コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 bly to generate a 15.87 Mb assembly of the Y chromosome.
2 ding kinetics and affinity for the bacterial chromosome.
3 ences as they are homologous to the bovine Y chromosome.
4 cking the replication of Chr2, the secondary chromosome.
5 s on isolation and sequencing of the ovine Y chromosome.
6 ss, telomere-to-telomere assembly of a human chromosome.
7 arger than the main body of their respective chromosomes.
8 eveal a remarkable flexibility of interphase chromosomes.
9 ow they topologically interact in replicated chromosomes.
10 ed virus genome were comparable to the other chromosomes.
11 coverage depth between viruses and bacterial chromosomes.
12 rst telomere-to-telomere assemblies of whole chromosomes.
13 n size, of which 80% has been anchored to 13 chromosomes.
14 altered allelic imbalance patterns between X chromosomes.
15 sive histone methylation marks on eukaryotic chromosomes.
16 lative positions and movement of segregating chromosomes.
17 e associations between EBV episomes and host chromosomes.
18 retaining their orientation within 3 mum of chromosomes.
19 n loop that is distinct from the rest of the chromosomes.
20 encompassing vast regions of the mating-type chromosomes.
21 expression and DNAm levels in fetal brain at chromosomes 1 and 17 that were associated with ADHD and
22 ed a uniform pattern of insertion in all the chromosomes (1-5) without any preference for a particula
23 Phosphatase and tensin homolog located on chromosome 10 (PTEN) is a tumor suppressor gene and one
24 identify the parental origin of each copy of chromosome 10 in the materials using oligonucleotide-bas
25 We previously identified a 210 kb region on chromosome 11 (50.37-50.58 Mb, mm10) containing two prot
26 hived at the MRC Harwell Institute lacks the chromosome 11 modifier but instead harbors an ~37 Mb reg
27 as shown to carry a non-B6-derived region of chromosome 11 that protected against B6.Y (POS) sex reve
29 pter protein-coding gene, SHANK2, located on Chromosome 11q13, was disrupted by SVs in 14% of MYCN no
30 The strong conserved synteny between mouse chromosome 12aF1 and human chromosome 14q32 has enabled
31 g Intergenic Co-Induced transcript (NICI) on chromosome 12p13.31 which is regulated by hypoxia via HI
32 5 x 10(-8) at chromosome 6p24.1 in PHACTR1, chromosome 12q13.3 in LRP1, and in females-only, at chro
34 tic leukaemia (including trisomy 12, loss of chromosomes 13q and 13q, and copy-neutral loss of hetero
35 eny between mouse chromosome 12aF1 and human chromosome 14q32 has enabled the use of mouse models to
37 temporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) and can contribute to Alzheimer'
39 support for the role of genetic variants on chromosome 18q23 in regulating neural connectivity and a
40 ABBR2, RUFY3, and in an intergenic region on chromosome 2 replicated with the same direction of effec
43 ders, three significant associations, all on chromosome 20, were identified: rs4809706 (p-value: 2.8
44 duals with DS supports the identification of chromosome 21 genes that protect against cancer when ove
45 S, involving trisomy of all or part of human chromosome 21 or orthologous mouse genomic regions, are
49 condition caused by a hemizygous deletion on chromosome 22-is associated with an elevated risk of psy
50 hin the epidermal differentiation complex on chromosome 25; (2) within a feather, micro-regional spec
53 .2 M SNP dataset, major QTLs were located on chromosomes 3 and 7 for Mn containing six candidate gene
54 including Rec114 and Mer2, which assemble on chromosomes(3-7) and are nearly universal in eukaryotes(
56 e to Phytophthora crown rot were detected on chromosome 4 (QtlPC-C04), 11 (QtlPC-C11) and 14 (QtlPC-C
59 m a conserved mouse pachytene piRNA locus on chromosome 6 (pi6) produce sperm with defects in capacit
62 ent at the major histocompatibility locus on chromosome 6, consistent with admixture-enabled selectio
63 entified associations with P < 5 x 10(-8) at chromosome 6p24.1 in PHACTR1, chromosome 12q13.3 in LRP1
64 al activity of HMAs in AML/MDS patients with chromosome 7 deletions and other monosomal karyotypes.Se
65 9B, and MYD88), losses of 17p13 and gains of chromosome 7, 11q12.3-q25, whereas DLBCL, NOS was predom
67 ns (sensitivity = 0.94, specificity = 0.92), chromosome 7/10 aneuploidies (sensitivity = 0.90, specif
68 ) identified one novel genomic risk locus on chromosome 8 (lead SNP rs17052966, p = 4.53 x 10(-9), od
69 low DNA damage (low genomic scar score with chromosome 9 gain) and a superior outcome (100% overall
70 carriers (n=185) of a pathogenic mutation in chromosome 9 open reading frame 72 (C9orf72), progranuli
72 monstrated that Grh remains bound to mitotic chromosomes, a property shared with other pioneer factor
73 ocated at 11q23, are among the most frequent chromosome aberrations in acute myeloid leukemia (AML).
74 on mitotic chromosomes, defects in metaphase chromosome alignment, and elevated rates of chromosome m
76 igned epigenetic states simultaneously along chromosomes and across cell types, precisely and compreh
78 assemble the 1.07 Gb genome sequence into 24 chromosomes and annotate 32,690 protein-coding genes.
80 egabase-pair scale haplotypes for individual chromosomes and identify 23 genomic regions that have re
81 alpha (TOP2A) is a core component of mitotic chromosomes and important for establishing mitotic chrom
82 ructure that assembles on the centromeres of chromosomes and provides the major attachment point for
84 ed progeny exhibited aneuploidy for multiple chromosomes and showed improved fertility with both pare
85 dients most important to align and segregate chromosomes and simultaneously assemble a bipolar spindl
86 ultiple modes of organization in prokaryotic chromosomes and yield insights into the evolution of euk
87 tly lower for segmental as compared to whole-chromosome aneuploidies (70.8% versus 97.18%, respective
88 ary to the prevalent meiotic origin of whole-chromosome aneuploidies, we show that sub-chromosomal ab
89 ing high-resolution descriptions of archaeal chromosome architectures, our data provide evidence of m
91 However, even in nucleosome-free regions, chromosomes are highly decorated with associated protein
93 Using this technology, we identified which chromosome arm harbors the virus genome and obtained a h
94 functions require localization first to the chromosome arms and then centromeres in mitosis and subs
95 matological and solid cancers initially gain chromosome arms, while only solid cancers subsequently p
96 the general attenuation of transcription on chromosome arms, yet how the cell regulates nuclear and
98 patitis B virus (HBV) integration in the HCC chromosome, as a circulating biomarker for this clinical
99 trand break (DSB) introduced on the paternal chromosome at the EYS locus, which carries a frameshift
101 ted by the three-dimensional organization of chromosomes at multiple levels, including compartments(1
105 between PRDM9-bound hotspots and the nascent chromosome axis through its component cohesin pREC8.
110 t as genes become silenced on the paternal X chromosome but linger in regions that escape X chromosom
111 leads to reduced spreading of roX2 on the X chromosome, but surprisingly also to relocalization to s
114 ads to complete destruction of the bacterial chromosome, causing cell death prior to completion of ph
115 se from cells entering anaphase with lagging chromosomes, cellular mechanisms allowing late-segregati
117 n Petunia inflata using bacterial artificial chromosome clones collectively containing all 17 SLF gen
120 nuclear and chromatin-associated RNAs after chromosome condensation and nuclear envelope breakdown i
123 d by chromatin structure, through the use of Chromosome Conformation Capture (3C), we identified sequ
127 ing an optimized single-cell high-throughput chromosome conformation capture (HiC) protocol(12,13), d
136 g meiosis, which leads to crossovers between chromosomes critical for production of healthy offspring
137 se microfluidic systems to probe the growth, chromosome cycle and division mechanism of Bacillus subt
140 cumulation of SAF-A-RNA complexes on mitotic chromosomes, defects in metaphase chromosome alignment,
142 specific structure formed between homologous chromosomes during prophase that promotes DSB formation
145 , pharmacological activation of the murine X chromosome-encoded receptor proteins Toll-like receptor
149 howed that ecDNAs preferentially tether near chromosome ends, where they re-integrate when DNA damage
150 res, the structures that protect the ends of chromosomes, eventually triggering cellular senescence.
151 rgene does not follow standard models of sex chromosome evolution, in which distinct evolutionary str
152 is enabled us to establish a model of spurge chromosome evolution, since the common paleopolyploid ev
157 dying model bacteria has revealed aspects of chromosome folding that are applicable to many species.
160 atory regions and in telomers at the ends of chromosomes frequently contain tandem repeats of guanine
161 tic approaches, we evaluated influences of X chromosome genomic imprinting and hormone replacement th
163 hnique revealed that the telomere lengths of chromosomes harboring the integrated virus genome were c
167 lot, quantitative polymerase chain reaction, chromosome immunoprecipitation, cell invasion, and lucif
170 maternal alleles were detected on 5 (of 12) chromosomes in high-fitness individuals of both reciproc
171 uce 3D maps of 36 genomic targets across six chromosomes in hundreds to thousands of cells, implying
173 ange of genetic information between parental chromosomes in meiosis is an integral process for the cr
176 early X chromosome inactivation-imprinted X chromosome inactivation prevents biallelic X silencing.
178 protein 1 (SMCHD1) has been implicated in X-chromosome inactivation, imprinting, and DNA damage repa
179 he hypothesis that-in organisms with early X chromosome inactivation-imprinted X chromosome inactivat
182 one deleterious hot-spot mutation increased chromosome instability in a wild-type (WT) background, s
184 t these CNVs appear to arise via a dicentric chromosome intermediate and breakage-fusion-bridge cycle
185 ow that subtelomeric DNA replication, unlike chromosome-internal DNA replication, is sensitive to hyd
187 he Escherichia coli SMC complex, MukBEF, the chromosome is organized as a series of loops around a th
192 6.49%, indicating the success in the ovine Y chromosome isolation and the high quality of the Y chrom
193 Hi-C scaffolding produces highly contiguous, chromosome-length scaffolds, and we identify hundreds of
199 analyzed transcriptional induction kinetics, chromosome looping, and enhancer RNA production to under
200 ually high expression located at the apex of chromosome loops protruding from the nuclear periphery i
202 ta point to a role for TOP2A as a structural chromosome maintenance enzyme locking in condensation st
203 De novo mutations arising on the paternal chromosome make the largest known contribution to autism
204 shortest length assay (TeSLA), we show that chromosome mis-segregation due to imperfect DDR signalin
208 s moubata cell line OME/CTVM22 had the modal chromosome number 33 instead of 2n = 20 chromosomes for
210 peciation (HHS), which involves no change in chromosome number, is an important mechanism of speciati
213 monstrate that under conditions of increased chromosome occupancy of the Escherichia coli SMC complex
215 ich was successfully applied to flow-sorting chromosomes of sheep, with a focus on isolation and sequ
217 gative correlation between the loss of the Y chromosome or linc-SPRY3-2/3/4 and overall survival.
218 pecies that present extensive differences in chromosome organization, phenotype, evolutionary history
223 vels-ranging from cell cycle organization to chromosome ploidy to replication mode and nature of the
226 ht and length were detected on a total of 18 chromosomes, reflecting the polygenic nature of growth.
228 sely with distance to nuclear speckles, with chromosome regions of unusually high expression located
229 esults indicated that 68.90% of reads were Y chromosome-related sequences as they are homologous to t
230 er-counting mechanism partitions holocentric chromosomes relative to the crossover site, which ultima
233 has examined mutations in genes involved in chromosome remodelling (for example, PBRM1, BAP1 and SET
236 que, we were able to unequivocally count the chromosomes resulting in 2n = 4x = 168, a revised chromo
237 inetochore-fibers pivot around poles but not chromosomes, retaining their orientation within 3 mum of
244 rates through genomic comparisons with a new chromosome-scale sequence of the invertebrate chordate a
247 gous recombination, which facilitates proper chromosome segregation and enables the reciprocal exchan
248 However, mutations in genes that control chromosome segregation are rare in human tumors as these
249 olar body and be fertilised, despite chaotic chromosome segregation at the first meiotic division.
250 nsitive and systematic quantitation of these chromosome segregation defects in cells undergoing mitos
253 on of the mitotic spindle to ensure faithful chromosome segregation during mitosis, cell polarization
258 a demonstrate that Cdc23 is required for the chromosome segregation through regulating the spindle as
267 induced super-Mendelian inheritance of the X-chromosome-shredding I-PpoI nuclease by coupling this to
268 m the PacBio sequencing platform and shorter chromosome size from the hybrid Oxford Nanopore-Illumina
270 KNL-1 and KNL-3 are required for preanaphase chromosome stretching, suggesting a role in pulling forc
274 O directly affects the formation of distinct chromosome subdomains during meiotic chromosome remodeli
276 e encoding phosphatase and tensin homolog on chromosome ten (PTEN) are diagnosed with PTEN hamartoma
278 nomalies in their gene arrays coded on the X chromosome that result in significantly decreased spectr
279 re we show that RNA is evicted from prophase chromosomes through Aurora-B-dependent phosphorylation o
281 ellular mechanisms allowing late-segregating chromosomes to rejoin daughter nuclei remain underexplor
282 us revealed that distances of the homologous chromosomes to the center of nucleus are almost the same
283 ified factors that revealed the link between chromosome translocation and peptidoglycan remodeling.
284 In Emu-Myc mice, which model the MYC/IGH chromosome translocation in Burkitt's lymphoma, homozygo
285 ence shows that DSBs are a primary source of chromosome translocations or deletions, making them a ma
286 a ring that encircled and cohered replicated chromosomes until its cleavage triggered the metaphase-t
287 ns for each parental genome (including the X chromosome), using an optimized single-cell high-through
288 f the significance of maternally inherited X chromosome variants in males with neurocognitive phenoty
289 n of fission yeast DNA inserted into a mouse chromosome was previously observed to adopt a mitotic or
290 A dominant karyotype with three aneuploid chromosomes was observed in 25 cells, while two differen
291 otic chromosome pairing between homoeologous chromosomes was reported in many nascent allopolyploids.
292 properties of gene-flanking regions on the X Chromosome, we find evidence that adaptive cis-regulator
294 d correct segregation of multiple homologous chromosomes, which can form complex multivalent configur
295 id de novo genome assembly that combines the chromosome-wide phasing and scaffolding capabilities of
297 report that elevated expression of CXorf67 (chromosome X open reading frame 67), which frequently oc
300 tegration of viral genomic DNA into the host chromosomes, yet remarkably, the timing and cellular loc