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1 anisotropy to orient division in the rounded mitotic cell.
2 otein SPD-2/CEP192 and CDK activity from the mitotic cell.
3 n early neurological event occurring in post-mitotic cells.
4 entially phosphorylates Cdc25A and Cdc25B in mitotic cells.
5 eIF4G1) in interphase or nocodazole-arrested mitotic cells.
6 ng of microtubule dynamics in interphase and mitotic cells.
7 t for the faster rate of PGK-FRET folding in mitotic cells.
8 ols the levels of hMSH4 by ubiquitination in mitotic cells.
9 pindle orientation and ectopically localized mitotic cells.
10 o SF3B1 in the nucleoplasm of interphase and mitotic cells.
11 that they are essential for HJ resolution in mitotic cells.
12 pment or differentiation of neighboring post-mitotic cells.
13 hin secondary lymphoid organs that contained mitotic cells.
14 n homolog BLM control crossover formation in mitotic cells.
15  is enriched in the nucleolus of meiotic and mitotic cells.
16 c effector pathways used by RhoA and Rac1 in mitotic cells.
17 negative EB1 protein fragment into mammalian mitotic cells.
18 recombination in yeast meiosis and mammalian mitotic cells.
19 not show a WNK1-like localization pattern in mitotic cells.
20 ression of meiotic transcripts expression in mitotic cells.
21 ir of stalled/collapsed replication forks in mitotic cells.
22 ng rapid migration to the cleavage furrow of mitotic cells.
23 xes are dissociated by these translocases in mitotic cells.
24  footprint, and often even disseminate their mitotic cells.
25  persistent microtubule bridges between post-mitotic cells.
26 t of the cell cycle and is only dispersed in mitotic cells.
27  skeleton controls hexagonal packing of post-mitotic cells.
28 tected in terminally differentiated and post-mitotic cells.
29 s a fundamental difference in meiotic versus mitotic cells.
30 K was found to co-localize in centrosomes in mitotic cells.
31 d that HP1 proteins interact with ASF/SF2 in mitotic cells.
32 nditional gene disruption and rescue in post-mitotic cells.
33 ell cycle and eEF2 phosphorylation is low in mitotic cells.
34 y than wild type topo I after isolation from mitotic cells.
35 ereby permit protein synthesis to proceed in mitotic cells.
36 lex that holds sister chromatids together in mitotic cells.
37 rosophila cannot be easily performed in post-mitotic cells.
38 ting homologous recombination in meiotic and mitotic cells.
39 ed, including early apoptotic events and pre-mitotic cells.
40 e cell cycle regulator is repurposed in post-mitotic cells.
41 s, is sufficient to segregate chromosomes in mitotic cells.
42 cantly increases the viability of irradiated mitotic cells.
43 d to be required for S303 phosphorylation in mitotic cells.
44 sed stability of the Mcd1 cohesin subunit in mitotic cells.
45 ], retains interphase-like behaviour even in mitotic cells.
46 ge of physicochemical properties observed in mitotic cells.
47 dentifying a novel function for CCNY in post-mitotic cells.
48 hase (2K1N), duplication to four EGJ in post-mitotic cells (2K2N) and segregation of two EGJ to each
49                           In yeast and human mitotic cells, a similar regulatory network restrains th
50  Although some tumors exhibited increases in mitotic cells after dosing, others displayed decreases,
51 ervations indicate that DDR is suppressed in mitotic cells after the step of gammaH2AX formation.
52 on of > 1000 genes to the rounding of single mitotic cells against confinement.
53 opically positioned around the cortex of the mitotic cell and we show that the mitotic spindle does n
54 rm that was used for the previous studies in mitotic cells and a novel, shorter mitotic isoform.
55 nd PPP1R12C phosphorylation are increased in mitotic cells and are important for mitosis completion.
56   When wild type topo I was pulled down from mitotic cells and dephosphorylated with alkaline phospha
57 wl, its association with PP1 is disrupted in mitotic cells and egg extracts.
58 dRrp6 elicits a decrease in the frequency of mitotic cells and in the mitotic marker phospho-histone
59  with microtubule-unattached kinetochores in mitotic cells and is a component of the spindle assembly
60 ngaged in the formation of a rigid cortex in mitotic cells and is therefore unavailable for deploymen
61 trast, HSF2 occupied hundreds of loci in the mitotic cells and localized to the condensed chromatin a
62 s the rounding force, pressure and volume of mitotic cells and localizes selected proteins.
63 rmatogenesis that ensures the maintenance of mitotic cells and normal spermiogenesis.
64 intain G2/M-specific genes repressed in post-mitotic cells and restrict the time window of mitotic ge
65  The activation of these typically quiescent mitotic cells and subsequent shifting of wild-type mtDNA
66  mRNAs within the nucleocytoplasmic space of mitotic cells and suggest that MT-RNAs are likely to con
67 , we reveal how the mechanical properties of mitotic cells and their response to external forces are
68 ve view of ER organization in interphase and mitotic cells and to address a discrepancy in the field
69 in-2B blocks tubulin polymerization, ablates mitotic cells, and induces mitochondria-dependent apopto
70 n is the major astrin-interacting protein in mitotic cells, and is required for astrin targeting to m
71 f cells occupying S phase, at the expense of mitotic cells, and kinetic analyses demonstrate that Id2
72                         Increased numbers of mitotic cells, apoptotic bodies, and polyploid keratinoc
73 athway regulates exit from the SAC only when mitotic cells are challenged by retained catenation and
74                                              Mitotic cells are extremely susceptible to apoptotic sig
75                            In addition, when mitotic cells are fused with interphase cells, "wait ana
76               Terminally differentiated post-mitotic cells are generally considered irreversibly deve
77  including HSF1-mediated expression of Hsps, mitotic cells are highly vulnerable to stress.
78                             Neurons, as post-mitotic cells, are devoid of replicative associated agin
79                                              Mitotic cells arrested by the spindle assembly checkpoin
80 e, we identify CDK5, a kinase active in post mitotic cells, as a new and important mediator of PKD pr
81 e6Delta, mus81Delta and nse6Delta mus81Delta mitotic cells, as well as the meiotic defects of nse6Del
82 tially co-localized at cell junctions and in mitotic cells, at the midbody during cytokinesis.
83 o represent a minor pathway of DSB repair in mitotic cells, being detected at about tenfold lower lev
84 omal passenger complex (CPC) distribution in mitotic cells, but associates with integrin complexes an
85 o be the main cue for spindle positioning in mitotic cells, but new evidence suggests that, in the co
86      The spindle assembly checkpoint arrests mitotic cells by preventing degradation of cyclin B1 by
87 chromosomes, and extrachromosomal regions of mitotic cells by quantitative confocal Raman microspectr
88                                  However, if mitotic cells cannot create sufficient space, their roun
89                To provide a clearer picture, mitotic cell chromosome alignment and spindle bipolarity
90                               Maintenance of mitotic cell clusters such as meristematic cells depends
91 ted protein, TCAB1, was released from hTR in mitotic cells coincident with TCAB1 delocalization from
92 ters, but express collier, a marker for post mitotic cells committed to a neural fate, while they are
93 show that activated RhoA is localized at the mitotic cell cortex, and Rho-associated kinase inhibitio
94                             Specifically, in mitotic cells, CRAF becomes phosphorylated on Ser338 and
95 to cycling cells and retained throughout the mitotic cell cycle ('Cell Cycle Common'), versus those t
96 d that KRP6 acts downstream of GA to inhibit mitotic cell cycle activation during germination.
97 testinal necroptosis was linked to increased mitotic cell cycle arrest via Per1/2-controlled Wee1, re
98 M inhibition caused catastrophic DNA damage, mitotic cell cycle arrest, and apoptosis specifically in
99 PC) activator best known for its role in the mitotic cell cycle at M-phase exit, in G1, and in mainta
100         This response is correlated with the mitotic cell cycle but is not coupled to nuclear osmolyt
101 ew and demonstrate that mouse embryos in the mitotic cell cycle can also directly reprogram sperm for
102 ase (AD) exhibit evidence of re-entry into a mitotic cell cycle even before the development of substa
103  a subset of human transcripts, enriched for mitotic cell cycle factors, leading to mitotic arrest.
104 lopment of Xenopus laevis embryos, the first mitotic cell cycle is long ( approximately 85 min) and t
105 lled by layers of regulation imposed on core mitotic cell cycle machinery components by the program o
106 ion of DNA content and quantification of the mitotic cell cycle phases by applying supervised machine
107  of GWAS data was significantly enriched for mitotic cell cycle processes (P = 0.001), the immune res
108 liferation and differentiation by prolonging mitotic cell cycle progression and promoting giant cell
109  late M/G(1) induction, and (iii) couple the mitotic cell cycle progression machinery to cellular pho
110                                              Mitotic cell cycle progression occurs rapidly, continuou
111 m-cell proliferative fate, despite promoting mitotic cell cycle progression of those germ cells that
112                       In addition to driving mitotic cell cycle progression, CYE-1 and CDK-2 also pla
113 -10 null allele reveals that METT-10 enables mitotic cell cycle progression.
114  protein type ubiquitin E3 ligase, regulates mitotic cell cycle progression.
115          The endocycle represents a modified mitotic cell cycle that in plants is often coupled to ce
116 daughter cells switch synchronously from the mitotic cell cycle to endoreduplication.
117 njury, quiescent hepatocytes can reenter the mitotic cell cycle to restore tissue homeostasis.
118 evealed that MeJA delays the switch from the mitotic cell cycle to the endoreduplication cycle, which
119 , multiple genes involved in maintaining the mitotic cell cycle were rapidly down-regulated and senes
120 dk2 is dispensable for the regulation of the mitotic cell cycle with both Cdk4 and Cdk1 covering for
121 f oogenesis, when follicle cells undergo the mitotic cell cycle, and at midoogenesis when these cells
122 ed with centromeres during all stages of the mitotic cell cycle, except from metaphase to mid-anaphas
123                                   During the mitotic cell cycle, Geminin can act both as a promoter a
124 B(S) classifier, including those involved in mitotic cell cycle, microtubule organization, and chromo
125 cohesin dissociation from DNA throughout the mitotic cell cycle, modulating sister chromatid cohesion
126 f CYCD3;1 or E2FB, both of which promote the mitotic cell cycle, strongly impaired CaLCuV infection.
127  cells progressing synchronously through the mitotic cell cycle, while preserving the coupling of cel
128 r this particular KRP as an activator of the mitotic cell cycle.
129 eiosis and suggest a similar function in the mitotic cell cycle.
130 quence of a block in the G(2)/M stage of the mitotic cell cycle.
131 cells in early, mid, and late S phase of the mitotic cell cycle.
132 lasm and progresses through G1 into the next mitotic cell cycle.
133  TTP/HuR mRNA ratios and was involved in the mitotic cell cycle.
134 clin with the CDK protein Cdc2 can drive the mitotic cell cycle.
135                        Thus, while the major mitotic cell-cycle activity is blocked after DNA damage,
136                      Moreover, TTP augmented mitotic cell-cycle arrest as demonstrated by flow cytome
137                                   Control of mitotic cell cycles by the anaphase-promoting complex or
138                                     Although mitotic cell cycles can take place in the absence of cen
139 of which p57 is essential for switching from mitotic cell cycles to endocycles.
140 ut not p27, the CDK inhibitor that regulates mitotic cell cycles.
141 nt of the prereplication complex (pre-RC) in mitotic cell cycles.
142 depletion resulted in a dramatic increase in mitotic cell death upon challenge with spindle poisons.
143 on prolonged mitotic progression and induced mitotic cell death, both of which are indicative of mito
144 amics, prometaphase arrest, tetraploidy, and mitotic cell death.
145 ily member, Noxa, is a critical initiator of mitotic cell death.
146 ubule dynamics and mitotic abnormalities and mitotic cell death.
147 ation-induced centrosome overduplication and mitotic cell death.
148 d cells are a specialized population of post-mitotic cells decorated with dozens of motile cilia that
149 ence of other spindle proteins, we show that mitotic cells deficient in MCAK fail to maintain spindle
150 e demonstrate that CME can be 'restarted' in mitotic cells despite high membrane tension, by allowing
151 igration during development or wound repair, mitotic cell detachment, and physiological shedding.
152 1 and H3K9me2 signals between interphase and mitotic cells disappeared.
153                                     However, mitotic cells display no detectable recruitment of the E
154 ces neurogenesis and increases the number of mitotic cells dividing away from the ventricular surface
155 matogonial stem cells into spermatocytes via mitotic cell division and the production of haploid sper
156 tion is correlated with the decision to exit mitotic cell division and to enter cell expansion, which
157                                              Mitotic cell division ensures that two daughter somatic
158                                              Mitotic cell division is controlled by cyclin-dependent
159                           How BRCA2 controls mitotic cell division is debated.
160                      Finally, we report that mitotic cell division is not required for genomic reprog
161 te SMC2 transcription as a key player in the mitotic cell division machinery.
162 requires a tightly controlled orientation of mitotic cell division relative to the apical polarity ax
163                      Successful execution of mitotic cell division requires the tight synchronisation
164        Here we employ computer simulation of mitotic cell division to determine how factors such as t
165           We find that convergent-extension, mitotic cell division, and daughter cell rearrangement d
166  arise from defects in DNA recombination and mitotic cell division, respectively.
167 dle assembly and microtubule dynamics during mitotic cell division.
168 tages of female meiotic cell development and mitotic cell division.
169 ng female mouse meiotic cell development and mitotic cell division.
170 s germ line stem cells to self-renew through mitotic cell division.
171 t, germline specification of the oocyte, and mitotic cell division.
172  of an event on the concerted process of the mitotic cell division.
173  the fundamental physiological properties of mitotic cell divisions, evokes a new view of the meiotic
174 n chromosome organization during meiotic and mitotic cell divisions.
175 between lipogenesis and protein synthesis in mitotic cell divisions.
176 ution of genetic material during meiotic and mitotic cell divisions.
177                                           In mitotic cells, double HJs are primarily dissolved by the
178 n 2 (MLC2) in the contractile ring region of mitotic cells during cytokinesis.
179                             In 4.1R-depleted mitotic cells, efficient centrosome separation is reduce
180 ctivation only ensuing when a DSB-containing mitotic cell enters G1.
181         Indeed, Rad51 foci do not persist in mitotic cells even after G2 checkpoint suppression, sugg
182 in the transition from cell division to post-mitotic cell expansion and concomitant petal maturation.
183 egulation of cell-cycle progression and post-mitotic cell expansion that together sculpt organ form.
184                                   While most mitotic cells express two AURK isoforms (AURKA and AURKB
185 Pin1 binding to different phosphoproteins in mitotic cell extracts was modulated by I-2, and binding
186                                              Mitotic cells facilitate this process by generating intr
187                                          How mitotic cell fate is regulated in the developing mammali
188 , the functional importance of the spherical mitotic cell for the success of cell division has been t
189 n caused by depletion of endogenous Rad21 in mitotic cells, further indicating the physiological sign
190                                           In mitotic cells, Fus2p-GFP is nuclear but becomes cytoplas
191    Here, we show that in maize (Zea mays L.) mitotic cells, H3T3ph is concentrated at pericentromeric
192 protein (APC) and its binding partner EB1 in mitotic cells has come from siRNA studies.
193                                              Mitotic cells have a distinctive intranuclear heterochro
194 hanical properties of symmetrically dividing mitotic cells have been well characterized, whereas the
195             Using different methods to limit mitotic cell height, we show that a failure to round up
196          O. tauri cultures were enriched for mitotic cells, high-pressure frozen, and then imaged in
197 nd transactivating capacity of HSF1, leaving mitotic cells highly susceptible to proteotoxicity.
198 sient inactivation of ATM and DNA-PK renders mitotic cells hypersensitive to DSB-inducing agents.
199 ble in mature postmitotic neurons as well as mitotic cells in mice brain by combining CRISPR-Cas9-med
200 ows a reduction in the number of neurons and mitotic cells in olfactory rosettes, mirroring the pheno
201 omous effects on the differentiation of post-mitotic cells in the bristle lineage.
202 tral retinal cells, and increased numbers of mitotic cells in the dorsal region, indicating that Tbx2
203                              For labeling of mitotic cells in the hippocampus, bromodeoxyuridine was
204 oriented centrosomes in a rare population of mitotic cells in the mutant retinas.
205    Loss of eIF4A-1 reduces the proportion of mitotic cells in the root meristem and perturbs the rela
206 protocols, FACS separation of interphase and mitotic cells, including mitotic subphases, can be combi
207  and Spr28 colocalize with Cdc3 and Cdc10 in mitotic cells, indicating that incorporation requires a
208 s ability involves dedifferentiation of post-mitotic cells into progenitors that in turn form new str
209 ion was reduced and re-intercalation of post-mitotic cells into the elongating gut tube epithelium wa
210  mitotic exit, the cytoskeleton of monopolar mitotic cells is initially radially symmetric but underg
211 centration of nuclear-localized CDKG1 in pre-mitotic cells is set by mother cell size, and its progre
212                                           In mitotic cells, it was observed that the gamma -tubulin s
213                                           In mitotic cells, knockdown of Kif5b leads to centrosome am
214                           Although most post-mitotic cells lack CDK1 and cyclins, lens fiber cells ma
215                                           In mitotic cells lacking Cep192, microtubules become organi
216 port here that Lis1 and Ndel1 reduction in a mitotic cell line impairs prophase nuclear envelope (NE)
217                        We also found that in mitotic cells Mad1 co-immunoprecipitated with Plk1.
218 o assess the impact of autonomous changes in mitotic cell mechanics within a stretched monolayer.
219                                           In mitotic cells, membrane tension is increased and this in
220                   EBP50 is not necessary for mitotic cell microvilli, and PKC activation causes a rea
221  the division site by localising Gef2 to the mitotic cell middle.
222                                           In mitotic cells, mitotic centromere associated kinesin (MC
223 rge-scale screening data sets on nuclear and mitotic cell morphologies demonstrates that CellCognitio
224 a medium containing ON 01910.Na, accumulated mitotic cell number with a peak from 10 to 14 hours and
225 ions accumulate over the life course in post-mitotic cells of many species.
226 ar bioenergetics during degeneration of post-mitotic cells of ocular tissue.
227 s in cell-specific patterns in virtually all mitotic cells of the body.
228  (HR), which employs the sister chromatid in mitotic cells or the homologous chromosome in meiotic ce
229  (NHEJ) or aberrant replication suggesting a mitotic cell origin.
230 al body patterning in land plants acting via mitotic cell plane positioning.
231  number, while simultaneously producing post-mitotic cells (PMCs).
232  a broadly distributed, abundant, and highly mitotic cell pool.
233  without sT, reveals an orthogonal pH3(S10+) mitotic cell population having higher inactive p4E-BP1(T
234  comprises different phases characterized by mitotic cell proliferation, endoreduplication, the accum
235 hanisms of DDR in great detail; however, how mitotic cells respond to DNA damage remains less defined
236 contrast, mucosal epithelial cells and other mitotic cells responded robustly to type I IFNs and did
237                                  Analysis of mitotic cells reveals that pRB depletion compromises cen
238 ia and mouse pro-B cell lymphoid cell lines, mitotic cells reversibly increase their volume by more t
239                    Little is known about how mitotic cells round against epithelial confinement.
240 that moesin phosphorylation is essential for mitotic cell rounding and identify a new role for cell r
241 hese proteins can contribute functionally to mitotic cell rounding and spindle centralization during
242  PSK1-alpha/beta or PSK2 expression inhibits mitotic cell rounding as well as spindle positioning and
243                              We propose that mitotic cell rounding in columnar epithelia allows cells
244                    Despite the importance of mitotic cell rounding in tissue development and cell pro
245                                              Mitotic cell rounding is accompanied by changes in the a
246  between IKNM and the fundamental process of mitotic cell rounding.
247                                           In mitotic cells, S1P is active, but SREBP is not cleaved a
248 ll as the potential consequences of abnormal mitotic cell shape and size on chromosome segregation, t
249 ta reveals mitotic FAs as a key link between mitotic cell shape and spindle orientation, and may have
250                       Finally, we found that mitotic cell shape is also abnormal in the mutant VZ.
251                         Thus, interphase and mitotic cells share similar mechanisms for creating larg
252 ts may be important for spindle integrity in mitotic cells so that tensile forces generated at kineto
253 sm may be relevant to other highly polarized mitotic cells, such as mammalian neural progenitors.
254 shmoos lost actin polarity more rapidly than mitotic cells, suggesting that the maintenance of cell p
255                                           In mitotic cells, TACC3 knockdown substantially affected th
256 Moreover, RSK is likely to be more active in mitotic cells than in interphase cells, as evidenced by
257        Muscle fibres are multinucleated post-mitotic cells that can change dramatically in size durin
258                      We find that ES-derived mitotic cells that have been dorsalized by the sonic hed
259 nt to a new type of "waste" material in post-mitotic cells that may contribute to the senescent pheno
260 on of multiple centrosome-like structures in mitotic cells that result from the separation of paired
261 rs, primary odontoblasts are long-lived post-mitotic cells that secrete dentine throughout the life o
262                                           In mitotic cells, this process depends on the activity of n
263                                   Thus, post-mitotic cells, though terminally differentiated, remain
264  of the centrosome is malleable; fusion of a mitotic cell to a differentiated or interphase cell resu
265 mponents of the cell cycle machinery in post-mitotic cells to control glucose homeostasis independent
266 antiviral strategies employed by neurons and mitotic cells to control HSV-1 infection.
267 e to produce strong pushing forces, allowing mitotic cells to round up; it might also, by lowering cy
268 approach to circumvent the inability of post-mitotic cells to support homologous recombination-based
269  relocalization from the nuclear interior in mitotic cells to the periphery at or proximal to telomer
270                                 Moreover, in mitotic cells, transcription termination of meiotic RNAs
271 matin compaction mediates progenitor to post-mitotic cell transitions and modulates gene expression p
272                           Here, we show that mitotic cells treated with DSB-inducing agents activate
273                  ChIP-seq of highly purified mitotic cells uncovered that key hematopoietic regulator
274 ion, spindle tension was markedly reduced in mitotic cells upon exposure to GF-15.
275 analyses of the microtubular cytoskeleton of mitotic cells using wild-type, mpk6-2 mutant and plants
276               Furthermore, EDD siRNA reduced mitotic cell viability and, in nocodazole-treated cells,
277 nnels to functionally cooperate and regulate mitotic cell volume and tumor progression.
278 , we found that the absence of a full DDR in mitotic cells was associated with the high cyclin-depend
279 nd the number of phospho-histone H3 staining mitotic cells was decreased, consistent with G2/M checkp
280                  The number of Ki67-positive mitotic cells was more than doubled, consistent with the
281                  By tracking oscillations in mitotic cells, we reveal that a robust cell-autonomous,
282                                           In mitotic cells, we show that the ER undergoes both spatia
283 n the vast majority of the previous studies, mitotic cells were chemically fixed at room temperature,
284                         Increased numbers of mitotic cells were observed following overexpression of
285 1 IRIF could be detected when the irradiated mitotic cells were treated with a CDK1 inhibitor.
286 e transcriptional response to stress also in mitotic cells where the chromatin is tightly compacted.
287 alizes to the cleavage furrow and midbody of mitotic cells, where it is required for the completion o
288 g mitosis, especially in nocodazole-arrested mitotic cells, where these kinases exhibit both an incre
289 ade around DNA damage sites did not occur in mitotic cells, which explains, at least in part, why BRC
290          Expression of cx43 is identified in mitotic cells, which further suggests that Cx43 may cont
291 removal of Rad51 from undamaged chromatin in mitotic cells, which prevents formation of nonrecombinog
292 s, had marked decreases in the percentage of mitotic cells with aligned chromosomes and bipolar spind
293 sted for an exposure-effect relationship for mitotic cells with defects in chromosome alignment and s
294 pression leads to an increased population of mitotic cells with dynein delocalized from the mitotic s
295 ation of endocytic proteins is maintained in mitotic cells with restored CME, indicating that direct
296                                 Treatment of mitotic cells with Trichostatin A, an HDAC inhibitor, re
297 d that DNA-damage signaling is attenuated in mitotic cells, with full DDR activation only ensuing whe
298 r biopsies were assessed for accumulation of mitotic cells within proliferative tumor regions.
299   Skin biopsies were evaluated for increased mitotic cells within the basal epithelium.
300 stimuli cause proliferative effects (PHH3(+) mitotic cells, YAP translocation, PDGF secretion) or inc

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