1 ted to BRCA1 by a combination of linkage and
mutation analyses.
2 rough HBV whole single-strand (-)-DNA genome
mutation analyses.
3 analysis, and results were compared with DNA
mutation analyses.
4 of expression, copy number, methylation, and
mutation analyses.
5 MafG using chromatin immunoprecipitation and
mutation analyses.
6 er structure for DI RNA replication based on
mutation analyses.
7 c amplification of sequence target assay and
mutation analyses.
8 present the mutations are not tested for in
mutation analyses.
9 These results combined with
mutation analyses allow us to propose a molecular model
10 to perform simultaneous germline and somatic
mutation analyses among individuals without leukemogenic
11 Mutation analyses and analogies to ribonuclease H indica
12 Here, using
mutation analyses and complementation, we demonstrated t
13 EGFR and K-ras
mutation analyses and EGFR gene copy number analyses wer
14 Our structure integrates results from
mutation analyses and previous cross-linking and fluores
15 Transactivation experiments,
mutation analyses,
and electrophoretic mobility shift as
16 from methylation, open chromatin and somatic
mutation analyses,
and functional studies in organoid mo
17 we used a combination of biochemical assays,
mutation analyses,
and in vitro bone marrow differentiat
18 es important for catalysis are identified by
mutation analyses,
and the results provide insights into
19 Genome-wide cancer
mutation analyses are revealing an extensive landscape o
20 Deletion and
mutation analyses as well as chromatin immunoprecipitati
21 Deletion and
mutation analyses as well as chromatin immunoprecipitati
22 ly lead to misinterpretation when performing
mutation analyses based on cDNA templates.
23 monstrated that many fundamental features of
mutation analyses based on lambda transgenic rodents are
24 Mutation analyses by single-stranded conformation polymo
25 athies, we independently performed different
mutation analyses:
candidate-based sequencing of all IFT
26 In vivo deletion and site-directed
mutation analyses confirm that one GATA element in mtl-1
27 DNA ends in conjunction with splice acceptor
mutation analyses confirmed that all detected M2 gene tr
28 Deletion and
mutation analyses demonstrate that the ligand-binding ac
29 Mutation analyses demonstrated that binding of PDX-1 and
30 r chromatin immunoprecipitation and promoter
mutation analyses demonstrated that FOXO3a regulates the
31 that other such genes could be pinpointed by
mutation analyses designed to identify homozygous mutati
32 Gel shift and
mutation analyses determined that AGGTGT (-1254/-1249) i
33 Among the
mutation analyses discordant by these methods for TP53 s
34 Combining gene expression and
mutation analyses enhances the ability to noninvasively
35 fficient manner, we performed expression and
mutation analyses for FEN1 in human lung cancer cell lin
36 Deletion and
mutation analyses have identified a critical cis element
37 To date,
mutation analyses have suggested a broad genotype-phenot
38 Mutation analyses identified a promoter-proximal ER stre
39 Further deletion and
mutation analyses identified an E box motif as a positiv
40 Mutation analyses identified the cobalt-responsive seque
41 Deletion and
mutation analyses identified two positive regulatory seq
42 Transcriptome-wide
mutation analyses identify many cell-type-specific mutat
43 Transfection combined with deletion and
mutation analyses illustrated that the PRE contains a cl
44 Somatic
mutation analyses in >30 locations throughout the nervou
45 Haplotype and
mutation analyses in a pedigree transmitting myelokathex
46 mutation-calling is essential for insightful
mutation analyses in cancer studies.
47 nt of their peptide as confirmed by internal
mutation analyses in each uORF.
48 the IOSCA locus on chromosome 10q24, and for
mutation analyses in IOSCA patients isolated the corresp
49 Expression and
mutation analyses in mice suggest that the homeobox-cont
50 Serial deletion and point
mutation analyses in reporter gene assays, as well as a
51 Biochemical studies and deletion
mutation analyses indicate that the 11-amino acid sequen
52 Mutation analyses indicate that the C-terminal NLS was f
53 Deletion and point
mutation analyses indicate that the distal TIE located a
54 Promoter deletion and point
mutation analyses indicated that a region between nucleo
55 VEGF promoter deletion and point
mutation analyses indicated that a region between nucleo
56 Deletion/
mutation analyses indicated that each of the three Ca(v)
57 Further deletion and point
mutation analyses indicated that mutation of individual
58 Deletion and
mutation analyses indicated that the SH3 binding motif o
59 correlations, 3D-protein modeling, in vitro
mutation analyses,
magnetic resonance imaging (MRI) mark
60 Clinical differences and results of the
mutation analyses make it very unlikely that XLTT is ano
61 ated prognostic models incorporating somatic
mutation analyses may outperform prediction based on con
62 Extensive
mutation analyses of 40 unrelated patients only identifi
63 (i) In the first examination,
mutation analyses of a recently discovered long-range RN
64 nto two different peptides and site-directed
mutation analyses of acylation sites, often served as in
65 nto two different peptides and site directed
mutation analyses of acylation sites.
66 Deletion and
mutation analyses of CDIR were employed to identify the
67 We conducted systematic
mutation analyses of E. coli EDL933 and E. coli MG1655 b
68 med genome-wide and targeted copy number and
mutation analyses of germline DNA from 208 patients with
69 Mutation analyses of the 5'-tRNA(ValCAC/AAC) half identi
70 Deletion and
mutation analyses of the Aurora-A promoter revealed that
71 Mutation analyses of the cII transgene in cells treated
72 Deletion and
mutation analyses of the enhancer based on comparison of
73 Deletion and
mutation analyses of the murine Bim promoter identified
74 Moreover,
mutation analyses of the NAD+ interacting residues of PA
75 Deletion and
mutation analyses of the p21Waf1 promoter revealed that
76 NA sequencing on the proband were completed,
mutation analyses of the putative carriers and noncarrie
77 Deletion and
mutation analyses of the rat and human UbC promoters are
78 We have integrated these data with previous
mutation analyses of the Reference Sequence genes in the
79 Here, we used site-specific
mutation analyses of the thioredoxin domain active site
80 Mutation analyses of the two cysteines in human MRP1 rev
81 Sequential deletion and site-directed
mutation analyses of the VEGF promoter demonstrated that
82 Deletive
mutation analyses of the VEGF promoter revealed that the
83 Deletion and
mutation analyses of this promoter had defined an elemen
84 Mutation analyses of three fragments showed that their t
85 Mutation analyses of various consensus binding motifs wi
86 The
mutation analyses presented in this report represent a s
87 Furthermore, deletion and point
mutation analyses reveal that both the amino-terminal IK
88 Furthermore,
mutation analyses reveal that ORF1p can direct L1 RNP di
89 Kinetic and
mutation analyses reveal that these RNAs cleave site-spe
90 Deletion and
mutation analyses revealed functional nuclear export sig
91 Mutation analyses revealed that a CCAAT enhancer binding
92 Promoter deletion and point
mutation analyses revealed that a region between nucleot
93 Mutation analyses revealed that a region of 86 amino aci
94 Our
mutation analyses revealed that C/EBPalpha drove Il4 pro
95 Deletion and point
mutation analyses revealed that part of the hinge domain
96 Deletion and
mutation analyses revealed that two proximal E box seque
97 Deletion and
mutation analyses revealed the functional importance of
98 Point
mutation analyses revealed two essential residues within
99 Using point
mutation analyses,
serine 2 (Ser-2) of Nanog has been id
100 HBV genome-wide
mutation analyses showed that A1 cofactors significantly
101 Point-
mutation analyses showed that ERK5 is covalently modifie
102 Mutation analyses showed that the full-length 1a protein
103 Deletion and
mutation analyses showed the requirement for a single hy
104 Together, the deletion and
mutation analyses suggest that the entire CAD provides a
105 gel mobility shift assays and site-directed
mutation analyses suggest that the putative NF-kappaB si
106 Further
mutation analyses suggested that a specific electrostati
107 sites in the survivin promoter, deletion and
mutation analyses suggested that neither site is require
108 By applying deep learning and motif
mutation analyses to epigenetic data for macrophages fro
109 esent a series of deletion and site-directed
mutation analyses to identify amino acids in RIN4 requir
110 on impacts and underscore the need for multi-
mutation analyses to uncover genetic factors underlying
111 A combination of
mutation analyses,
trans-protection analyses, and in vitr
112 ty single-nucleotide polymorphism array, and
mutation analyses using formalin-fixed ICC samples from
113 DNA mobility shift assays and
mutation analyses using recombinant SnaH protein express
114 sults demonstrate the feasibility of in vivo
mutation analyses using transgenic fish and illustrate t
115 clear receptors and mammalian two-hybrid and
mutation analyses we now show that interaction with the
116 Supported by promoter activity and
mutation analyses,
we demonstrate that a large fraction
117 Utilizing competition peptides and
mutation analyses,
we discovered two unique regions (ami
118 By deletion mapping and scanning
mutation analyses,
we have identified three putative RTA
119 cient preferential translation, deletion and
mutation analyses were conducted in a truncated Hsp70 5'
120 KRAS and BRAF
mutation analyses were obtained in 498 (88%) and 457 pat
121 luorescent in situ hybridization (FISH), and
mutation analyses were performed in 318 patients.
122 Patients and Methods
Mutation analyses (
wild-type [WT] and mutant) for TP53,