrophages, pneumocytes

9 190-B RhoGAP exhibit excessive Rho activity, are defective for adipogenesis, but undergo myogenesis i

10 ly up-regulates B-cell TACI expression, this was defective for all subjects with mutations.

11 ts lacking the unc-104 kinesin motor protein were defective for anterograde movement of dense-core ve

12 siological ATP concentrations, these mutants are defective for ATP hydrolysis but not ATP binding in

13 bstitution results in a dimeric kinesin that is defective for ATP hydrolysis and a motor that cannot

14 for MutS E694A, a protein that binds ATP but is defective for ATP hydrolysis.

15 s, the mutant complex binds mispaired bases, is defective for ATP-induced sliding clamp formation and

16 the mutant complex binds mispaired bases and is defective for ATP-induced sliding clamp formation but

17 in motif II and Q804A and R808A in motif VI were defective for ATP hydrolysis and mRNA release from

18 d Q685A, G688A, R689A, and R692A in motif VI were defective for ATP hydrolysis and step 2 transesteri

19 en of the eleven residues that were targeted were defective for ATP hydrolysis, and seven of these we

20 dometrial cell lines harboring ATR mutations are defective for ATR-dependent responses.

21 racellular and extracellular TACI expression was defective for B cells of all subjects with mutations

22 roblasts to anchorage-independent growth and were defective for B-lymphoid transformation in vitro an

23 expressing a mutant of E6, E6(I128T), which is defective for binding at least a subset of the alpha-

24 antigen that inactivates the pRb-family, but is defective for binding p53, exhibit hyperplasia but do

25 TFIIA-gammaY65A is defective for binding to the beta-sheet domain of TBP

26 containing a single R44A replacement, which was defective for binding at its mutant surface but boun

27 e in a manner similar to wild-type BvgA, but was defective for binding the fhaB promoter in the absen

28 Zta C171S was defective for binding to these promoters in vivo, as

29 ) or the entire gene cluster (strain KKF457) are defective for biofilm formation.

30 /p110 PI 3-kinase binding sites (PDGFR-F/F), are defective for both p85 binding and ligand-stimulated

31 ns within the E2 transactivation domain that are defective for both transcriptional transactivation a

32 alize MECs with low efficiency were found to be defective for both p53 and hAda3 degradation.

33 lacks expression of the PrrF and PrrH sRNAs, is defective for both iron and heme homeostasis.

34 encodes an altered form of TFIIB (E62K) that is defective for both start site selection and gene loop

35 Furthermore, an S. flexneri ydeP mutant was defective for both glutamate-independent and glutama

36 nts, but not their complemented derivatives, were defective for both surface translocation and film p

37 Another mutant, H358A, was defective for capsid assembly.

38 ureB-deficient H. pylori mutants were defective for CASP1 activation in murine bone marro

39 roline-rich region deletion mutant BRG1 that is defective for CBP binding inhibited p53 destabilizati

40 virions with mutant Envs that bind CXCR4 but are defective for CD4 binding or membrane fusion induced

41 One of the seven Nefs was defective for CD4 downregulation, two others were de

42 X and clpP deletions in several strains that are defective for cell division.

43 e, several mutants have been identified that are defective for cell fusion, and yet the molecular mec

44 mplantation, and preimplantation blastocysts are defective for cell outgrowth and/or survival in vitr

45 DeltahtrA strains were additionally found to be defective for cell invasion and vacuole escape in sel

46 The pcry mutant is defective for central properties of the circadian clo

47 do not extravasate to sites of infection and are defective for chemotaxis.

48 However, several mutated proteins that were defective for chromosomal interaction could associa

49 ubstrate mutants dam1 spc34 and ndc80, which are defective for chromosome biorientation.

50 ed randomly, indicating that the ptd mutants are defective for CO formation in the interference-sensi

51 al evidence that a C316S/E350Q mutant, which is defective for cognate substrate lysine acetylation; a

52 ion mutant that mimics in vivo Scc2 cleavage is defective for cohesin deposition.

53 vA and zevB grew normally in rich medium but were defective for colonization in a mouse lung model.

54 Smc3-K113Q is defective for condensation, whereas eco1Delta wpl1Del

55 nd we show that while the Ub-CR conformation is defective for conjugation, it demonstrates improved b

56 The Vpr mutant (Q65R) that was defective for DCAF1 interaction also had a defect in

57 ants failing to produce A-signal or C-signal are defective for developmental expression of asgE.

58 eta TA cassettes in B. subtilis mutants that were defective for different proteases.

59 401L substitutions (but not W401F) and W414L were defective for dimerization in vitro.

60 itutions at three positions in the CB domain are defective for DNA cleavage but still proficient in l

61 H3-G34R mutants are defective for DNA damage repair by homologous recomb

62 e early region E4 deleted (E4-deleted virus) are defective for DNA replication and late protein synth

63 ants of MTBP without a functional CTM domain are defective for DNA replication in Xenopus egg extract

64 ltiple residues on the surface of the E1 DBD are defective for DNA replication without affecting the

65 The other mutant was defective for DNA binding in vitro yet was still rec

66 ime quantitative PCR showed that BAC-IN84/Ep was defective for DNA synthesis in that no increase in t

67 infectious virus upon treatment with TPA and was defective for DNA synthesis.

68 r defects in ATP hydrolysis, these complexes were defective for DNA binding.

69 This Nef mutant is defective for downregulating CD4 and, in addition, fo

70 Here we show that an hfq mutant strain is defective for DsrA-mediated regulation of both rpoS a

71 stingly, a partial-penetrance Rb mutant that is defective for E2F binding retains full activity in in

72 Here we report that these mutants are defective for early gastric recruitment of CD4(+) T

73 We also found that the nla4 mutant is defective for early developmental events and for vege

74 he core enzyme; however, R275Q, E295K, A302D were defective for Efinal sigma(70) holoenzyme formation

75 ion-of-function alleles were identified that are defective for either FEAR signaling or aspects of an

76 undergo regulated nuclear translocation but are defective for Elk-1/TCF transactivation and target g

77 cdc13-1 mutants, suggesting ten1-ts strains are defective for end protection.

78 ormal expression and localization in the ER, were defective for endosomal alkalization.

79 demonstrate that a GP mutant, GP-F88A, which is defective for entry into a variety of human cell type

80 Therefore, TRDeltagO is defective for entry into all three cell types.

81 Temperature-sensitive mutants of TFIIB that are defective for essential interactions were isolated.

82 The mutants were defective for Exo activity on all primer templates

83 Mutant Mlh1-Pms1 and PCNA proteins that were defective for Exo1-independent but not Exo1-depende

84 s and initiate assembly of pilus fibres, but were defective for extending the pilus fibres, as measur

85 trate that in the presence of ATP, RecA K72R is defective for extension of RecA filaments on DNA.

86 ed biofilm formation in E. coli strains that were defective for extracellular, surface, or regulatory

87 es of macrophages, whereas Raji cells, which are defective for Fas-induced PS exposure, remained unen

88 Stimulated PBMCs from the patient were defective for Fas-independent cytotoxicity.

89 er, virions with the aptamers 70.8 and 70.15 were defective for first-strand transfer, suggesting an

90 titution within its Tap42 binding domain and is defective for formation of the Tap42-Sit4 complex.

91 amined a number of M. xanthus genotypes that were defective for fruiting-body development, including

92 p mutants undergo conformational changes but are defective for fusion because they fail to make produ

93 We find that E99V mutant viruses are defective for fusion with cell membranes and thus ar

94 thoprim (trim) cassette in the envelope gene were defective for Gag protein production and the nuclea

95 PGCs that are defective for Gbetagamma signaling failed to polariz

96 titutions within its Dbl homology domain and is defective for GEF activity, inhibits Src-promoted cel

97 expression of HBV carrying the V124W mutant was defective for genome replication.

98 Moreover, bazooka mutants are defective for germband extension.

99 in those BR and auxin signaling mutants that were defective for Glc-induced LR production.

100 utant of the glycosyltransferase gacI, which is defective for GlcNAc side-chain addition, is attenuat

101 rpoH1 mutants are defective for growth at high temperature and form in

102 her assays, verification that mutant strains are defective for growth in specific host tissues, and i

103 is, and therefore cells lacking SRE1 or STP1 are defective for growth in the presence of low levels o

104 cking unfed-ticks and badR-deficient strains are defective for growth under these same conditions.

105 hph mutant cells are defective for growth, and, remarkably, ectopic expre

106 n of the first gene in the mel2 locus, melF, is defective for growth in IFN-gamma-plus-lipopolysaccha

107 Therefore, the DeltaICP0 HSV-1 virus is defective for growth in most cells, except the human

108 The mutant virus, pm8002, was defective for growth in 293 cells, although it repli

109 enotype, we found that the DeltasecA2 mutant was defective for growth in macrophages from C57BL/6 mic

110 that a DeltasecA2 mutant of M. tuberculosis was defective for growth in the early stages of low-dose

111 nes lacking the lipoate protein ligase LplA1 was defective for growth specifically in the host cytoso

112 e deletion of fslE and found that the mutant was defective for growth under iron limitation.

113 ough none of the single OSH deletion mutants was defective for growth, gene expression profiles revea

114 Next, the mutants that were defective for growth at 30 degrees C, a non-permiss

115 ions within the identified gene menD or pepP were defective for growth in primary murine macrophages

116 LANA mutants that were defective for GSK-3beta interaction were unable to

117 at strains lacking the ubiquitin ligase Bre1 are defective for H3 methylation, suggesting that there

118 II and associate with gene-specific loci but is defective for H3 K36 di- and trimethylation.

119 to the MLL1 SET domain and observed that all are defective for H3K4 dimethylation by the MLL1 core co

120 Cells transfected with Zta variants that were defective for helicase binding still formed replica

121 etic assays we identify mutants of MvaT that are defective for higher-order oligomer formation.

122 tive and dNTPase-positive SAMHD1Q548A mutant is defective for HIV-1 restriction.

123 er genetic tools, we show that DmBlm mutants are defective for homologous repair but show a compensat

124 important, as macrophages lacking HIF-1alpha are defective for IFN-gamma-dependent control of infecti

125 at mutations that cause one viral DNA end to be defective for IN-mediated integration led to abnormal

126 mutant Rna15 with decreased affinity for RNA is defective for in vitro RNA processing and lethal in v

127 Third, V165A and R166A mutants were defective for in vitro integration activity, when a

128 ll Piv mutants altered in conserved residues were defective for in vivo inversion of the M. lacunata

129 l or temperature-sensitive CK2 yeast mutants are defective for induction of H4 S1 phosphorylation upo

130 UPR, we identified a UPR reporter gene that was defective for induction in IRE1alpha-null mouse embr

131 iate-early and early phases of infection but are defective for infectious progeny virus production.

132 Two tumor mutants, E146K and R343H, were defective for inhibition of cell growth and migrati

133 performed to isolate an allele of MCM2 that is defective for interaction with HBO1; this allele was

134 whereas overexpression of a mutant CPEB that is defective for interaction with molecular motors inhib

135 ows defects in the ATPase of the complex and is defective for interaction with Rad17/3/1 and for load

136 the small subunit of TFIIA (toa2-I27K) that is defective for interaction with TAF11.

137 proved biochemical activity, one of the TBPs was defective for interaction with polymerase II preinit

138 Yet, J domain mutants of ERdj3 that were defective for interaction with Ssa1 restored the gr

139 most pronounced in dmc1Delta mutants, which are defective for interhomolog repair, and explain the p

140 sing single, defined surface polysaccharides are defective for intestinal colonization compared with

141 A nonflagellated strain expressing EPS is defective for intestinal colonization in the suckling

142 The delta flgP mutant strain was defective for intestinal colonization (approximately

143 er and spleen in susceptible BALB/c mice and were defective for intestinal persistence in Salmonella-

144 tant strains lacking any of the translocases were defective for intimate attachment.

145 ains lacking the translocated substrate SdhA are defective for intracellular replication and activate

146 la species, was identified in this screen to be defective for intracellular growth within both macrop

147 he Y. pseudotuberculosis YPIII(p(-)) strain, was defective for intracellular replication.

148 imited in proline because proline auxotrophs were defective for intramacrophage survival and virulenc

149 llular signal-regulated kinase 2 (ERK2) that are defective for intrinsic mitogen-activated protein ki

150 tested, one carrying an insertion in Cj1496c was defective for invasion into INT-407 cells; this defe

151 tized less efficiently by macrophages and it was defective for invasion of non-phagocytic cells and s

152 Strains expressing the mutant SspC alleles were defective for invasion, translocation of effector m

153 urin-deficient yeast mutant (cnb1Delta) that is defective for ion homeostasis, but had no effect on t

154 ments showed that the phoPTn10 mutant strain is defective for killing both cultured and primary human

155 Substitution mutation Y390F was defective for kinase function.

156 a2p variants with changes at these positions are defective for Krh1p binding in vivo.

157 tion and DSB-independent homolog pairing but is defective for later events, formation of DSBs, and sy

158 Mutants lacking lbtA or lbtB were defective for legiobactin, producing 40 to 70% less

159 The PALB2-S59A/S64E mutant is defective for localization to DNA damage sites and HR

160 chemical evidence that a K268M mutant, which is defective for Lys-274 chemical acetylation in the con

161 KplE1 is defective for lysis but fully competent for site-spec

162 105 to glutamate produces a Mos protein that is defective for M-phase activation, as assessed by in v

163 Furthermore, mgtE variants that were defective for magnesium transport could still compl

164 elta hsp82-T101I and hsc82 Delta cpr7 Delta, are defective for maltase induction and exhibit signific

165 ntroduction of I383>L into a Myc mutant that is defective for Max binding substantially restored its

166 Energy-coupled transport was defective for melibiose accumulation, but detectable

167 Heat-treated prt1-1 extracts are defective for Met-tRNA(i)Met binding to 40S subunits

168 h Ala is substituted for Glu(38) is shown to be defective for mismatch repair in vivo.

169 reviously characterized mutant of c-Myc that is defective for Miz-1 inactivation, we examined whether

170 e apoptotic potential of a c-MYC mutant that is defective for MIZ-1 inhibition.

171 erminal amino acids 604 to 613 or 608 to 613 is defective for MotA-dependent activation.

172 l pathogenic properties; the deletion strain was defective for motility in semisolid agar, biofilm fo

173 We isolated mutants of INI1 that are defective for multimerization using a reverse yeast

174 We found that a mobABD mutant was defective for murine host colonization and that a ca

175 standing observation that pol32Delta strains are defective for mutagenesis.

176 Using mutant viruses that are defective for nuclear entry, we observed a 90% decre

177 incorporate nup214/CAN, nup153, or nup98 and were defective for nuclear import of lamin B3.

178 mbryos expressing mutant forms of Sall1 that are defective for NuRD binding.

179 cells expressing mutant forms of FOG-1 that are defective for NuRD binding.

180 rco function through phosphorylation at S289 are defective for odor-guided behavior.

181 rant receptor Or43b and find that the mutant is defective for odor-evoked activity in ab8A neurons, a

182 ags mutated at the tip of the "beta-hairpin" are defective for oligomerization on duplex DNA; however

183 that ori mutants that fail to melt correctly are defective for ori unwinding and DNA replication in v

184 defective for PAK-2 activation, and one Nef was defective for PAK-2 activation and major histocompat

185 defective for CD4 downregulation, two others were defective for PAK-2 activation, and one Nef was def

186 also observed that HIV-1 zinc finger mutants were defective for particle production and exhibited a s

187 both wt E5, and transforming E5 mutants that are defective for PDGF-R activation, constitutively acti

188 y with galactose as a sole carbon source and was defective for phosphoglucomutase activity, suggestin

189 ine expressing an MT allele (Y315F) known to be defective for PI3K binding displayed a markedly reduc

190 ddition, MS11 recB mutants are also shown to be defective for pilE/pilS recombination.

191 A Shigella flexneri degP mutant, which was defective for plaque formation in Henle cell monolay

192 new DHBV M variants indicated that they too were defective for primer translocation/utilization and

193 of miRNA precursors, whereas dicer-2 mutants are defective for processing siRNA precursors.

194 the C. elegans ortholog of PC type 2 (PC2), were defective for processing endogenously expressed FMR

195 sing the nonshuttling UL84 mutant (NS84 BAC) was defective for production of infectious virus.

196 Animals lacking zygotic dronc are defective for programmed cell death (PCD) and arrest

197 A TFIIB R78C mutant extract was defective for promoter-specific run-on transcription

198 All three SecA mutant proteins were defective for promoting cell growth unless they wer

199 retain the ability to down regulate HIF but are defective for promotion of fibronectin matrix assemb

200 pression and viral factory formation, but it was defective for proteolytic processing of the precurso

201 L. pneumophila mutants lacking SidD were defective for Rab1 removal from LCVs, identifying S

202 sidue or generated M18T and T37R alterations were defective for recombination.

203 heckpoint-deficient mutant of RPA, rfa1-t11, is defective for recruiting Ddc2 to ssDNA both in vivo a

204 train carrying an F832A mutation in Rb1 that is defective for recruitment to repetitive sequences.

205 Yeast expressing an Rga2 mutant that is defective for regulation by calcineurin display incre

206 nt with a direct role in HR, Cebrc-2 mutants are defective for repair of meiotic and radiation-induce

207 tions, which prevent Sap1p binding in vitro, are defective for replication fork arrest in vivo, where

208 r plaques than wild-type (WT) virus, and AM2 is defective for replication at higher temperatures.

209 Our data demonstrate that these mutants were defective for replication in primary human monocyte

210 ir SLCs replaced with two different CMV SLCs were defective for replication.

211 Interestingly, PKR mutant cells were defective for response to double-stranded (ds) RNA

212 romoter for efficient transcription in vitro were defective for response to growth rate changes in vi

213 These cells were defective for restarting stalled replication forks

214 Here, we show that dsl1 mutants are defective for retrograde Golgi-to-ER traffic, even u

215 CO-Ty1 is defective for retrotransposition, suggesting a sequen

216 to the cytoplasm, confirming that SSKH cells are defective for Rev-mediated RNA export.

217 seen when a Sam68 point mutant (G178E) that is defective for RNA binding was used.

218 4B gene from the closely related H77 isolate is defective for RNA replication in a transient assay, s

219 frame 2 (ORF2) that disrupts VP1 expression was defective for RNA replication, as quantified by luci

220 y RNAi, and lysates from armi mutant ovaries are defective for RNAi in vitro.

221 III in Saccharomyces cerevisiae strains that were defective for RNase H1, H2, or both.

222 Luria-Bertani medium, none of these mutants was defective for rpoS stationary-phase induction.

223 hrough a reverse-genetic screen and shown to be defective for rps12 trans-splicing.

224 mains active even if a constituent SecY copy is defective for SecA binding.

225 way and that cancer-associated SFRP1 mutants are defective for senescence induction.

226 -75 mutants, most ncs cla4-75 double mutants were defective for septin localization during budding.

227 HL-60 A2 is a clonal cell line that is defective for sialylation and alpha1,3-fucosyltransfe

228 wild-type levels of FlgS and FlgR, but they were defective for signaling through the FlgSR system.

229 All mutants that were defective for silencing suppression were also non-f

230 peron display abnormal colony morphology and are defective for sliding motility, properties that sugg

231 cribed spacer 1, indicate that bud23 mutants are defective for small-subunit export.

232 The pta1-Delta75 mutant is defective for snoRNA termination, RNA polymerase II C

233 ion resulted in a neutralized cytoplasm that was defective for SPI-2 secretion.

234 Cells deleted for fin are defective for spore formation and exhibit increased

235 Second, we found that siz1 mutants, which are defective for Srs2 recruitment to replication forks,

236 h a deletion of RAD59, a homologue of RAD52, was defective for SSA, especially when the homologous-se

237 and s/s mice that express LRb(S1138) [which is defective for STAT3 (signal transducer and activator

238 critical for differentiation, since mutants are defective for stationary phase survival, flagellar g

239 ltered cell surface in stationary phase, and is defective for stationary-phase survival and recovery

240 d-type alpha-factor receptor, and while both are defective for Ste3p constitutive internalization, bo

241 We found that the Mcm10-4A mutant was defective for stimulating DDK phosphorylation of Mcm

242 We isolated three mutants that were defective for surfactant.

243 s identified in our screen were confirmed to be defective for survival in blood bactericidal assays.

244 The Delta iglC mutant, however, is defective for survival, replication, and the ability

245 row on D-Ala-D-Ala as sole carbon source and was defective for survival in nutrient-poor conditions.

246 d more Fe(III) than the wild-type strain and was defective for survival in soil, suggesting that thes

247 The DeltaABCH mutant was defective for survival/growth within human and murin

248 a KIM6+ galU mutant and a KIM6+ wecBC mutant were defective for survival in murine macrophages.

249 The latter strains have been shown to be defective for swarming because the agar remains dry.

250 es, yet the inactive Y324F and R173K mutants are defective for synapsis.

251 ing three mutants (unc-4, cha-1, and unc-17) are defective for synthesis or packaging of acetylcholin

252 ld-type B. melitensis, while the vjbR mutant was defective for systemic spread in IRF-1(-/-) mice, su

253 We found that csm4Delta strains, which are defective for telomere-led chromosome movements, sho

254 The patA1 and patA2 mutants are defective for the assembly of EA1 in the envelope bu

255 mutants have a functional Icm/Dot system yet are defective for the expression of many genes encoding

256 ast (Schizosaccharomyces pombe) cells, which are defective for the G(2)/M DNA damage checkpoint, Hus1

257 mutants that target to focal adhesions, yet are defective for the induction of paxillin phosphorylat

258 ytic subunit-deficient CHO cell lines, which are defective for the nonhomologous end-joining DNA repa

259 d potently activated CF mutant channels that are defective for the normal ATP-dependent mode of gatin

260 , Lmna(G609G/+) vascular smooth muscle cells are defective for the production and extracellular accum

261 n this paper, we show that mice lacking Mia3 are defective for the secretion of numerous collagens, i

262 In addition to being defective for the tumor-suppressor function, mutan

263 the classical mouse dysmyelination mutants, is defective for the expression of myelin-associated gly

264 We find that srb4ts Mediator is defective for the stimulation of basal RNA polymerase

265 int mutant of RASSF1A showed that the mutant was defective for the MOAP-1 interaction and for Bax act

266 The TAT mutant was defective for the symbiosis, forming nodules incapab

267 quired for A20 effector function because A20 was defective for the targeting and inactivation of TBK1

268 virus 40, resulted in T antigen mutants that were defective for the ability to support viral growth,

269 Furthermore, p21CIP1-/- 3T3 cells were defective for the DeltaMEKK3:ER*-induced G1 cell cy

270 We determined that all BCG strains were defective for the induction of two dormancy genes:

271 Conversely, VDR KO iNKT cells were defective for the production of multiple cytokines

272 Furthermore, the RNA-binding motif mutants are defective for their export through the XPO1 (CRM1/Ex

273 thway, and worms defective for germline RNAi are defective for these heritable effects.

274 of farnesol and that Or83c receptor mutants are defective for this behavior.

275 Mutants in either Myo2 or Sro7 that are defective for this interaction show hypersensitivity

276 The silencing-defective BAH mutants are defective for this interaction.

277 the medium, whereas the fadA5 mutant strain is defective for this activity.

278 sC mutant defective in interaction with TnsB is defective for Tn7 transposition both in vitro and in

279 A ctp1(CtIP) deletion is defective for Top2 removal but overproficient for Top

280 Similarly, in yeast cells that are defective for transcription termination, collisions

281 identify a new class of histone mutants that is defective for transcription-dependent nucleosome occu

282 ld interface of adeno-associated virus (AAV) was defective for transcription of the packaged genome.

283 ls comparable to that of wild-type virus but were defective for transduction.

284 However the kar2 mutant was defective for transfer of NE lumenal GFP, but not di

285 luding a U3 mutation which has been shown to be defective for transposition in vivo.

286 ished CNC, even when the suppressing element was defective for transposition.

287 1p contain a misassembled i-AAA protease and are defective for turnover of mitochondrial inner membra

288 Furthermore, nla18 mutant cells are defective for two of the earliest events in developm

289 e provide evidence that RSK2-deficient cells were defective for UV-induced Ser(727) phosphorylation o

290 of serine 20 to alanine into p53(-/-) cells, were defective for UVB-induced apoptosis.

291 nal or C-terminal kinase-dead mutant of MSK1 were defective for UVB-induced serine 112 phosphorylatio

292 model of latency, viruses lacking only UL135 were defective for viral genome amplification and reacti

293 boring the resistance-inducing substitutions were defective for viral integration.

294 es show that the N-Myc equivalent of c-Myc-S is defective for virtually all transcriptional activatio

295 Yersinia pestis KIM D27 mutants lacking yopR were defective for virulence in a mouse model of septice

296 (YopM Delta 12-C) or PRK2 (YopM Delta 6-15) were defective for virulence in this assay, indicating t

297 be expressed as RNAs; however, the majority are defective for virus production.

298 ther mutants (Y700A and Y730A) were found to be defective for virus assembly.

299 lished in staphylococcal tagO mutants, which are defective for wall teichoic acid synthesis.

300 Mutant forms of FOI that are defective for zinc transport also fail to rescue mor