ライフサイエンスコーパス: point mutant

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

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

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

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

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

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

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

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

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

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

11 activities associated with these four single point mutants.

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

13 est determined comprehensive fitness maps of point mutants.

14 dated by chain assembly kinetics of selected point mutants.

15 nging to achieve highly precise detection of point mutants.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 Using point mutants and chimeras with defined biochemical and

36 n clinically relevant BCR-ABL1 kinase domain point mutants and further sensitized Ba/F3 BCR-ABL1 cell

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

38 Through analysis of point mutants and naturally occurring Vif variants, we f

39 in-IV sequence, we produced a library of 373 point mutants and tested them for Na(v)1.7 and Na(v)1.2

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

48 ne scanning mutagenesis was used to generate point mutants at all possible residues within a GFP-Dbp5

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

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

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

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

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

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

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

56 mined wild-type SOD1 and six disease-related point mutants by using tandem MS and ion-mobility MS as

57 Remarkably, an inactive NSH1 point mutant can activate NSH2 in vivo, fully preventing

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

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

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

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

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

63 Our work represents a comprehensive single-point mutant characterization and mapping of the 70S rib

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

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

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

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

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

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

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

71 Intracellular truncation and point mutants demonstrate that EphB2 catalytic activity

72 ls structural differences between DHFR and a point mutant (DHFR-G121V).

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

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

75 wild-type DQ2, versus a DM-susceptible, DQ2 point mutant DQ2alpha+53G.

76 nificantly absent for catalytically inactive point mutant (E219Q) of MMP1 and could be modulated by a

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

78 monstrated that these catalytically inactive point mutants enable robust detection and visualization

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

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

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

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

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

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 n, containing Ag NPs, ds-DNA of EGFR exon 21 point mutant gene, GEM as a template molecule, 3-(aminop

87 evaluating its interaction with EGFR exon 21-point mutant gene.

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

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

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

91 The H18R point mutant has been previously shown to reduce aggrega

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

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

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

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

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

97 An ASNA1 point mutant identified using CRISPR-mediated mutagenesi

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

99 Point mutants identified the importance of four positive

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

101 g the maturation cycle of tubulin by using a point mutant in beta-tubulin confers hyperstable microtu

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

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

104 rt this model through functional analysis of point mutants in both AimB and MreB, photo-cross-linking

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

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

107 Point mutants in Spo0J that disrupt DNA bridging are def

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

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

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

111 The point mutants in the WPD loop alter the loop equilibrium

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

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

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

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

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

117 Two single-point mutants increased beta-ionone yields almost 3-fold

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

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

120 Results with catalytically inactive point mutants indicated that OGT-1 glycosyltransferase a

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

122 e new hENM model allows integrins and single-point mutant integrins to explore various conformational

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

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

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

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

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

128 -binding properties, with disease-associated point mutants known to increase as well as decrease affi

129 The W317A TAT-RasGAP(317-326) point mutant, known to have impaired killing activities,

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

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

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

133 LH receptor point mutants lacking potential palmitoylation sites rem

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

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

136 on is associated with human infertility, the point mutant mice are fertile despite meiotic defects.

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

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

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

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

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

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

143 ARAP3 PH domain point mutant neutrophils are characterized by disturbed

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

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

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

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

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

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

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

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

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

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

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

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

156 n we used this method to assess all possible point mutants of a canonical T7 RNAP promoter, our resul

157 these effects, we used differentially stable point mutants of a single protein, TEM-1 beta-lactamase.

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

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

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

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

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

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

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

165 Two point mutants of ENH_DsD designed to recover the monomer

166 Point mutants of FIH were prepared to test the functiona

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

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

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

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

171 Finally, we identify several point mutants of Merlin associated with neurofibromatosi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 A structure-guided point mutant (R118E) in F1, which blocks Rap1 binding, a

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

200 ied whether WT p53 and cancer-associated p53 point mutants regulate ICMT levels and whether ICMT over

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

202 ution and a selected glaucoma-causing single-point mutant rescued in vitro folding and stability defe

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

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

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

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

207 Molecular genetic analyses of both point mutants reveal an important role for MEIOB in cros

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

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

210 sidase activity of wild-type TSP3 to various point mutants revealed that catalysis requires the carbo

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

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

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

214 omparative analysis of thrombin and a single-point mutant reveals that the simulation analysis can di

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

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

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

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

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

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

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

222 16 in LRRK2 (equivalent to Ala147 in CHK1 10-point mutant structure).

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

224 with inserted lacZ reporter gene; (2) a C59S point mutant substitution and (3) an R141C point mutant

225 S point mutant substitution and (3) an R141C point mutant substitution.

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

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

228 d shifts) on the CTD of both wild type and a point mutant (T142A) within the S/T region of the first

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

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

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

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

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

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

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

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

237 ned the vTA complex as a whole, and an ORF18 point mutant that failed to bind ORF30 was unable to com

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

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

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

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

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

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

244 PLY non-pore-forming point mutants that are trapped at various stages of pore

245 ferent pools of KIF4A, we generated specific point mutants that are unable to interact with either co

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

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

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

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

250 ur findings are based on a library of double point mutants that contain each one loss-of-function wit

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

252 Point mutants that disrupt their ability to stimulate ac

253 Double cysteine point mutants that engineer extra interdomain disulfide

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

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

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

257 ted using mice lacking DEL-1 or expressing a point mutant thereof, or mice with T cell-specific delet

258 AlfC and certain point mutants thereof have been used to add and remove f

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

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

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

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

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

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

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

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

267 Examination of additional point mutants unexpectedly revealed that the CTS of Bim

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

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

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

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

272 Point mutant viruses indicated that K90 is critical for

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

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

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

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

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

278 Using chimeras and point mutants we have mapped the binding site of the P2X

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 Here, we describe the phenotype of 2 Cdk2 point mutants with elevated or decreased activity, respe

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

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

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

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

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