1 oscopic and immunohistological features with
mutational analyses.
2 ity of the P. furiosus Rad50 structure-based
mutational analyses.
3 be assigned to these key interactions using
mutational analyses.
4 erform coimmunoprecipitation experiments and
mutational analyses.
5 DP2 was confirmed by peptide competition and
mutational analyses.
6 tivation is supported by our structure-based
mutational analyses.
7 teraction using structural, biophysical, and
mutational analyses.
8 prompt detailed DNA promoter methylation or
mutational analyses.
9 k for understanding and interpreting earlier
mutational analyses.
10 tion of its substrate MepS by structural and
mutational analyses.
11 The use of bioinformatics,
mutational analyses,
a substrate competitor peptide, and
12 p molecular models that, in conjunction with
mutational analyses,
allow us to propose an active site
13 Statistical coupling and correlated
mutational analyses along with clustering revealed a hig
14 We demonstrate, through
mutational analyses and domain replacement experiments,
15 Mutational analyses and domain swapping experiments were
16 Mutational analyses and functional assays have identifie
17 FLT3, NPM1, CEBPA, WT1, and MLL
mutational analyses and gene- and microRNA-expression pr
18 membrane), we performed domain swapping and
mutational analyses and identified a C-terminal di-leuci
19 Mitochondrial DNA damage was analyzed by
mutational analyses and measurement of mtDNA copy number
20 Using
mutational analyses and phosphorylated peptides, we show
21 and regulation of these three operons using
mutational analyses and promoter-reporter fusions.
22 Mutational analyses and simulations in the presence and
23 Mutational analyses and structural comparisons with othe
24 transcriptional regulation of SLICK/Slick by
mutational analyses and studying gene expression by luci
25 NMR data together with
mutational analyses are consistent with Zn(2+) coordinat
26 However, results from
mutational analyses are open to alternative interpretati
27 Biophysical and
mutational analyses are used to map regions of the PI31
28 Guided by our
mutational analyses as well as hydroxyl radical footprin
29 mplexes between these components and perform
mutational analyses based on the structures.
30 Mutational analyses both in vitro and in vivo provide ev
31 Previous
mutational analyses centered on mutants with substitutio
32 A combination of promoter deletion and
mutational analyses,
chromatin immunoprecipitation assay
33 Mutational analyses confirm that several residues identi
34 Mutational analyses confirm the essential structural rol
35 Mutational analyses confirm the importance of these resi
36 Mutational analyses confirmed identified HSUR2-mRNA inte
37 Mutational analyses confirmed that the small cold shock
38 Supershift and
mutational analyses confirmed the binding of YY1 to this
39 Mutational analyses confirmed the functional relevance o
40 Further,
mutational analyses confirms that the atypical CRD is cr
41 Mutational analyses corroborated the results of the tran
42 lix (M1TH) protective element using in vitro
mutational analyses coupled with biochemical and biophys
43 Mutational analyses defined the requirements for the IN-
44 interactions only with Vdelta1(+) TCRs, and
mutational analyses demonstrate a role of the Vdelta1 do
45 Mutational analyses demonstrate analogous interactions i
46 Our
mutational analyses demonstrate that pore loop 2 residue
47 Our
mutational analyses demonstrate that, similar to other 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 Mutational analyses demonstrated that this immunosuppres
54 Here, we report results from
mutational analyses demonstrating that yeaR-yoaG operon
55 Mutational analyses disclosed that amino acids substitut
56 Protein-protein interaction and
mutational analyses established that the antiviral effec
57 We utilise structural and
mutational analyses,
fibril growth kinetics and solubili
58 Mutational analyses found that sequences within the IME4
59 Our
mutational analyses further indicate that the N-terminal
60 SAXS and
mutational analyses further reveal that the preformed di
61 Mutational analyses further showed that the conserved Cy
62 Crystallographic studies and
mutational analyses have contributed to a general unders
63 Mutational analyses have established that an interaction
64 Mutational analyses have identified several key PCD comp
65 Genetic and
mutational analyses have identified the transmembrane (T
66 Mutational analyses have indicated that the carboxyl-ter
67 Although
mutational analyses have indicated that transmembrane (T
68 Mutational analyses have recently revealed that these mo
69 Mutational analyses have revealed many genes that are re
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 Mutational analyses identified a FxxxLxxxK binding motif
75 s-linking coupled with mass spectrometry and
mutational analyses identified a new interaction between
76 Structural and
mutational analyses identified conserved residues within
77 Mutational analyses identified distinct crucial binding
78 In addition,
mutational analyses identified functional domains of r12
79 Mutational analyses identified no coding or intron junct
80 Structure-guided
mutational analyses identified residues critical for act
81 Previous
mutational analyses identified residues within the Gag m
82 Mass spectrometric and
mutational analyses identified Ser730 as the only phosph
83 Deletional and
mutational analyses identified that Plk1 phosphorylated
84 Mass spectrometry and
mutational analyses identified Thr-18 and Thr-33 as the
85 Mutational analyses identify Glu(276), Phe(280), and Val
86 Our
mutational analyses identify the D261, E262, and C-termi
87 Through
mutational analyses in 7325 individuals, we report four
88 e the roles of active-site residues by using
mutational analyses in a peptide synthesis assay with in
89 idated our computational predictions through
mutational analyses in cell transfection experiments.
90 Mutational analyses in situ confirmed expression of muta
91 an enormous hydrophobic groove implicated by
mutational analyses in tail-anchored protein binding.
92 pts the other, confounding interpretation of
mutational analyses in the context of the virus.
93 ding to mutations indicate the importance of
mutational analyses in the future.
94 This idea is consistent with
mutational analyses in various sensory systems, where mu
95 Through a series of
mutational analyses,
in combination with biochemical and
96 Bioinformatics and
mutational analyses indicate that a conserved Gly117 (he
97 Limited
mutational analyses indicate that arginine 488 located w
98 logical and molecular genetic approaches and
mutational analyses indicate that extracellular signal-r
99 e S-transferase fusion pulldown and receptor
mutational analyses indicate that GRIN1-MOR interaction
100 Structural and
mutational analyses indicate that high flexibility and d
101 Mutational analyses indicate that neither phosphorylatio
102 Together, structural and
mutational analyses indicate that only two of the four C
103 However,
mutational analyses indicate that SmgGDS utilizes a dist
104 Biochemical analyses and
mutational analyses indicate that SpoIVA and SipL direct
105 ently suppress the expression of STAT-1, and
mutational analyses indicate that the E6 targeting E6-as
106 Mutational analyses indicate that the high sensitivity o
107 Recent
mutational analyses indicate that this process is more c
108 Mutational analyses indicate the importance of specific
109 AC) found for other SBP domain proteins, but
mutational analyses indicated that at least one addition
110 For one such individual,
mutational analyses indicated that four polymorphisms se
111 Accordingly,
mutational analyses indicated that GATA sites are requir
112 Mutational analyses indicated that nuclear localization
113 Mutational analyses indicated that the C-terminal region
114 Mass-spectrometry and
mutational analyses indicated that the PRF occurred thro
115 Mutational analyses indicated that the transmembrane dom
116 Mutational analyses indicated that the turnover of the p
117 The combined structural and
mutational analyses lead to the detailed understanding o
118 Structure-based
mutational analyses mapped the binding site for the [GS]
119 ell as the results from previous genetic and
mutational analyses,
methylotrophy is enabled by methano
120 Our structural and
mutational analyses not only establish structural bases
121 Mutational analyses of ATG3 confirm that four residues w
122 Point
mutational analyses of C21 revealed that a conserved pro
123 Mutational analyses of consensus-type glmS ribozymes sup
124 obank" agrees well with previous large-scale
mutational analyses of CRC.
125 Mutational analyses of CTCL patient peripheral blood mal
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 We performed
mutational analyses of IFITM3 and identified multiple re
136 Mutational analyses of intragenic suppressors and coexpr
137 Mutational analyses of IRF8 showed that its ability to b
138 Comprehensive
mutational analyses of KCNQ1 (KV7.1, LQTS type 1), KCNH2
139 Mutational analyses of LAT, Gads, and SLP-76 indicated t
140 Mutational analyses of MARCH1 defined discrete domains r
141 Biological and
mutational analyses of our peptide provide new insights
142 In vivo and in vitro
mutational analyses of Phe91 and Trp93 emphasize the imp
143 Furthermore, truncation and
mutational analyses of PknK revealed that PknK is autore
144 Mutational analyses of protein-DNA contacts, which were
145 Mutational analyses of RecA1/RecA2 domains confirmed the
146 Structure-guided
mutational analyses of RopB dimer interface demonstrated
147 Mutational analyses of Sdh1 implicate C-terminal region
148 Mutational analyses of SNAP190 support a model wherein C
149 Mutational analyses of structurally conserved regions of
150 Further transcriptional, binding, and
mutational analyses of the 5' promoter have identified t
151 Mutational analyses of the 5'-leader of ATF5 mRNA fused
152 ction, we used solution NMR spectroscopy and
mutational analyses of the active fragment, PR11, which
153 provide a null genetic background to perform
mutational analyses of the Ago2 protein.
154 Mutational analyses of the alpha-internexin promoter dem
155 The
mutational analyses of the CHV-1/EP713 infectious cDNA c
156 Furthermore,
mutational analyses of the conserved EAL and GGDEF resid
157 Site-specific
mutational analyses of the conserved residues within WRD
158 Our
mutational analyses of the Ede1 UBA domain-ubiquitin int
159 try, fluorescence in situ hybridization, and
mutational analyses of the EGFR gene have all been propo
160 Taken together, our structural and
mutational analyses of the Hda-beta clamp complex indica
161 Chemical modification and
mutational analyses of the longer and shorter forms of t
162 Mutational analyses of the Nop5 protein interface sugges
163 Here, we perform systematic statistical and
mutational analyses of the overlapping HIV-1 genes tat a
164 Immunohistochemical and
mutational analyses of the patient's melanocytic tumors
165 Mutational analyses of the positionally conserved sORF o
166 Mutational analyses of the promoter region combined with
167 Mutational analyses of the secreted recombinant insulin
168 Mutational analyses of the two EAL motifs of DipA sugges
169 putational modeling, circular dichroism, and
mutational analyses of the zinc finger domain of MDM2 an
170 Mutational analyses of these PrP(Sc)-binding regions rev
171 Mutational analyses of two components of the CheIV clust
172 Mutational analyses of VPg indicate that a subset of the
173 Coupled with
mutational analyses,
our studies reveal the critical rol
174 tein function has been probed extensively by
mutational analyses,
particularly in plants where large
175 studies, cryo-electron microscopy (cryo-EM),
mutational analyses,
peptide binding analysis, linker-sc
176 Mutational analyses performed following acquired ibrutin
177 revious array studies, the glycosylation and
mutational analyses presented here suggest a unique glyc
178 Modeling and
mutational analyses provide evidence that SpoIIGA is a n
179 Structural and
mutational analyses provide new insights into a putative
180 Mutational analyses provided evidence that this stem-loo
181 Mutational analyses provided insights into sequence reco
182 Mutational analyses resulted in the identification of ei
183 The structure and associated
mutational analyses reveal molecular details of Ubc12 re
184 Mutational analyses reveal multiple phosphorylation site
185 Mutational analyses reveal that cFLIPL nuclear localizat
186 In vivo
mutational analyses reveal that either the DNase activit
187 Mass spectrometric and
mutational analyses reveal that K133 of pro-IL-1beta is
188 Mutational analyses reveal that self-interaction is crit
189 Sequence and
mutational analyses reveal that the cleavage occurs with
190 However,
mutational analyses reveal that the helicase function of
191 AGO structure modelling and
mutational analyses reveal that the QF-V motif within th
192 Our
mutational analyses reveal the individual contributions
193 ith a H4K16ac peptide along with binding and
mutational analyses reveal unique mechanistic features u
194 Mutational analyses revealed combinatorial, non-exchange
195 Mutational analyses revealed differential binding affini
196 Importantly,
mutational analyses revealed extensive auto-inhibitory m
197 Mutational analyses revealed that a conserved leucine re
198 Biochemical, mass spectrometric, and
mutational analyses revealed that CM14 inhibits HlyU fro
199 Mutational analyses revealed that DAB2 interacts with TN
200 Phospho-proteomic and
mutational analyses revealed that eIF4G1 is a substrate
201 Subsequent
mutational analyses revealed that HvgA and capsule, but
202 omputationally predicted targets followed by
mutational analyses revealed that let-7 and miR-18 down-
203 Mutational analyses revealed that MC159 and cIAP1 each b
204 Positional cloning and
mutational analyses revealed that nbl results from a V32
205 Mutational analyses revealed that sequences throughout t
206 Further
mutational analyses revealed that the "NF" sequence with
207 Mutational analyses revealed that the conserved Phox2 an
208 Further
mutational analyses revealed that the first 10 amino aci
209 sphatase activity and a series of subsequent
mutational analyses revealed that the N terminus of HDAC
210 Mutational analyses revealed that the N-terminus of AurA
211 ing proteins RIP1 and RIP3, and deletion and
mutational analyses revealed that the RHIM in TRIF was e
212 mapping, selective amino acid labeling, and
mutational analyses revealed the peptidyl transferase ce
213 Mutational analyses revealed the sites of modification o
214 Mutational analyses revealed two conserved cysteines and
215 ere, small angle X-ray scattering (SAXS) and
mutational analyses show APLF is largely an intrinsicall
216 Comparison with other helicases and
mutational analyses show how it threads single-stranded
217 of the MT1-MMP-mediated cleaved products and
mutational analyses show that cleavage of DDR1 takes pla
218 Time course and
mutational analyses show that DNA bending occurs after r
219 Mutational analyses show that most residues interacting
220 Mutational analyses show that the contacts of both recog
221 Mutational analyses show that the GluN2A preference of S
222 Furthermore,
mutational analyses show that there is a strong correlat
223 Cross-competition assays and
mutational analyses showed evidence for at least three d
224 ding determinants or "recognition elements."
Mutational analyses showed that all three recognition el
225 Molecular dynamics and
mutational analyses showed that alphaKG binds TDG on Arg
226 Sequence and
mutational analyses showed that auto-repression involves
227 Mutational analyses showed that autosomal recessive hypo
228 Mutational analyses showed that bombesin-enhanced cyclin
229 Mutational analyses showed that both CMD-1 and HTH-4 are
230 Mutational analyses showed that both Valpha/Vbeta interf
231 Mutational analyses showed that CRTCs possess distinct f
232 Further
mutational analyses showed that most of the 93 bp MRR re
233 ved in the subgroup 3 tobamoviruses, and our
mutational analyses showed that nuclear localization of
234 Structural and
mutational analyses showed that ribosome-bound NEMF recr
235 In vitro footprinting and in vivo
mutational analyses showed that SgrS base pairs with man
236 Metabolic, enzymatic and
mutational analyses showed that the gsIII-like gene enco
237 ment usage and different docking mechanisms,
mutational analyses showed that the TCRs shared a conser
238 Mutational analyses showed that these contacts are impor
239 Our
mutational analyses showed that these sites are required
240 Our sequence comparisons and
mutational analyses showed that this architecture of the
241 e alpha4 helix of the MLKL 4HB domain, which
mutational analyses showed was crucial for reconstitutio
242 TP53
mutational analyses spanned exons 4 to 8.
243 Although biochemical and
mutational analyses strongly suggest that the heptad-rep
244 Kinetic and
mutational analyses strongly suggest that these structur
245 Through
mutational analyses,
such a state is known to enhance th
246 Further
mutational analyses suggest a novel mechanism of Tau reg
247 Mutational analyses suggest that biphasic activation of
248 Mutational analyses suggest that further interaction bet
249 ser extent than hmx3a More surprisingly, our
mutational analyses suggest that Hmx3a may not require i
250 Furthermore, promoter deletion and
mutational analyses suggest that mevastatin induced KLF2
251 Collectively, these
mutational analyses suggest that minor sequence differen
252 Mutational analyses suggest that p22/p18 is synthesized
253 Mutational analyses suggest that this motif binds a repr
254 Mutational analyses suggest that Vpr interacts with DNA-
255 Subsequent
mutational analyses suggested that the ExoY oligomerizat
256 Mutational analyses suggested that the observed effects
257 Evidence from structure-guided
mutational analyses suggests that acyl-coenzyme A enters
258 Insertion and deletion
mutational analyses support a beta-barrel structure mode
259 Mutational analyses support that these mechanisms underl
260 Our
mutational analyses support the critical role of this co
261 Mutational analyses support the view that HIRA acts as a
262 Most RYR2
mutational analyses target 3 canonical domains encoded b
263 Therefore, we examined by
mutational analyses the reason for the resistance of hum
264 Based on structural and
mutational analyses,
the catalytic mechanism of Aly36B f
265 ed on co-immunoprecipitation, two-hybrid and
mutational analyses,
the E. coli c-di-GMP receptor YcgR
266 e we use high-resolution crystallography and
mutational analyses to characterize GFP variants that un
267 assays, high-resolution crystallography, and
mutational analyses to characterize the interaction betw
268 at Ccm2l binds Ccm1 and perform deletion and
mutational analyses to define the regions of Ccm1 that m
269 tructure in combination with biophysical and
mutational analyses to define the XLF-XRCC4 interactions
270 In this study, we used in silico and
mutational analyses to identify and characterize the rol
271 eptidyl transferase center (PTC) active site
mutational analyses to inform design.
272 ers Rev phenotype, we undertook deletion and
mutational analyses to map functional domains and to ide
273 We have carried out
mutational analyses to show that the noncanonical residu
274 Here we use biochemical and
mutational analyses to study the structure/function of t
275 We further combine our structural data with
mutational analyses to understand how specificity is ach
276 roaches in Drosophila melanogaster, in which
mutational analyses together with genome-wide transcript
277 Mutational analyses transitioning PiCas12a to PdCas12a r
278 We have undertaken
mutational analyses (
truncations and alanine substitutio
279 Structure-based
mutational analyses uncovered kinetic competition betwee
280 Mutational analyses using SPOT arrays revealed the effec
281 P53 analyses were performed through germline
mutational analyses using standard molecular techniques.
282 Mutational analyses validate the interaction mode betwee
283 orter-based in vitro translation assays, and
mutational analyses,
we demonstrate here that eIF4GI and
284 Using
mutational analyses,
we demonstrate that, in addition to
285 Through
mutational analyses,
we identified an active canonical N
286 Using structural and
mutational analyses,
we identified key residues involved
287 Using 3-dimensional molecular modeling and
mutational analyses,
we identified the nucleotide bases
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 bioinformatics, quantitative proteomics, and
mutational analyses,
we show that Acinetobacter uses its
292 Through a series deletion and
mutational analyses,
we showed that the stem cell-associ
293 By
mutational analyses,
we supplied evidence that the N-ter
294 Mutational analyses were also performed in 105 Chinese a
295 ar basis of the interaction of FhbB with FH,
mutational analyses were conducted.
296 Mutational analyses were performed for 25 mutations (PIK
297 ctor H binding, truncation and site-directed
mutational analyses were performed.
298 mplementation in Nb was used for accelerated
mutational analyses while avoiding complex biotic intera
299 ple roles of the constituent nucleotides via
mutational analyses,
while high-throughput experimental
300 Mutational analyses within the GxxxG motif of the TM reg