1 tion of its substrate MepS by structural and
mutational analyses.
2 erform coimmunoprecipitation experiments and
mutational analyses.
3 DP2 was confirmed by peptide competition and
mutational analyses.
4 teraction using structural, biophysical, and
mutational analyses.
5 prompt detailed DNA promoter methylation or
mutational analyses.
6 k for understanding and interpreting earlier
mutational analyses.
7 been the subject of extensive structural and
mutational analyses.
8 ity of the P. furiosus Rad50 structure-based
mutational analyses.
9 be assigned to these key interactions using
mutational analyses.
10 The use of bioinformatics,
mutational analyses,
a substrate competitor peptide, and
11 p molecular models that, in conjunction with
mutational analyses,
allow us to propose an active site
12 Statistical coupling and correlated
mutational analyses along with clustering revealed a hig
13 We demonstrate, through
mutational analyses and domain replacement experiments,
14 Mutational analyses and domain swapping experiments were
15 Mutational analyses and functional assays have identifie
16 FLT3, NPM1, CEBPA, WT1, and MLL
mutational analyses and gene- and microRNA-expression pr
17 membrane), we performed domain swapping and
mutational analyses and identified a C-terminal di-leuci
18 Mitochondrial DNA damage was analyzed by
mutational analyses and measurement of mtDNA copy number
19 Using
mutational analyses and phosphorylated peptides, we show
20 and regulation of these three operons using
mutational analyses and promoter-reporter fusions.
21 Mutational analyses and simulations in the presence and
22 Mutational analyses and structural comparisons with othe
23 transcriptional regulation of SLICK/Slick by
mutational analyses and studying gene expression by luci
24 NMR data together with
mutational analyses are consistent with Zn(2+) coordinat
25 However, results from
mutational analyses are open to alternative interpretati
26 Biophysical and
mutational analyses are used to map regions of the PI31
27 Guided by our
mutational analyses as well as hydroxyl radical footprin
28 mplexes between these components and perform
mutational analyses based on the structures.
29 Mutational analyses both in vitro and in vivo provide ev
30 Previous
mutational analyses centered on mutants with substitutio
31 A combination of promoter deletion and
mutational analyses,
chromatin immunoprecipitation assay
32 Mutational analyses confirm that several residues identi
33 Mutational analyses confirm the essential structural rol
34 Mutational analyses confirm the importance of these resi
35 Mutational analyses confirmed that the small cold shock
36 Supershift and
mutational analyses confirmed the binding of YY1 to this
37 Mutational analyses confirmed the functional relevance o
38 Further,
mutational analyses confirms that the atypical CRD is cr
39 Mutational analyses corroborated the results of the tran
40 Mutational analyses defined the requirements for the IN-
41 Mutational analyses demonstrate a correlation between th
42 interactions only with Vdelta1(+) TCRs, and
mutational analyses demonstrate a role of the Vdelta1 do
43 Mutational analyses demonstrate analogous interactions i
44 Our
mutational analyses demonstrate that pore loop 2 residue
45 Mutational analyses demonstrate that the knot is importa
46 Our
mutational analyses demonstrate that, similar to other d
47 Mutational analyses demonstrated that both the InR and D
48 Although
mutational analyses demonstrated that conserved amino ac
49 Enzyme inhibition studies and
mutational analyses demonstrated that protein kinase CK2
50 Mutational analyses demonstrated that Raf-1 S471 is crit
51 Mutational analyses demonstrated that the basic patch re
52 Mutational analyses demonstrated that the majority of th
53 Sequence and
mutational analyses demonstrated that TRM contained a re
54 Here, we report results from
mutational analyses demonstrating that yeaR-yoaG operon
55 Protein-protein interaction and
mutational analyses established that the antiviral effec
56 We utilise structural and
mutational analyses,
fibril growth kinetics and solubili
57 Mutational analyses found that sequences within the IME4
58 Our
mutational analyses further indicate that the N-terminal
59 SAXS and
mutational analyses further reveal that the preformed di
60 Mutational analyses further showed that the conserved Cy
61 Crystallographic studies and
mutational analyses have contributed to a general unders
62 Mutational analyses have established that an interaction
63 Mutational analyses have identified several key PCD comp
64 Genetic and
mutational analyses have identified the transmembrane (T
65 Mutational analyses have indicated that the carboxyl-ter
66 Although
mutational analyses have indicated that transmembrane (T
67 Mutational analyses have recently revealed that these mo
68 Mutational analyses have revealed many genes that are re
69 Mutational analyses have revealed that separate domains
70 Comprehensive
mutational analyses have revealed that the mixed lineage
71 X-ray structural and
mutational analyses have shown that bovine heart cytochr
72 Mutational analyses have suggested that a central substr
73 Mutational analyses have suggested that the carboxyl-ter
74 s-linking coupled with mass spectrometry and
mutational analyses identified a new interaction between
75 Mutational analyses identified distinct crucial binding
76 In addition,
mutational analyses identified functional domains of r12
77 Mutational analyses identified no coding or intron junct
78 Previous
mutational analyses identified residues within the Gag m
79 Mass spectrometric and
mutational analyses identified Ser730 as the only phosph
80 Deletional and
mutational analyses identified that Plk1 phosphorylated
81 Mass spectrometry and
mutational analyses identified Thr-18 and Thr-33 as the
82 Mutational analyses identify Glu(276), Phe(280), and Val
83 Our
mutational analyses identify the D261, E262, and C-termi
84 Through
mutational analyses in 7325 individuals, we report four
85 e the roles of active-site residues by using
mutational analyses in a peptide synthesis assay with in
86 idated our computational predictions through
mutational analyses in cell transfection experiments.
87 Mutational analyses in situ confirmed expression of muta
88 an enormous hydrophobic groove implicated by
mutational analyses in tail-anchored protein binding.
89 pts the other, confounding interpretation of
mutational analyses in the context of the virus.
90 ding to mutations indicate the importance of
mutational analyses in the future.
91 This idea is consistent with
mutational analyses in various sensory systems, where mu
92 Through a series of
mutational analyses,
in combination with biochemical and
93 Bioinformatics and
mutational analyses indicate that a conserved Gly117 (he
94 Limited
mutational analyses indicate that arginine 488 located w
95 logical and molecular genetic approaches and
mutational analyses indicate that extracellular signal-r
96 e S-transferase fusion pulldown and receptor
mutational analyses indicate that GRIN1-MOR interaction
97 Structural and
mutational analyses indicate that high flexibility and d
98 Mutational analyses indicate that neither phosphorylatio
99 Together, structural and
mutational analyses indicate that only two of the four C
100 However,
mutational analyses indicate that SmgGDS utilizes a dist
101 Biochemical analyses and
mutational analyses indicate that SpoIVA and SipL direct
102 ently suppress the expression of STAT-1, and
mutational analyses indicate that the E6 targeting E6-as
103 Mutational analyses indicate that the high sensitivity o
104 Recent
mutational analyses indicate that this process is more c
105 AC) found for other SBP domain proteins, but
mutational analyses indicated that at least one addition
106 For one such individual,
mutational analyses indicated that four polymorphisms se
107 Accordingly,
mutational analyses indicated that GATA sites are requir
108 Mutational analyses indicated that nuclear localization
109 Mutational analyses indicated that the C-terminal region
110 Mass-spectrometry and
mutational analyses indicated that the PRF occurred thro
111 Mutational analyses indicated that the transmembrane dom
112 Mutational analyses indicated that the turnover of the p
113 Mutational analyses indicated that two of four G tracts
114 The combined structural and
mutational analyses lead to the detailed understanding o
115 Structure-based
mutational analyses mapped the binding site for the [GS]
116 ell as the results from previous genetic and
mutational analyses,
methylotrophy is enabled by methano
117 Our structural and
mutational analyses not only establish structural bases
118 Mutational analyses of a putative coiled coil region in
119 Mutational analyses of ATG3 confirm that four residues w
120 Point
mutational analyses of C21 revealed that a conserved pro
121 Positional cloning and
mutational analyses of candidate genes were performed to
122 Mutational analyses of consensus-type glmS ribozymes sup
123 obank" agrees well with previous large-scale
mutational analyses of CRC.
124 Mutational analyses of CTCL patient peripheral blood mal
125 activator for CYP7A1, we used deletional and
mutational analyses of CYP7A1 promoter sequences and def
126 Mutational analyses of differentially regulated genes re
127 tors (GABA(A)R) with an etomidate analog and
mutational analyses of direct activation of GABA(A)R by
128 Mutational analyses of DLS sequences confirmed their fun
129 nhancers, those who are undertaking detailed
mutational analyses of enhancer sequences, or those who
130 tic alterations, and the ability of unbiased
mutational analyses of entire tumor genomes is likely to
131 ccus furiosus Mre11 dimers bound to DNA with
mutational analyses of fission yeast Mre11.
132 Taken together, structural and
mutational analyses of gate residues suggest key roles o
133 Mutational analyses of genomic DNA from the Dicer and Dr
134 Here, using
mutational analyses of hepatitis B virus (HBV), we found
135 Mutational analyses of HPV16 E7 indicate that the major
136 Mutational analyses of Hsp70 and Hop were undertaken to
137 We performed
mutational analyses of IFITM3 and identified multiple re
138 Mutational analyses of intragenic suppressors and coexpr
139 Mutational analyses of IRF8 showed that its ability to b
140 Comprehensive
mutational analyses of KCNQ1 (KV7.1, LQTS type 1), KCNH2
141 Mutational analyses of LAT, Gads, and SLP-76 indicated t
142 Mutational analyses of MARCH1 defined discrete domains r
143 nterfaces has been limited to structural and
mutational analyses of natural binding partners or small
144 Biological and
mutational analyses of our peptide provide new insights
145 In vivo and in vitro
mutational analyses of Phe91 and Trp93 emphasize the imp
146 Furthermore, truncation and
mutational analyses of PknK revealed that PknK is autore
147 Mutational analyses of protein-DNA contacts, which were
148 Mutational analyses of RecA1/RecA2 domains confirmed the
149 Structure-guided
mutational analyses of RopB dimer interface demonstrated
150 Mutational analyses of Sdh1 implicate C-terminal region
151 Mutational analyses of SNAP190 support a model wherein C
152 Mutational analyses of some of these genes have implicat
153 Mutational analyses of structurally conserved regions of
154 Further transcriptional, binding, and
mutational analyses of the 5' promoter have identified t
155 Deletion and
mutational analyses of the 5'-flanking region of the HSD
156 Mutational analyses of the 5'-leader of ATF5 mRNA fused
157 ction, we used solution NMR spectroscopy and
mutational analyses of the active fragment, PR11, which
158 provide a null genetic background to perform
mutational analyses of the Ago2 protein.
159 Mutational analyses of the alpha-internexin promoter dem
160 The
mutational analyses of the CHV-1/EP713 infectious cDNA c
161 Furthermore,
mutational analyses of the conserved EAL and GGDEF resid
162 Site-specific
mutational analyses of the conserved residues within WRD
163 Our
mutational analyses of the Ede1 UBA domain-ubiquitin int
164 try, fluorescence in situ hybridization, and
mutational analyses of the EGFR gene have all been propo
165 Taken together, our structural and
mutational analyses of the Hda-beta clamp complex indica
166 Chemical modification and
mutational analyses of the longer and shorter forms of t
167 Mutational analyses of the Nop5 protein interface sugges
168 Here, we perform systematic statistical and
mutational analyses of the overlapping HIV-1 genes tat a
169 Mutational analyses of the p12 Gag phosphoprotein of Mol
170 Mutational analyses of the p51 YMDD aspartates indicated
171 Immunohistochemical and
mutational analyses of the patient's melanocytic tumors
172 Mutational analyses of the positionally conserved sORF o
173 g region of the viral genome was revealed by
mutational analyses of the predicted microRNA binding si
174 Mutational analyses of the PRKAR1A gene in 51 unrelated
175 Mutational analyses of the promoter region combined with
176 By deletion and
mutational analyses of the RNA structures, we have deter
177 Mutational analyses of the secreted recombinant insulin
178 ute to secondary tumorigenesis, we performed
mutational analyses of the TP53, BRCA1, and BRCA2 tumor
179 Mutational analyses of the two EAL motifs of DipA sugges
180 putational modeling, circular dichroism, and
mutational analyses of the zinc finger domain of MDM2 an
181 Mutational analyses of these PrP(Sc)-binding regions rev
182 ed with HSCR, in the Ednrb ENS enhancer, and
mutational analyses of these sites suggested that SOX10
183 Mutational analyses of two components of the CheIV clust
184 Mutational analyses of VPg indicate that a subset of the
185 family enzymes as a model, we have conducted
mutational analyses on AtEYA to query the roles of conse
186 Coupled with
mutational analyses,
our studies reveal the critical rol
187 tein function has been probed extensively by
mutational analyses,
particularly in plants where large
188 studies, cryo-electron microscopy (cryo-EM),
mutational analyses,
peptide binding analysis, linker-sc
189 drophobic pocket does not bind HLA class II,
mutational analyses presented here indicate that this do
190 Modeling and
mutational analyses provide evidence that SpoIIGA is a n
191 Structural and
mutational analyses provide new insights into a putative
192 Mutational analyses provided evidence that this stem-loo
193 Mutational analyses provided insights into sequence reco
194 Mutational analyses resulted in the identification of ei
195 The structure and associated
mutational analyses reveal molecular details of Ubc12 re
196 Mutational analyses reveal multiple phosphorylation site
197 Mutational analyses reveal that cFLIPL nuclear localizat
198 Mass spectrometric and
mutational analyses reveal that K133 of pro-IL-1beta is
199 Mutational analyses reveal that self-interaction is crit
200 Sequence and
mutational analyses reveal that the cleavage occurs with
201 However,
mutational analyses reveal that the helicase function of
202 AGO structure modelling and
mutational analyses reveal that the QF-V motif within th
203 Our
mutational analyses reveal the individual contributions
204 Mutational analyses revealed combinatorial, non-exchange
205 Mutational analyses revealed differential binding affini
206 Importantly,
mutational analyses revealed extensive auto-inhibitory m
207 Mutational analyses revealed that a conserved leucine re
208 Mutational analyses revealed that DAB2 interacts with TN
209 Phospho-proteomic and
mutational analyses revealed that eIF4G1 is a substrate
210 Subsequent
mutational analyses revealed that HvgA and capsule, but
211 omputationally predicted targets followed by
mutational analyses revealed that let-7 and miR-18 down-
212 Mutational analyses revealed that MC159 and cIAP1 each b
213 Positional cloning and
mutational analyses revealed that nbl results from a V32
214 Mutational analyses revealed that sequences throughout t
215 Further
mutational analyses revealed that the "NF" sequence with
216 Mutational analyses revealed that the acidic cluster and
217 Mutational analyses revealed that the conserved Phox2 an
218 Further
mutational analyses revealed that the first 10 amino aci
219 sphatase activity and a series of subsequent
mutational analyses revealed that the N terminus of HDAC
220 Mutational analyses revealed that the N-terminus of AurA
221 ing proteins RIP1 and RIP3, and deletion and
mutational analyses revealed that the RHIM in TRIF was e
222 mapping, selective amino acid labeling, and
mutational analyses revealed the peptidyl transferase ce
223 Mutational analyses revealed the sites of modification o
224 Mutational analyses revealed two conserved cysteines and
225 ere, small angle X-ray scattering (SAXS) and
mutational analyses show APLF is largely an intrinsicall
226 Comparison with other helicases and
mutational analyses show how it threads single-stranded
227 Deletion and site-specific
mutational analyses show that arginine 73 in ABI1 is ess
228 of the MT1-MMP-mediated cleaved products and
mutational analyses show that cleavage of DDR1 takes pla
229 Time course and
mutational analyses show that DNA bending occurs after r
230 Mutational analyses show that most residues interacting
231 Mutational analyses show that the contacts of both recog
232 Mutational analyses show that the GluN2A preference of S
233 Furthermore,
mutational analyses show that there is a strong correlat
234 Cross-competition assays and
mutational analyses showed evidence for at least three d
235 ding determinants or "recognition elements."
Mutational analyses showed that all three recognition el
236 Molecular dynamics and
mutational analyses showed that alphaKG binds TDG on Arg
237 Sequence and
mutational analyses showed that auto-repression involves
238 Mutational analyses showed that autosomal recessive hypo
239 Mutational analyses showed that bombesin-enhanced cyclin
240 Mutational analyses showed that both CMD-1 and HTH-4 are
241 Mutational analyses showed that both Valpha/Vbeta interf
242 Mutational analyses showed that CRTCs possess distinct f
243 Further
mutational analyses showed that most of the 93 bp MRR re
244 ved in the subgroup 3 tobamoviruses, and our
mutational analyses showed that nuclear localization of
245 Structural and
mutational analyses showed that ribosome-bound NEMF recr
246 In vitro footprinting and in vivo
mutational analyses showed that SgrS base pairs with man
247 Metabolic, enzymatic and
mutational analyses showed that the gsIII-like gene enco
248 ment usage and different docking mechanisms,
mutational analyses showed that the TCRs shared a conser
249 Mutational analyses showed that these contacts are impor
250 TP53
mutational analyses spanned exons 4 to 8.
251 Although biochemical and
mutational analyses strongly suggest that the heptad-rep
252 Kinetic and
mutational analyses strongly suggest that these structur
253 Through
mutational analyses,
such a state is known to enhance th
254 Further
mutational analyses suggest a novel mechanism of Tau reg
255 J protein in the chimera and the results of
mutational analyses suggest that an evolutionary correla
256 Mutational analyses suggest that biphasic activation of
257 Mutational analyses suggest that further interaction bet
258 Furthermore, promoter deletion and
mutational analyses suggest that mevastatin induced KLF2
259 Collectively, these
mutational analyses suggest that minor sequence differen
260 Mutational analyses suggest that p22/p18 is synthesized
261 Mutational analyses suggest that this motif binds a repr
262 Mutational analyses suggest that Vpr interacts with DNA-
263 Mutational analyses suggested that the observed effects
264 Insertion and deletion
mutational analyses support a beta-barrel structure mode
265 Mutational analyses support that these mechanisms underl
266 Mutational analyses support the view that HIRA acts as a
267 Most RYR2
mutational analyses target 3 canonical domains encoded b
268 Therefore, we examined by
mutational analyses the reason for the resistance of hum
269 ed on co-immunoprecipitation, two-hybrid and
mutational analyses,
the E. coli c-di-GMP receptor YcgR
270 e we use high-resolution crystallography and
mutational analyses to characterize GFP variants that un
271 assays, high-resolution crystallography, and
mutational analyses to characterize the interaction betw
272 We performed comparative and
mutational analyses to define more comprehensively the r
273 at Ccm2l binds Ccm1 and perform deletion and
mutational analyses to define the regions of Ccm1 that m
274 tructure in combination with biophysical and
mutational analyses to define the XLF-XRCC4 interactions
275 In this study, we used in silico and
mutational analyses to identify and characterize the rol
276 ers Rev phenotype, we undertook deletion and
mutational analyses to map functional domains and to ide
277 Therefore,
mutational analyses to resolve mechanical unfolding path
278 We have carried out
mutational analyses to show that the noncanonical residu
279 Here we use biochemical and
mutational analyses to study the structure/function of t
280 We further combine our structural data with
mutational analyses to understand how specificity is ach
281 roaches in Drosophila melanogaster, in which
mutational analyses together with genome-wide transcript
282 We have undertaken
mutational analyses (
truncations and alanine substitutio
283 Mutational analyses using SPOT arrays revealed the effec
284 P53 analyses were performed through germline
mutational analyses using standard molecular techniques.
285 Using a combination of biochemical and
mutational analyses,
we demonstrate that EGF induces the
286 Through
mutational analyses,
we identified an active canonical N
287 Using structural and
mutational analyses,
we identified key residues involved
288 By
mutational analyses,
we identified two regions in the C-
289 Through targeted
mutational analyses,
we identify missense mutations of V
290 Using nuclear magnetic resonance and
mutational analyses,
we identify the SSB-Ct binding pock
291 Using
mutational analyses,
we mapped the protein-protein inter
292 bioinformatics, quantitative proteomics, and
mutational analyses,
we show that Acinetobacter uses its
293 Through a series deletion and
mutational analyses,
we showed that the stem cell-associ
294 By
mutational analyses,
we supplied evidence that the N-ter
295 Mutational analyses were also performed in 105 Chinese a
296 Mutational analyses were also performed on the residues
297 ar basis of the interaction of FhbB with FH,
mutational analyses were conducted.
298 Mutational analyses were performed for 25 mutations (PIK
299 ctor H binding, truncation and site-directed
mutational analyses were performed.
300 ple roles of the constituent nucleotides via
mutational analyses,
while high-throughput experimental