ライフサイエンスコーパス: point mutant

1 r's ligase ((W37V)LplA) or any tryptophan 37 point mutant.

2 ng activity and can be replicated by a S120D point mutant.

3 y an N-WASp binding-deficient Arg SH3 domain point mutant.

4 but failed to repress an AR acetylation site point mutant.

5 wth and sorting defects of an rsp5 C2 domain point mutant.

6 if ezrin binding to NHE3 was inhibited by a point mutant.

7 tenin as well as Y654E or Y654F beta-catenin point mutants.

8 activities associated with these four single point mutants.

9 bserved of either wild-type or other similar point mutants.

10 dated by chain assembly kinetics of selected point mutants.

11 sitive to lapatinib inhibition than two HER2 point mutants.

12 es expressing FLT3-ITD or FLT3 kinase domain point mutants.

13 nging to achieve highly precise detection of point mutants.

14 lly verified and then recombined in multiple-point mutants.

15 gy surface of the wild type and other single-point mutants.

16 nd characterizing only a handful of multiple-point mutants.

17 ism hypothesis based on 18 structure-derived point mutants.

18 ication (FLT3/ITD) mutants and the FLT3/D835 point mutants.

19 Here, we extended our analysis to three syn point mutants: A855V, R858H, and A874P.

20 stability and the mechanisms by which these point mutants act.

21 Interestingly, the His(221) point mutant acted specifically as a cyclase without kin

22 A point mutant affecting the CENP-M/CENP-I interaction ham

23 d that functional cell-based assays of three point mutants affecting residues participating in sugar

24 We tested wild type (WT) and CFP-NKA-alpha1 point mutants (alanine substitution at F956, E960, L964,

25 ergetics of receptor activation, we designed point-mutants (alanine to phenylalanine) in the predicte

26 at a WMS deletion mutant, and five AD and GD point mutants all have disrupted heparin binding to TB5.

27 inculin is critical for this event because a point mutant (alpha-catenin L344P) lacking high affinity

28 However, deletion and point mutants altering conserved Zn-finger residues exhi

29 in the developing hair cells, and the dim1A point mutant alters the cell-specific expression of the

30 ion in the L-segment IGR, including a single point mutant and 35 nt partial deletion, were the only m

31 Expression of a L205R point mutant and a DnaJ-PKA fusion protein were found to

32 Both point mutant and DNMT1 (DeltaCXXC) enzyme displayed sign

33 n of 25 kDa (Snap-25): the blind-drunk (Bdr) point mutant and heterozygous Snap-25 knockout mice.

34 as inhibited approximately 50% for all three point mutants and >90% for the WRN double mutant (T1024G

35 this question, we generated a set of single point mutants and a double point mutant (tel1(KD)) of Te

36 or wild-type hTS up to about 1 mM for single-point mutants and agree with computational predictions o

37 Serum-mapping studies, using pseudovirus point mutants and antigen adsorption assays, indicated t

38 Using point mutants and chimeras with defined biochemical and

39 these residues was analyzed in vivo through point mutants and motif interchanges.

40 Structure-guided point mutants and the monobody abrogated the Prdm14-Mtgr

41 ophysical and functional characterization of point mutants and truncated versions of anophelin unambi

42 ivity as confirmed by fusion-restricted gp41 point mutants and use of the fusion inhibitor T20.

43 miniproteins, 1000 natural proteins, 10,000 point mutants, and 30,000 negative control sequences.

44 eflecting an aversive-like effect) in alpha2-point-mutant animals.

45 st, application of a highly selective FKBP51 point mutant antagonist, following FKBP51(mut) BLA-overe

46 nding site and creation of aptamer-resistant point mutants are consistent with a model of side-by-sid

47 The structures of a three-point mutant (Asn336Ser/Met348Lys/Ile246Met or MAO-N-D3)

48 /Met348Lys/Ile246Met or MAO-N-D3) and a five-point mutant (Asn336Ser/Met348Lys/Ile246Met/Thr384Asn/As

49 gle c-MYC G4 and several of its truncated or point mutants at 100 mM KCl concentration under mechanic

50 Other hedgehog point mutants at D303, also unreactive with cholesterol,

51 We showed that single point mutants at the interface altered the energy landsc

52 Here we report that a point mutant, BAL A28S, not only catalyzes the decarboxy

53 WT AID and active and inactive point mutants bind cooperatively to single-stranded DNA

54 In vivo, ARAP3 PH domain point mutant bone marrow chimeras exhibit reduced neutro

55 based on the failure of the known catalytic point mutant Bud2(R682A) to function in the checkpoint.

56 eprived wild-types and deprived CaMKII-T286A point mutants but not in undeprived animals of either ge

57 The BAH point mutants, but not the L738P mutant, disrupted the i

58 evoked, release can be rescued in a syntaxin point mutant by removing CPX-1.

59 uld be restored in several N- and C-terminal point mutants by directly tethering the minimal STIM1 ac

60 Disease-associated point mutants can reveal the unsuspected functional sign

61 n the other hand, expression of specific FAK point mutants can selectively disrupt distinct aspects o

62 Crystal structures of WT-T4L and point mutants captured a range of conformations that dif

63 Lastly, we show that the S381E point mutant caused the headpiece domain to associate wi

64 olished in constitutively inhibited Patched1 point mutants causing the Gorlin cancer syndrome, sugges

65 Because gating incompetent Blm10 C-terminal point mutants confers a loss of function phenotype, we p

66 fusion of Rh gL, EBV/Rh-LCV chimeras, and gL point mutants could be restored by replacing EBV gB with

67 type cystinosin or by the disease-associated point mutant CTNS-K280R, which has no cystine transporte

68 opic expression of wild-type CUL9, but not a point mutant CUL9 deficient in p53 binding, promotes apo

69 e bacteriophage P22 and its endorhamnosidase point mutant (D392N) with its ligands comprising two and

70 ntified an apparently nondesensitizing GluR6 point mutant (D776K) located at the apex of the ligand b

71 Point mutants defective for binding to WW domain or SMAD

72 -in mice expressing cancer-associated Aalpha point mutants defective in binding B' subunits, one knoc

73 Intracellular truncation and point mutants demonstrate that EphB2 catalytic activity

74 ng why the phenotype of cells expressing PHD point mutants differs from those expressing core Rag2 pr

75 These 6MI point mutant DNAzymes fall into three distinct functiona

76 Mn(2+), is abolished with EDTA, and an NSP4 point mutant, E(120)A, fails to bind alpha2 integrin I d

77 A series of point mutants, each lacking a single Walker A Lys residu

78 sing 53 RNAPII point mutants, we generated a point mutant epistatic miniarray profile (pE-MAP) compri

79 To assess this, we developed a point mutant estrogen receptor alpha (ERalpha) knockin m

80 Here, we show that a double point mutant EVI1-(1+6Mut), unable to bind Gata1, abroga

81 ll-surface display to screen 1341 PrP single point mutants for attenuated interaction with four anti-

82 Indeed, a point mutant from this site abolished interaction betwee

83 Point mutants further demonstrate that the primary nucle

84 Mapping with ICP27 deletion and point mutants further shows that the interaction require

85 n peptide, GLFGAIAGFIENGWEGMIDG, and its two point-mutant, fusion-incompetent peptides G1E and G13L,

86 and X-ray crystallography to characterize a point mutant, H41F, which retains actin-binding activity

87 le assembly, whereas other phospho-deficient point mutants had a minimal effect on spindle assembly.

88 Nine of the point mutants had reduced activity in vivo.

89 A panel of rho-PAR4 chimeras and PAR4 point mutants has mapped the dimer interface to hydropho

90 However, the point mutant helps reveal unexpected roles of Brg in CD2

91 roperties of no less than six of the G-->6MI point mutants highlight UV1C's built-in functional flexi

92 Using the catalytically inactive point mutant Hyal1-E131Q, we found that enzymatic activi

93 Expression of a HA-binding point mutant, Hyal1-Y202F, revealed that secretion of Hy

94 A designed point mutant, I26P-IAPP; a designed double mutant, G24P,

95 use cells, as well as the expression of BRG1 point mutants identified in human tumours, leads to anap

96 Point mutants identified the importance of four positive

97 mically inactivated toxin; however, even the point mutant impacted limits of detection, illustrating

98 t kinase TOR1) repeats 4A to 9A and a triple point mutant in repeat 9A, which showed a loss of functi

99 We identify a point mutant in the Rho-insert domain of CDC42, called c

100 eas AhpC* is inactive as a peroxidase, other point mutants in AhpC can confer the in vivo disulfide r

101 Additionally, point mutants in LLP-3 can maintain multiround propagati

102 rization-inhibiting drug A22 and by creating point mutants in mreB.

103 Point mutants in Spo0J that disrupt DNA bridging are def

104 hed by the appearance of naturally occurring point mutants in the A/M2 channel pore, among which the

105 ional essentiality of all possible nonnative point mutants in the entire hMC4R protein (332 residues)

106 The biochemical characterization of point mutants in the GTP-binding motifs of mGBP2 reveale

107 ing domain (LBD), we now report that several point mutants in the LBD have little effect on the bindi

108 k activity supported by a series of cysteine point mutants in TM6, TM7, and TM9 of mouse PS1.

109 s a template to produce a series of 21 Glut1 point mutants in which each residue along helix 6 was in

110 We developed a series of beta2-chimaerin point mutants in which intramolecular contacts that occl

111 ity measurements of the wild type and single-point mutants in which titrable residues are replaced wi

112 pic expression of wild-type S1PR2, but not a point mutant incapable of activating downstream signalin

113 deficient NK cells, expression of a PKCtheta point-mutant incapable of forming microclusters had litt

114 Significantly, several point mutants increased the inhibitory activity of nsp1,

115 ological inhibitors as well as expression of point mutants indicate that phosphorylation of TLE1 by c

116 TKI ponatinib is effective against BCR-ABL1 point mutants individually, but remains vulnerable to ce

117 We tested the model by generating 58 point mutants involving residues in and around the predi

118 mutant N12S/Q190L/H248Q, whereas each single point mutant is characterized by decelerated Pr to Pfr d

119 However, the double-point mutant is lethal, demonstrating that the essential

120 Three point mutants (K126V, K160V, and R187V) which did not fu

121 Lastly, we show that a BLAP75 point mutant (K166A), defective in Topo IIIalpha interac

122 ondrocytes, and a soluble recombinant double point mutant (K3R/Q102N) of S100A11 TG2 transamidation s

123 E126A) and a ubiquitylation-resistant double point mutant (KK90RR/KK91RR) rescued mitochondria to a l

124 We had previously generated point mutant knock-in mice and now report novel findings

125 onstructed chimeric Kv1.3-Kv1.5 channels and point-mutant Kv1.3 channels, which were expressed as GFP

126 normal B-cell development, whereas an Hdac3 point mutant lacking deacetylase activity failed to comp

127 or substrate dsRNA recognition, whereas a V2 point mutant lacking the suppressor function in vivo can

128 LH receptor point mutants lacking potential palmitoylation sites rem

129 Corresponding point mutants (M69E, A70D, L73E, S74D) were defective in

130 otide binding, and additional truncation and point mutants mapped the alterations of TCL biochemistry

131 d Cu(I) release from wild-type Atox1 and two point mutants (Met(10)Ala and Lys(60)Ala).

132 e failed to induce OIH in CaMKIIalpha(T286A) point mutant mice, although wild-type littermate mice de

133 s effect was abolished in alpha2- and alpha3-point-mutant mice, suggesting that these subunits are ne

134 These "active" point mutants mimic the behavior of WT AID for motif rec

135 n led to permanent reductions in deletion or point-mutant mtDNA in patient-derived cells, raising the

136 Among the mutants analyzed, two single point mutants, N170K and K297G, and a double mutant, N17

137 A single-point mutant near the SLIP1 homodimer interface abolishe

138 ARAP3 PH domain point mutant neutrophils are characterized by disturbed

139 rmining the reaction rate constant for every point mutant of a catalytic RNA, we demonstrated that ab

140 Second, we show that a point mutant of ARTEMIS at a putative active site residu

141 e origin of the lack of activity of the E24A point mutant of EcMazF in its inability to support the s

142 not cells with wild-type p53 and the double point mutant of fortilin lacking p53 binding, fail to in

143 In addition, fortilin, but not a double point mutant of fortilin lacking p53 binding, inhibits p

144 ated by overexpressing the acetylation-mimic point mutant of Hsp90.

145 A point mutant of IRS-1 (S270A) impaired association of IR

146 NMR studies were performed for each SMA-like point mutant of LEN followed by in silico analysis for a

147 re we show that the oncogenic potential of a point mutant of Myc (MycV394D) that is selectively defic

148 A single point mutant of P335A reduces the ability to bind syntax

149 the Rab3A Earlybird mouse which expresses a point mutant of Rab3A.

150 In this work, we study a point mutant of the C-terminal domain of ribosomal prote

151 Accordingly, a triple-point mutant of the ectodomain-deleted cadherin, which i

152 10(12) sequences, the calculation selects a point mutant of the native protein as the top solution (

153 However, binding to a panel of single-point mutants of adalimumab indicates markedly different

154 e three familial Parkinson's disease-related point mutants of alpha-synuclein, only the lipid-binding

155 Point mutants of alpha1 -antitrypsin (alpha1AT) form ord

156 e is well established, recent evidence links point mutants of betaS to dementia with Lewy bodies.

157 man chimeric CD4 molecules and site-directed point mutants of CD4, amino acids L96, P121, P122, and Q

158 Activity was severely reduced in alanine point mutants of conserved residues D138 and D139, which

159 Furthermore, analysis of point mutants of conserved residues of Bcl10 shows that

160 Kinetic data from two point mutants of CRALBP support an essential role of Glu

161 Two point mutants of ENH_DsD designed to recover the monomer

162 Point mutants of FIH were prepared to test the functiona

163 mine the inhibition sensitivity of different point mutants of highly conserved amino acid residues.

164 To address this, we identified point mutants of human IMPDH2 that either prevent or pro

165 constructed a library of randomly generated point mutants of IAPP.

166 ere confirmed in cells overexpressing single point mutants of IRS2 (S303A or S675A) containing a PKCb

167 ein function, we previously generated E gene point mutants of mouse hepatitis virus (MHV) that were d

168 Expression of Arg-to-Lys point mutants of p65 demonstrated that both Arg-30 and A

169 tention at the IS, we generated deletion and point mutants of PKCtheta.

170 Although several point mutants of Ras exhibit a dominant negative effect,

171 this by testing the ability of A13P and F15D point mutants of rat IAPP to inhibit amyloid formation b

172 Finally, point mutants of residues in the conserved metal-binding

173 We show here that point mutants of Saccharomyces cerevisiae eRF1 display s

174 Three single- or double-point mutants of the C4-symmetric protein RhuA were desi

175 ctions are poorly understood, truncation and point mutants of the integrin alpha1 subunit cytoplasmic

176 se compounds were tested against a series of point mutants of the ligand-binding domain residue Gln-5

177 S1P(2) point mutants of the ligand-binding pocket were characte

178 Steady-state kinetic analysis of multiple point mutants of the lipid-binding pocket pinpoints crit

179 We therefore examined 49 point mutants of the pore-lining residues, representing

180 ed COS cells using a battery of truncated or point mutants of the three proteins.

181 We have isolated several point mutants of the toxin CcdB that fail to bind to its

182 sis of the structure, we identify truncation/point mutants of the TPRs that have differential effects

183 With reverse genetics reassortants and point mutants of the two clinical isolates, we further s

184 n) is inserted into functionally-inactivated point mutants of two target proteins (staphylococcal nuc

185 ll microscopy and specific calpain-resistant point-mutants of talin (L432G) and FAK (V744G), we find

186 silico saturation mutagenesis the effects of point mutants on its structural stability.

187 to investigate the effects of all ubiquitin point mutants on yeast growth rate.

188 sociation defect, while patient-derived SBDS point mutants only partially improved subunit associatio

189 dominant negative and human- disease-allele point mutants or knock-out and knockdown models, we show

190 anines within the amphipathic helix (M2 five-point mutant, or 5PM) reduced scission and also filament

191 entia, the deletion mutant DeltaK280 and the point mutant P301L.

192 (2)IValpha mutant (PLA(2)IValpha(1-525)) and point mutant (PLA(2)IValpha-S228C) also promotes recover

193 rent mutants, three JS-causing variants, two point mutants predicted to alter guanine nucleotide hand

194 We identify PSD-95 point mutants (Q15A, E17R) that maintain PSD-95's influe

195 ion of wild-type L1CAM, but not of the L1CAM point mutants R1166X and S1224L, rescued the decrease in

196 ore, a C-terminally truncated Vpr mutant and point mutants R80A and Q65R, all of which lack G2 arrest

197 We conclude that conditional point mutants, rarely used in mammalian genetics, can he

198 An L2 double point mutant renders the TM domain nonfunctional and blo

199 Both hydrolytically active and inactive FlhF point mutants restored polar flagellar assembly, as seen

200 Four point mutants retained catalytic activity at 1/3rd to 1/

201 A subset of PilA point mutants retained the ability to interact with PilS

202 mplexes of wild-type and the Leu28Phe (L28F) point mutant reveal conformational exchange between an o

203 rmal titration calorimetry studies of single-point mutants reveal that residue F309, which is located

204 Point mutants revealed a structural role of this N-termi

205 Surprisingly, analysis of profilin point mutants revealed that differences in highly conser

206 Characterization of several of designs and point mutants revealed that in all cases, the mutations

207 chimeric molecules, isolated C2 domains, and point mutants revealed that the C2B domain of the fly pr

208 arge panoply of known natural and artificial point mutants revealed that this general dominant negati

209 minus (NT) and extracellular loops, and CCR5 point mutants revealed that, relative to parental R3A, R

210 Systematic comparison of Pkd1l1 and Pkd2 point mutants reveals strong phenocopying, evidenced by

211 inant-negative CREB1 mutant (K-CREB) or of a point mutant (S133A) resulted in a decreased ability of

212 Interestingly, none of the point mutants seemed to perturb the ability of Kar3Vik1

213 Targeted intracellular point mutants showed that axon pruning requires tyrosine

214 We generated AQP9 point mutants showing that this effect is independent fr

215 Four new site point mutants showing the effects of side-chain alterati

216 xibility improves the accuracy of predicting point-mutant side-chain conformations over fixed backbon

217 tohydroxylation, it is more likely that this point mutant simply mispositions the HIF-Asn(803) side c

218 pleted of Prp43 or expressing only catalytic point mutants, six snoRNAs that guide modifications clos

219 ed 12 different familial melanoma-associated point mutants spanning the p16 coding region and analyze

220 16 in LRRK2 (equivalent to Ala147 in CHK1 10-point mutant structure).

221 uency and scale of the changes within single point mutant structures are generally larger than those

222 ar modeling and functional analyses of Bcl10 point mutants suggest that residues Asp(80) and Glu(84)

223 inetic analysis of 20 G. max ATP sulfurylase point mutants suggests a reaction mechanism in which nuc

224 phenotypes of key ChpA phosphorylation site point mutants supported a scheme whereby ChpArec functio

225 type 3 Dearing (T3D) and T3D-sigma1R202W, a point mutant T3D derivative that does not bind sialic ac

226 d a set of single point mutants and a double point mutant (tel1(KD)) of Tel1p that were kinase defici

227 Moreover, AhpC* and several point mutants tested in vitro exhibit an enhanced reduct

228 this processing and a catalytically inactive point mutant, TG1-FLAG(C377A), accumulates in the endopl

229 eir effect in pathology, but we identify one point mutant that abrogates complex formation without af

230 We identify a point mutant that abrogates this interaction and show th

231 versely, the slower disassembly of foci in a point mutant that constitutively binds Rad51 correlates

232 In contrast, an ICP27 point mutant that does not interact with Nup62 had no su

233 Furthermore, by employing a pnp-R100D point mutant that encodes a catalytically inactive PNPas

234 Instead, foci disassemble more rapidly in a point mutant that fails to bind Rad51, associated with f

235 own deacetylase of Hsp90, or overexpressed a point mutant that mimics the hyperacetylated state of Hs

236 Characterization of a vinculin point mutant that specifically disrupts F-actin binding

237 We also report a Ras point mutant that stabilizes the protein in the open con

238 stance and virulence, we constructed a HSV-2 point mutant that synthesizes full-length vhs protein la

239 a strain of B. burgdorferi carrying an rrp2 point mutant that was defective in its ability to activa

240 models of pulmonary fibrosis, a 3-amino acid point mutant that was unable to bind pSMAD3 proved ineff

241 t genetic screening system, we identify Lhx3 point mutants that bind to NLI but not Isl1.

242 to efficiently generate plasmid libraries of point mutants that can then be transformed to generate l

243 Nase or dNTPase activity, we identify SAMHD1 point mutants that cause loss of one or both functions.

244 rategy for predicting highly stable multiple-point mutants that combines energy- and evolution-based

245 Characterization of ARL2 point mutants that disrupt binding to TBCD suggested tha

246 Point mutants that disrupt their ability to stimulate ac

247 Double cysteine point mutants that engineer extra interdomain disulfide

248 However, point mutants that increase or decrease the affinity of

249 We investigated five known mGluR6 point mutants that lead to CSNB1 to determine the molecu

250 berculosis pathogenesis, we generated RelMtb point mutants that were either synthetase dead (RelMtb(H

251 sitions into KIR2DL1 and KIR2DL3 produced 38 point mutants that were tested for binding to 95 HLA- A,

252 Out of a panel of 554 point mutants throughout SERT, 10 were found to improve

253 tration upon binding, we engineered a single-point mutant to destabilize the interface of Pfk-2.

254 n (SHAPE) chemistry coupled with analysis of point mutants to map long-range interactions in this RNA

255 structures, we engineered a series of GCaMP2 point mutants to probe the mechanism of GCaMP2 function

256 ts, we could effectively substitute selected point mutants to test these in the cellular recombinatio

257 active isoform of human HIF-1a (HIF-1a three point mutant (TPM)), in a doxycycline-dependent manner.

258 reconstituted with wild-type (wt) alpha3 or point mutants unable to engage laminin 5 (G163A) or epit

259 EVI1 interaction sites, we show that an EVI1 point mutant, unable to bind PU.1, restores the activati

260 ion mutants of unc-68, and in particular the point mutant UNC-68(R4743C), analogous to the establishe

261 rmine the fitness of all possible individual point mutants under controlled conditions for a nine-ami

262 Kinetic analysis of VR1 point mutants using VWF115 as a short substrate revealed

263 mportance of the IXVXI motif, we created the point mutant V181A, which, as expected, disrupts the Hsp

264 ve adsorption with native gp120 and specific point mutant variants, chimeric virus analysis, and pept

265 Using a dominant-negative, deacetylase-dead point mutant virus (AAV-HDAC3(Y298H)-v5), we found that

266 ction of mice with the macrodomain catalytic point mutant virus (N1347A) resulted in reductions in le

267 ling of the pore formation process, and in a point mutant, W165T, for which the pore formation proces

268 During this work, two point mutants, W348R and E349K, were identified as trans

269 The CHK1 10-point mutant was preferred, following assessment of surr

270 urgdorferi expressing individual dbpA lysine point mutants was assessed in mice challenged via needle

271 A panel of Runx2 deletion and point mutants was used to examine RUNX2-SMAD protein-pro

272 extensive analysis of receptor deletion and point mutants we have discovered that position 602 resid

273 Using a translocation-deficient MspA point mutant, we showed that susceptibility of M. smegma

274 For both wild-type PDZ domains and single point mutants, we find that 70-80% of the most frequentl

275 studies of ATPase inactive full-length Spa47 point mutants, we find that Spa47 oligomerization and AT

276 expressing a series of PECAM-1 deletion and point mutants, we found that the PECAM-1 cytoplasmic dom

277 ng experiments with a series of deletion and point mutants, we further demonstrate that the ciliary l

278 Using 53 RNAPII point mutants, we generated a point mutant epistatic min

279 Ectopically expressed FANCC point mutants were capable of fully complementing the mi

280 Point mutants were constructed and expressed in Xenopus

281 Eight single-point mutants were designed at these sites, of which fiv

282 ght into the protein's function, a number of point mutants were generated altering both DNA binding a

283 esidues in ADAMTS1 or ADAMTS2) and 18 single-point mutants were generated in these VRs and expressed.

284 these residues are important for catalysis, point mutants were prepared in the human enzyme.

285 s involved in self-cleavage were identified; point mutants were produced and characterized structural

286 Additional point mutants were used to identify two GC-rich regions

287 vage activity at the 3'-end of 18 S rRNA, as point mutants where this interaction is abolished in vit

288 e first time that combining a synaptic mouse point mutant with a controlled prenatal stressor paradig

289 t VSV-Lassa and VSV-Junin), including an SFV point mutant with a lower pH threshold for fusion (SFV E

290 cance of the CARMIL1-CP interaction, using a point mutant with a well-defined biochemical defect.

291 However, neither point mutants with alterations in this region nor the co

292 y antibody affinity, we compared a series of point mutants with known affinities and show that even s

293 ned space), and predicts the conformation of point mutants with similar accuracy and generates biolog

294 We show that naturally occurring HIV-1 Vif point mutants with suboptimal anti-APOBEC3G activity ind

295 aring the effects of asymmetric histone tail point mutants with those of symmetric double mutants rev

296 Two Axin point mutants within the Armadillo binding domain were w

297 Specifically, two point mutants within the Shaggy binding domain showed lo

298 molecular dynamics simulations of the single-point mutant Y169G.

299 coccal Enterotoxin B (SEB) mutants, a single point mutant (Y89A), and a mutant with three amino acids

300 pha-bergamotene and (E)-beta-farnesene, or a point mutant ZmTPS10M, which produces primarily (E)-beta