1 of expression, copy number, methylation, and
mutation analyses.
2 ted to BRCA1 by a combination of linkage and
mutation analyses.
3 MafG using chromatin immunoprecipitation and
mutation analyses.
4 er structure for DI RNA replication based on
mutation analyses.
5 c amplification of sequence target assay and
mutation analyses.
6 present the mutations are not tested for in
mutation analyses.
7 analysis, and results were compared with DNA
mutation analyses.
8 Mutation analyses and analogies to ribonuclease H indica
9 Here, using
mutation analyses and complementation, we demonstrated t
10 EGFR and K-ras
mutation analyses and EGFR gene copy number analyses wer
11 Our structure integrates results from
mutation analyses and previous cross-linking and fluores
12 Transactivation experiments,
mutation analyses,
and electrophoretic mobility shift as
13 we used a combination of biochemical assays,
mutation analyses,
and in vitro bone marrow differentiat
14 es important for catalysis are identified by
mutation analyses,
and the results provide insights into
15 Genome-wide cancer
mutation analyses are revealing an extensive landscape o
16 Deletion and
mutation analyses as well as chromatin immunoprecipitati
17 Deletion and
mutation analyses as well as chromatin immunoprecipitati
18 ly lead to misinterpretation when performing
mutation analyses based on cDNA templates.
19 monstrated that many fundamental features of
mutation analyses based on lambda transgenic rodents are
20 Mutation analyses by single-stranded conformation polymo
21 athies, we independently performed different
mutation analyses:
candidate-based sequencing of all IFT
22 In vivo deletion and site-directed
mutation analyses confirm that one GATA element in mtl-1
23 DNA ends in conjunction with splice acceptor
mutation analyses confirmed that all detected M2 gene tr
24 Deletion and
mutation analyses demonstrate that the ligand-binding ac
25 Mutation analyses demonstrated that binding of PDX-1 and
26 r chromatin immunoprecipitation and promoter
mutation analyses demonstrated that FOXO3a regulates the
27 that other such genes could be pinpointed by
mutation analyses designed to identify homozygous mutati
28 Gel shift and
mutation analyses determined that AGGTGT (-1254/-1249) i
29 Among the
mutation analyses discordant by these methods for TP53 s
30 fficient manner, we performed expression and
mutation analyses for FEN1 in human lung cancer cell lin
31 Deletion and
mutation analyses have identified a critical cis element
32 To date,
mutation analyses have suggested a broad genotype-phenot
33 Mutation analyses identified a promoter-proximal ER stre
34 Further deletion and
mutation analyses identified an E box motif as a positiv
35 Mutation analyses identified the cobalt-responsive seque
36 Deletion and
mutation analyses identified two positive regulatory seq
37 Transfection combined with deletion and
mutation analyses illustrated that the PRE contains a cl
38 Somatic
mutation analyses in >30 locations throughout the nervou
39 Haplotype and
mutation analyses in a pedigree transmitting myelokathex
40 mutation-calling is essential for insightful
mutation analyses in cancer studies.
41 nt of their peptide as confirmed by internal
mutation analyses in each uORF.
42 the IOSCA locus on chromosome 10q24, and for
mutation analyses in IOSCA patients isolated the corresp
43 Expression and
mutation analyses in mice suggest that the homeobox-cont
44 Serial deletion and point
mutation analyses in reporter gene assays, as well as a
45 Biochemical studies and deletion
mutation analyses indicate that the 11-amino acid sequen
46 Mutation analyses indicate that the C-terminal NLS was f
47 Deletion and point
mutation analyses indicate that the distal TIE located a
48 Promoter deletion and point
mutation analyses indicated that a region between nucleo
49 VEGF promoter deletion and point
mutation analyses indicated that a region between nucleo
50 Deletion/
mutation analyses indicated that each of the three Ca(v)
51 Further deletion and point
mutation analyses indicated that mutation of individual
52 Deletion and
mutation analyses indicated that the SH3 binding motif o
53 Clinical differences and results of the
mutation analyses make it very unlikely that XLTT is ano
54 ated prognostic models incorporating somatic
mutation analyses may outperform prediction based on con
55 Extensive
mutation analyses of 40 unrelated patients only identifi
56 (i) In the first examination,
mutation analyses of a recently discovered long-range RN
57 nto two different peptides and site-directed
mutation analyses of acylation sites, often served as in
58 nto two different peptides and site directed
mutation analyses of acylation sites.
59 Deletion and
mutation analyses of CDIR were employed to identify the
60 We conducted systematic
mutation analyses of E. coli EDL933 and E. coli MG1655 b
61 med genome-wide and targeted copy number and
mutation analyses of germline DNA from 208 patients with
62 Deletion and
mutation analyses of the Aurora-A promoter revealed that
63 Mutation analyses of the cII transgene in cells treated
64 Deletion and
mutation analyses of the enhancer based on comparison of
65 Deletion and
mutation analyses of the murine Bim promoter identified
66 Deletion and
mutation analyses of the p21Waf1 promoter revealed that
67 NA sequencing on the proband were completed,
mutation analyses of the putative carriers and noncarrie
68 Deletion and
mutation analyses of the rat and human UbC promoters are
69 We have integrated these data with previous
mutation analyses of the Reference Sequence genes in the
70 Mutation analyses of the two cysteines in human MRP1 rev
71 Sequential deletion and site-directed
mutation analyses of the VEGF promoter demonstrated that
72 Deletive
mutation analyses of the VEGF promoter revealed that the
73 Deletion and
mutation analyses of this promoter had defined an elemen
74 Mutation analyses of three fragments showed that their t
75 Mutation analyses of various consensus binding motifs wi
76 Furthermore, deletion and point
mutation analyses reveal that both the amino-terminal IK
77 Furthermore,
mutation analyses reveal that ORF1p can direct L1 RNP di
78 Deletion and
mutation analyses revealed functional nuclear export sig
79 Mutation analyses revealed that a CCAAT enhancer binding
80 Promoter deletion and point
mutation analyses revealed that a region between nucleot
81 Mutation analyses revealed that a region of 86 amino aci
82 Our
mutation analyses revealed that C/EBPalpha drove Il4 pro
83 Deletion and point
mutation analyses revealed that part of the hinge domain
84 Deletion and
mutation analyses revealed that two proximal E box seque
85 Deletion and
mutation analyses revealed the functional importance of
86 Point
mutation analyses revealed two essential residues within
87 Using point
mutation analyses,
serine 2 (Ser-2) of Nanog has been id
88 Point-
mutation analyses showed that ERK5 is covalently modifie
89 Mutation analyses showed that the full-length 1a protein
90 Deletion and
mutation analyses showed the requirement for a single hy
91 Together, the deletion and
mutation analyses suggest that the entire CAD provides a
92 gel mobility shift assays and site-directed
mutation analyses suggest that the putative NF-kappaB si
93 Further
mutation analyses suggested that a specific electrostati
94 sites in the survivin promoter, deletion and
mutation analyses suggested that neither site is require
95 esent a series of deletion and site-directed
mutation analyses to identify amino acids in RIN4 requir
96 A combination of
mutation analyses,
trans-protection analyses, and in vitr
97 ty single-nucleotide polymorphism array, and
mutation analyses using formalin-fixed ICC samples from
98 DNA mobility shift assays and
mutation analyses using recombinant SnaH protein express
99 sults demonstrate the feasibility of in vivo
mutation analyses using transgenic fish and illustrate t
100 clear receptors and mammalian two-hybrid and
mutation analyses we now show that interaction with the
101 Supported by promoter activity and
mutation analyses,
we demonstrate that a large fraction
102 Utilizing competition peptides and
mutation analyses,
we discovered two unique regions (ami
103 By deletion mapping and scanning
mutation analyses,
we have identified three putative RTA
104 cient preferential translation, deletion and
mutation analyses were conducted in a truncated Hsp70 5'
105 KRAS and BRAF
mutation analyses were obtained in 498 (88%) and 457 pat
106 luorescent in situ hybridization (FISH), and
mutation analyses were performed in 318 patients.
107 Patients and Methods
Mutation analyses (
wild-type [WT] and mutant) for TP53,