1 ion of CENH3 in maize by over-expression and
mutational analysis.
2 nal miR-214-3p-binding sites as confirmed by
mutational analysis.
3 ed by negative-stain electron microscopy and
mutational analysis.
4 e sites has been discovered and validated by
mutational analysis.
5 acterize its dinucleotide-binding site using
mutational analysis.
6 ence typing (MLST), and pertactin gene (prn)
mutational analysis.
7 on, P was subjected to mass spectrometry and
mutational analysis.
8 K1 and mapped binding energy hot spots using
mutational analysis.
9 fferent substrates, provides context for the
mutational analysis.
10 ombination of genetics, in vitro assays, and
mutational analysis.
11 r function has not been studied in detail by
mutational analysis.
12 hemical and physiologic activities utilizing
mutational analysis.
13 structural modeling, molecular docking, and
mutational analysis.
14 sociated with SCN resistance, supporting our
mutational analysis.
15 Comprehensive alanine
mutational analysis across 553 residues of E1E2 also res
16 structure with functional and immunological
mutational analysis across E1E2 in order to propose an i
17 Mutational analysis allowed us to split the mRNA unwindi
18 Thus, random mutagenesis and
mutational analysis allows for the achievement of high s
19 Using
mutational analysis and a minigenome system, we identifi
20 f P(O) and P(C) in viral RNA synthesis using
mutational analysis and a minigenome system.
21 eed for a high-resolution structure to guide
mutational analysis and cautions against relying on olde
22 Through
mutational analysis and chemical complementation assays,
23 moter of DNM3os was demonstrated by promoter
mutational analysis and ChIP.
24 In combination with
mutational analysis and electrophoretic mobility shift a
25 Mutational analysis and enzymatic activity assays identi
26 uclear magnetic resonance data and performed
mutational analysis and functional assays to identify th
27 Mutational analysis and immunophenotyping have been prop
28 rdiac calsequestrin filament with supporting
mutational analysis and in vitro filamentation assays.
29 The structural data are supported by
mutational analysis and indicate that Snu17p provides an
30 Mutational analysis and inspection of the 3D structures
31 ogy to previously known cereblon substrates,
mutational analysis and modelling indicate that the cere
32 The present work employs
mutational analysis and molecular modeling of the bindin
33 Using
mutational analysis and NMR, we find that Pru binding in
34 Further
mutational analysis and quantum chemical calculations pr
35 Mutational analysis and solution studies confirmed that
36 characterization previously required expert
mutational analysis and specialized NMR or chemical mapp
37 By combining
mutational analysis and super-resolution imaging, we ide
38 By
mutational analysis and uncoupling of ISW1a's dinucleoso
39 ediate the protein interaction with DCTN3 by
mutational analysis and, based on that information, we d
40 ctroscopy, together with molecular modeling,
mutational analysis,
and fluorescent polarization bindin
41 The results of the
mutational analysis are highly relevant for the future s
42 Our
mutational analysis,
based on the electron cryomicroscop
43 ng, we employed the complementary methods of
mutational analysis,
binding studies, X-ray crystallogra
44 deficiency subgroups on the basis of tumour
mutational analysis:
BRCA mutant (deleterious germline o
45 address these issues, we performed extensive
mutational analysis by high-throughput sequencing in 215
46 analysis was compared to the current MAPREC (
mutational analysis by polymerase chain reaction and res
47 his is the first comprehensive TSC1 and TSC2
mutational analysis carried out in TSC patients in Greec
48 Functional analysis of the complex via
mutational analysis combined with RNA-binding assays and
49 Mutational analysis,
combined with bacterial two-hybrid
50 Mutational analysis confirmed an essential function for
51 Kinetic and
mutational analysis confirmed several features seen in t
52 Mutational analysis confirmed that changes in modificati
53 Mutational analysis confirmed that these modifications p
54 Mutational analysis confirmed the critical importance of
55 Mutational analysis confirmed the hypotheses, indicating
56 Finally, structure-guided
mutational analysis confirms the importance of RNA bindi
57 Mutational analysis confirms the importance of several s
58 Global and local phylogenomics, coupled with
mutational analysis,
consistently revealed that these vi
59 Structure-guided
mutational analysis converted KATms from a cAMP-regulate
60 Mutational analysis coupled with molecular docking and m
61 Mutational analysis defines a chymotrypsin-like serine p
62 Mutational analysis definitively demonstrates that TbPRM
63 Comprehensive
mutational analysis demonstrated that nearly all G/U pai
64 Mutational analysis demonstrates that FnrS and ArcZ bind
65 Mutational analysis demonstrates that the majority of th
66 Mutational analysis demonstrates that the methionine res
67 Mutational analysis demonstrates that the Wap super-enha
68 Mutational analysis demonstrates that two conserved resi
69 Mutational analysis demonstrates that VP35 interaction i
70 C with bile salt, along with biophysical and
mutational analysis,
demonstrates that the hydrophobic c
71 Mutational analysis determined that only genes in cluste
72 e applications such as nanobody development,
mutational analysis,
drug discovery, and studies of GPCR
73 Here, we have performed
mutational analysis followed by a genotype-phenotype cor
74 hat included a serum tryptase determination,
mutational analysis for KIT D816V, and bone marrow evalu
75 g of metastatic colorectal cancer (including
mutational analysis for KRAS, NRAS, BRAF, PIK3CA, and ot
76 Mutational analysis found that residues R329 and G330 in
77 Mutational analysis found that the NSs-A46 mutant, which
78 Mutational analysis has identified EcRppH residues cruci
79 to the nematode infestation, functional and
mutational analysis has shown the absence of functional
80 uctures, molecular dynamics simulations, and
mutational analysis have previously indicated that an ex
81 Furthermore,
mutational analysis identified a high-risk group of pati
82 Site-directed
mutational analysis identified a TQ motif at amino acid
83 Structure modeling and
mutational analysis identified amino acid residues impor
84 Mutational analysis identified an extended RNA-binding s
85 Molecular modeling and
mutational analysis identified residues for glucosinolat
86 1 (CK1) activity, and mass spectrometry and
mutational analysis identified serine 334 as an importan
87 Structural modeling, confirmed by
mutational analysis,
identified slc26a6 and NaDC-1 resid
88 In this study, we used
mutational analysis,
immunoblotting, HEK293 cells, and i
89 of signal intensity in the 2:1 complex, and
mutational analysis implicated the distal surface away f
90 trans relieved translational inhibition, and
mutational analysis implied a mechanism in which the clo
91 e, we have applied a combination of targeted
mutational analysis in a cell-based system and structura
92 s of the psaL, psaJ, chlN, and cpcA mRNAs by
mutational analysis in a heterologous reporter system.
93 to date followed by N/KRAS, PIK3CA, and AKT1
mutational analysis in BRAF wild-type patients.
94 By a
mutational analysis in combination with a BCR rebuilding
95 Phylogenetic and
mutational analysis in combination with activity and phe
96 Here we use
mutational analysis in combination with measurements of
97 VIPER-inferred protein activity outperformed
mutational analysis in predicting sensitivity to targete
98 Mutational analysis in the putative RNA1-contacting resi
99 e docking, molecular dynamics and systematic
mutational analysis in three Fur transporters with disti
100 However,
mutational analysis in vitro and in vivo led to the surp
101 etic resonance studies in lipid bicelles and
mutational analysis indicate differences in structure ex
102 Pulse chase and
mutational analysis indicated that HRD1 inhibits STT3B-d
103 Mutational analysis indicated that human TPP1 does not r
104 Mutational analysis indicated that multiple regions of t
105 Mutational analysis indicated that the acidic residues,
106 Mutational analysis indicated that the active site for b
107 Mutational analysis indicated that the kinase and the tr
108 Mutational analysis indicated that the presence of an A
109 Mutational analysis indicated that the TCP target motif
110 Our
mutational analysis indicates roles for different olfact
111 negatively charged alpha-Fe2O3 surface, and
mutational analysis indicates that electrostatic interac
112 Our kinetic and
mutational analysis indicates that the two double stand
113 s most commonly a clinical diagnosis because
mutational analysis is challenging in mosaic conditions.
114 We performed targeted
mutational analysis of 194 patients with rigorously defi
115 cancer metastatic process, we performed deep
mutational analysis of 676 genes in 107 stages II to IV
116 Mutational analysis of a cyclin F-specific amino acid mo
117 Mutational analysis of a rhomboid enhancer reveals at le
118 Mutational analysis of AD-5 identified tyrosine 280 in c
119 Mutational analysis of all residues of the (extracellula
120 Mutational analysis of amino acids in the binding interf
121 We also performed targeted
mutational analysis of an additional 24 such tumors and
122 Mutational analysis of bicistronic minigenomes and recom
123 Genome-wide
mutational analysis of breast and lung cancer cohorts (n
124 A recent molecular and
mutational analysis of breast cancers revealed that inac
125 uctural elucidation, molecular modeling, and
mutational analysis of BvnE, and quantum chemical calcul
126 Mutational analysis of c-kit demonstrated kinase-indepen
127 We performed
mutational analysis of CALM1, CALM2, and CALM3 gene-codi
128 Mutational analysis of candidate genes in an 11.9-Mb lin
129 Mutational analysis of celR demonstrated that the cyclas
130 Mutational analysis of conserved active site residues su
131 Structure-activity studies and
mutational analysis of contact residues define the optim
132 Mutational analysis of cysteine residues in CNPYb identi
133 Mutational analysis of eIF1A and eIF5B revealed distinct
134 Mutational analysis of exon 12 of CACNA1C was completed
135 Detailed
mutational analysis of four CRP binding sites upstream o
136 Using these data and
mutational analysis of full-length proteins, we pinpoint
137 Additionally, results from
mutational analysis of Gag revealed that membrane-bindin
138 Mutational analysis of GNB3 in a cohort of 58 subjects w
139 Here we report a
mutational analysis of HA stability utilizing a panel of
140 We report the first comprehensive
mutational analysis of HC-RES/INT ET patients and highli
141 Mutational analysis of HDAC4 suggests that the peptide i
142 Complementing this with
mutational analysis of HDAC7, we show that HDAC7, via it
143 rates the power of mouse reverse genetics in
mutational analysis of human genetic disorders and attes
144 and 24 depressed tumors, were subjected for
mutational analysis of KRAS (exon 2), BRAF (exon 11 and
145 Mutational analysis of lipin 1beta and its peptides indi
146 aralog in Saccharomyces cerevisiae Extensive
mutational analysis of Nap1 has revealed that Nap1 affin
147 Mutational analysis of nuclear and plastid isoforms demo
148 have performed an elaborate structure-based
mutational analysis of numerous Epa paralogs to generall
149 Mutational analysis of p53 and EGFR was performed on DNA
150 Mutational analysis of PE2 suggest that its signaling ab
151 Using mass spectrometry and
mutational analysis of purified proteins, we found that
152 However,
mutational analysis of R1-7 reveals differences in bindi
153 Mutational analysis of residues within the CBM65 of Ra18
154 Mutational analysis of SD motifs located upstream of the
155 Here, we performed
mutational analysis of Set5, combined with phosphoproteo
156 The
mutational analysis of swapping the residues at the +2 a
157 Here we report comprehensive
mutational analysis of the ACKR3 interaction with its ch
158 Hence, we have performed a
mutational analysis of the AMPAR region that links the f
159 Structural analysis, molecular modeling, and
mutational analysis of the ARD identified two adjacent s
160 Subsequent
mutational analysis of the candidate gene was performed
161 Mutational analysis of the cas6 gene reveals three amino
162 Here, we performed a comprehensive
mutational analysis of the conserved residues in ORF18,
163 ng a CRISPR/Cas-based method, we performed a
mutational analysis of the cwps genes.
164 Using a D2-truncation RPTPalpha variant and
mutational analysis of the D1/D2 interfaces, we show tha
165 Extensive
mutational analysis of the DBP7 promoter revealed a comp
166 Mutational analysis of the ectopic VSG 3'UTR demonstrate
167 Through
mutational analysis of the element, we demonstrate that
168 Alanine-scanning
mutational analysis of the first 62 amino acids of Vif2
169 We present an extensive
mutational analysis of the frameshift stimulators (mRNA
170 ace force apparatus combined with systematic
mutational analysis of the functional surfaces to direct
171 Mutational analysis of the i-motif DNA revealed that bin
172 pR interaction with the hcp promoter through
mutational analysis of the inverted repeat present withi
173 Mutational analysis of the LLI sequence with alanine and
174 A
mutational analysis of the major long-QT syndrome-suscep
175 Finally,
mutational analysis of the metal ligands of AdcR caused
176 Truncation and
mutational analysis of the miR-155 promoter confirmed th
177 We carried out
mutational analysis of the N-terminal 62 amino acids of
178 Cytogenetic array and
mutational analysis of the parental tumors and the corre
179 Mutational analysis of the pigmented lesions did not ide
180 biochemical and genetic approaches including
mutational analysis of the promoter, Fe(2+) cleavage ass
181 Here, we performed a large-scale
mutational analysis of the RBS of A/WSN/33 (H1N1) and A/
182 Subsequent NMR structure-based
mutational analysis of the region highlighted the critic
183 odel was tested in the current study using a
mutational analysis of the Sac7d region of the chromodom
184 y, we conducted an extensive and family-wide
mutational analysis of the serine recombinase DNA-bindin
185 We performed a comprehensive
mutational analysis of the three extracellular loops of
186 Mutational analysis of the trailer HSPA8 binding motif r
187 Mutational analysis of these hotspots reveals that the r
188 Mutational analysis of these stem loops supports a model
189 Mutational analysis of this aromatic cage supports its r
190 e performed an alanine- and glycine-scanning
mutational analysis of this pore-loop segment to systema
191 Mutational analysis of this region identified four disti
192 a striking example of convergent evolution,
mutational analysis of this terpene synthase revealed an
193 Subsequent
mutational analysis of TRDN revealed either homozygous o
194 However,
mutational analysis of tumours has largely been exhauste
195 Mutational analysis of Vps1 in a helix of the stalk doma
196 Here, we conducted a
mutational analysis of Yhc1, guided by the U1C NMR struc
197 We performed targeted
mutational analysis on samples obtained before transplan
198 Mutational analysis,
photoaffinity labeling, and structu
199 ChiLS is essential for Pygo binding, and our
mutational analysis places the NPFxD pockets on either s
200 Previously, computer modeling and
mutational analysis predicted two pyrethroid receptors,
201 Using
mutational analysis,
real-time RT-PCR, transcriptional f
202 cleotide-conversion strategy for large-scale
mutational analysis (
RESA-bisulfite).
203 Structural modeling combined with
mutational analysis revealed a highly conserved catalyti
204 Mutational analysis revealed an alpha-helical region of
205 Mutational analysis revealed an overlap between LRP1 bin
206 This high-throughput
mutational analysis revealed dominant characteristics fo
207 Mutational analysis revealed that a single amino acid (T
208 Our
mutational analysis revealed that a tripeptide motif ((2
209 Mutational analysis revealed that CS induced SCVs emerge
210 Mutational analysis revealed that KIR residues involved
211 A systematic
mutational analysis revealed that Tfp biogenesis in S. s
212 Moreover, competition experiments and
mutational analysis revealed that the helicase activity
213 Mutational analysis revealed that the patient achieving
214 showed that their interaction is direct, and
mutational analysis revealed that the pleckstrin homolog
215 Mutational analysis revealed that the VEGFR2-epsin inter
216 Mutational analysis revealed that Thr-1007 dephosphoryla
217 Mutational analysis revealed that viral clearance from t
218 Computational modeling and cellular
mutational analysis revealed the hydrophobic face of two
219 Mutational analysis revealed the remarkable importance o
220 Mutational analysis revealed Tyr747, located in the firs
221 demonstrate the presence of oligomers; (ii)
mutational analysis reveals a trans-arginine finger, R15
222 Structural and
mutational analysis reveals how nature evolves a classic
223 Structure-based
mutational analysis reveals how this enzyme recognizes t
224 Mutational analysis reveals that a riboguanosine residue
225 Furthermore,
mutational analysis reveals that all isolated EMS mutant
226 Our findings support that
mutational analysis should be considered in patients rec
227 Mutational analysis showed a role for TET13 in primary r
228 Mutational analysis showed that induction of hyphae in a
229 Mutational analysis showed that its efficient splicing r
230 Although docking and
mutational analysis showed that LDK1229 forms similar in
231 Our
mutational analysis showed that loop-1 of A3A is respons
232 Mutational analysis showed that mefenamic acid's effect
233 Mutational analysis showed that mutations in prrB impart
234 Further
mutational analysis showed that N(1575)Y could also syne
235 Mutational analysis showed that the GXXG loop in the KH
236 Mutational analysis showed that these differences result
237 Mutational analysis showed that three ABA RESPONSE ELEME
238 Furthermore,
mutational analysis shows p21 repression requires intera
239 Mutational analysis shows that Ca(2+) binding is necessa
240 Our
mutational analysis shows that differences between NtA a
241 Mutational analysis shows that key residues important fo
242 Mutational analysis shows that ligand type I specificity
243 Detailed
mutational analysis shows that one polycysteine short OR
244 Mutational analysis shows that residues forming the Ash2
245 The resolved structure, as well as
mutational analysis,
shows that the interaction is prima
246 ays with monoclonal antibody (MAb) C179, and
mutational analysis suggest that the compounds bind in t
247 Additionally, the results of
mutational analysis suggest that the membrane-binding ac
248 an N-terminal mutation in the Tyr motif and
mutational analysis suggest that transmembrane alpha-hel
249 Mutational analysis suggested that Cys(609) in GC1 is in
250 Mutational analysis suggested that differences in the N-
251 confer high Rca activity to rice Rca Further
mutational analysis suggested that Glu-217 restricts the
252 B complexes bound up to two LIS1 dimers, and
mutational analysis suggested that LIS1 binds directly t
253 Protein structure modeling and
mutational analysis suggested that the thermostability o
254 Mutational analysis suggests that Ca(2+) coordinates an
255 Mutational analysis suggests that multisite ubiquitinati
256 Broadly, our
mutational analysis suggests that there are key genes an
257 Mutational analysis suggests that while the ssDNA-bindin
258 Mutational analysis suggests the involvement of an N-ter
259 sed on recent crystal structures, along with
mutational analysis,
suggests that each subunit within a
260 Extensive
mutational analysis supports a previously unrecognized f
261 Mutational analysis supports the bifunctional PH domain
262 We also show by
mutational analysis that both of these motifs are requir
263 minal sequencing, pharmacologic studies, and
mutational analysis that proprotein convertases (PCs) pr
264 ription start site, and demonstrated through
mutational analysis that this sequence is crucial for C/
265 ble electron microscopy data, we validate by
mutational analysis the mechanism of Cdc45 association w
266 We performed
mutational analysis to define a PML interaction motif wi
267 We used a
mutational analysis to demonstrate that the EUO binding
268 luding genomics, network reconstruction, and
mutational analysis to identify and validate molecular n
269 Here we used confocal microscopy and
mutational analysis to identify the residues within the
270 Finally, we combined protein expression with
mutational analysis to map somatic genotype and clonal a
271 Using a
mutational analysis to quantify the energetic contributi
272 We also performed structure-guided
mutational analysis to survey the functions of 36 residu
273 Mutational analysis,
together with negative-staining ele
274 Mutational analysis uncovered two dsRNA-binding domains
275 Furthermore, the
mutational analysis uncovers the TM1 region of Mgr2 crit
276 Based on
mutational analysis using bacteria found resistant to on
277 Mutational analysis verified consensus sequence nucleoti
278 Comprehensive
mutational analysis was performed on I(to)-encoding KCNA
279 apping in 2 families with HIES from Tunisia,
mutational analysis was performed with selector-based, h
280 SLC6A3
mutational analysis was undertaken in all patients.
281 hrough the use of biophysical approaches and
mutational analysis,
we characterize both interfaces and
282 n with homologous HPr kinases and subsequent
mutational analysis,
we confirmed the essential catalyti
283 By systematic
mutational analysis,
we define conserved dual bi-arginin
284 Through
mutational analysis,
we demonstrate that PagPBPa is requ
285 By in vitro assays and
mutational analysis,
we demonstrate that protein arginin
286 Here, using
mutational analysis,
we determine the significance of ea
287 compartment-specific chemical labeling, and
mutational analysis,
we found that activated integral me
288 the viral 3C-like proteinase NS6(Pro) Using
mutational analysis,
we identified the FCV-induced cleav
289 Through
mutational analysis,
we identified two glutamine residue
290 On the basis of sequence and
mutational analysis,
we identify a small hydrophobic reg
291 Together with a broad
mutational analysis,
we identify essential residues dire
292 80) and an LR deletion mutant, combined with
mutational analysis,
we show here that these full-length
293 Performing biochemical and
mutational analysis,
we show that Bacillus subtilis delt
294 experiments on living cells, biochemical and
mutational analysis,
we show that CD8 binding to pMHC in
295 Through
mutational analysis,
we show that disrupting the N-termi
296 Using
mutational analysis,
we show that domains of Vpr involve
297 Using
mutational analysis,
we show that Nck sequesters WTIP an
298 Using
mutational analysis,
we show that the accessory subunits
299 Through
mutational analysis,
we validated the RPN2-binding inter
300 We combined yeast genetics and Gag
mutational analysis with Gag-ESCRT binding studies and t