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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-dependent regulation of PPP holoenzymes in mitotic cells.
4 ed, including early apoptotic events and pre-mitotic cells.
5 e cell cycle regulator is repurposed in post-mitotic cells.
6 s, is sufficient to segregate chromosomes in mitotic cells.
7 cantly increases the viability of irradiated mitotic cells.
8 d to be required for S303 phosphorylation in mitotic cells.
9 ittle is known about their functions in post-mitotic cells.
10 sed stability of the Mcd1 cohesin subunit in mitotic cells.
11 ], retains interphase-like behaviour even in mitotic cells.
12 ge of physicochemical properties observed in mitotic cells.
13 dentifying a novel function for CCNY in post-mitotic cells.
14 n early neurological event occurring in post-mitotic cells.
15 entially phosphorylates Cdc25A and Cdc25B in mitotic cells.
16 eIF4G1) in interphase or nocodazole-arrested mitotic cells.
17 t for the faster rate of PGK-FRET folding in mitotic cells.
18 ols the levels of hMSH4 by ubiquitination in mitotic cells.
19 pindle orientation and ectopically localized mitotic cells.
20 that they are essential for HJ resolution in mitotic cells.
21 pment or differentiation of neighboring post-mitotic cells.
22 hin secondary lymphoid organs that contained mitotic cells.
23 n homolog BLM control crossover formation in mitotic cells.
24  is enriched in the nucleolus of meiotic and mitotic cells.
25 c effector pathways used by RhoA and Rac1 in mitotic cells.
26 negative EB1 protein fragment into mammalian mitotic cells.
27 recombination in yeast meiosis and mammalian mitotic cells.
28  from medioapical myosin loss in neighboring mitotic cells.
29 not show a WNK1-like localization pattern in mitotic cells.
30 ir of stalled/collapsed replication forks in mitotic cells.
31 ng rapid migration to the cleavage furrow of mitotic cells.
32 xes are dissociated by these translocases in mitotic cells.
33  footprint, and often even disseminate their mitotic cells.
34  persistent microtubule bridges between post-mitotic cells.
35 t of the cell cycle and is only dispersed in mitotic cells.
36  skeleton controls hexagonal packing of post-mitotic cells.
37 tected in terminally differentiated and post-mitotic cells.
38  sort cardiomyocyte populations enriched for mitotic cells.
39 ing with ETAA1 having a dominant function in mitotic cells.
40 owers a turbulent microtubule network inside mitotic cells.
41 or cell nuclei, with high expression in some mitotic cells.
42  NPC quality control is compromised in aging mitotic cells.
43 orylation in vivo and interacts with Cse4 in mitotic cells.
44 hase assembly is a major challenge for aging mitotic cells.
45 n interactome in spread interphase and round mitotic cells.
46 ng of microtubule dynamics in interphase and mitotic cells.
47 o SF3B1 in the nucleoplasm of interphase and mitotic cells.
48 ression of meiotic transcripts expression in mitotic cells.
49 nditional gene disruption and rescue in post-mitotic cells.
50 rosophila cannot be easily performed in post-mitotic cells.
51 ting homologous recombination in meiotic and mitotic cells.
52 hase (2K1N), duplication to four EGJ in post-mitotic cells (2K2N) and segregation of two EGJ to each
53                           In yeast and human mitotic cells, a similar regulatory network restrains th
54 peractivity alters centrosome positioning in mitotic cells, affecting oriented cell division and prom
55  Although some tumors exhibited increases in mitotic cells after dosing, others displayed decreases,
56 ervations indicate that DDR is suppressed in mitotic cells after the step of gammaH2AX formation.
57 on of > 1000 genes to the rounding of single mitotic cells against confinement.
58 ical cell division orientation by elongating mitotic cells along the main tension axis.
59       To ensure faithful genome propagation, mitotic cells alternate one round of chromosome duplicat
60 , relying on a balance of forces between the mitotic cell and the surrounding tissue.
61 opically positioned around the cortex of the mitotic cell and we show that the mitotic spindle does n
62 rm that was used for the previous studies in mitotic cells and a novel, shorter mitotic isoform.
63 nd PPP1R12C phosphorylation are increased in mitotic cells and are important for mitosis completion.
64 f adhesion structure, which is emphasized by mitotic cells and cells in long-term culture, identifies
65 as upregulated in a Drak-dependent manner in mitotic cells and colocalized with phosphorylated Sqh in
66 wl, its association with PP1 is disrupted in mitotic cells and egg extracts.
67 ngaged in the formation of a rigid cortex in mitotic cells and is therefore unavailable for deploymen
68 trast, HSF2 occupied hundreds of loci in the mitotic cells and localized to the condensed chromatin a
69 s the rounding force, pressure and volume of mitotic cells and localizes selected proteins.
70 rmatogenesis that ensures the maintenance of mitotic cells and normal spermiogenesis.
71 intain G2/M-specific genes repressed in post-mitotic cells and restrict the time window of mitotic ge
72  mRNAs within the nucleocytoplasmic space of mitotic cells and suggest that MT-RNAs are likely to con
73 , we reveal how the mechanical properties of mitotic cells and their response to external forces are
74 ve view of ER organization in interphase and mitotic cells and to address a discrepancy in the field
75 n is the major astrin-interacting protein in mitotic cells, and is required for astrin targeting to m
76 f cells occupying S phase, at the expense of mitotic cells, and kinetic analyses demonstrate that Id2
77                         Increased numbers of mitotic cells, apoptotic bodies, and polyploid keratinoc
78 athway regulates exit from the SAC only when mitotic cells are challenged by retained catenation and
79                                              Mitotic cells are extremely susceptible to apoptotic sig
80                            In addition, when mitotic cells are fused with interphase cells, "wait ana
81               Terminally differentiated post-mitotic cells are generally considered irreversibly deve
82  including HSF1-mediated expression of Hsps, mitotic cells are highly vulnerable to stress.
83                             Neurons, as post-mitotic cells, are devoid of replicative associated agin
84                                              Mitotic cells arrested by the spindle assembly checkpoin
85 e, we identify CDK5, a kinase active in post mitotic cells, as a new and important mediator of PKD pr
86 e6Delta, mus81Delta and nse6Delta mus81Delta mitotic cells, as well as the meiotic defects of nse6Del
87 tially co-localized at cell junctions and in mitotic cells, at the midbody during cytokinesis.
88                                              Mitotic cells attenuate the DNA damage response (DDR) by
89 o represent a minor pathway of DSB repair in mitotic cells, being detected at about tenfold lower lev
90 omal passenger complex (CPC) distribution in mitotic cells, but associates with integrin complexes an
91 o be the main cue for spindle positioning in mitotic cells, but new evidence suggests that, in the co
92      The spindle assembly checkpoint arrests mitotic cells by preventing degradation of cyclin B1 by
93 chromosomes, and extrachromosomal regions of mitotic cells by quantitative confocal Raman microspectr
94                                  However, if mitotic cells cannot create sufficient space, their roun
95 hosphorylation-specific H2B S6 antibodies in mitotic cells caused anaphase defects with impaired chro
96                To provide a clearer picture, mitotic cell chromosome alignment and spindle bipolarity
97                               Maintenance of mitotic cell clusters such as meristematic cells depends
98 ted protein, TCAB1, was released from hTR in mitotic cells coincident with TCAB1 delocalization from
99 ters, but express collier, a marker for post mitotic cells committed to a neural fate, while they are
100 on was not inhibited but rather increased in mitotic cells, consistent with active translation initia
101 show that activated RhoA is localized at the mitotic cell cortex, and Rho-associated kinase inhibitio
102                             Specifically, in mitotic cells, CRAF becomes phosphorylated on Ser338 and
103 to cycling cells and retained throughout the mitotic cell cycle ('Cell Cycle Common'), versus those t
104 d that KRP6 acts downstream of GA to inhibit mitotic cell cycle activation during germination.
105 arvation, Schizosaccharomyces pombe exit the mitotic cell cycle and become irreversibly committed to
106 testinal necroptosis was linked to increased mitotic cell cycle arrest via Per1/2-controlled Wee1, re
107 M inhibition caused catastrophic DNA damage, mitotic cell cycle arrest, and apoptosis specifically in
108 PC) activator best known for its role in the mitotic cell cycle at M-phase exit, in G1, and in mainta
109         This response is correlated with the mitotic cell cycle but is not coupled to nuclear osmolyt
110 ew and demonstrate that mouse embryos in the mitotic cell cycle can also directly reprogram sperm for
111 rk, no such comprehensive model of the human mitotic cell cycle existed.
112  a subset of human transcripts, enriched for mitotic cell cycle factors, leading to mitotic arrest.
113 lopment of Xenopus laevis embryos, the first mitotic cell cycle is long ( approximately 85 min) and t
114 lled by layers of regulation imposed on core mitotic cell cycle machinery components by the program o
115 ion of DNA content and quantification of the mitotic cell cycle phases by applying supervised machine
116  of GWAS data was significantly enriched for mitotic cell cycle processes (P = 0.001), the immune res
117                                          The mitotic cell cycle program can be activated by simultane
118                                              Mitotic cell cycle progression occurs rapidly, continuou
119                       In addition to driving mitotic cell cycle progression, CYE-1 and CDK-2 also pla
120  protein type ubiquitin E3 ligase, regulates mitotic cell cycle progression.
121 -10 null allele reveals that METT-10 enables mitotic cell cycle progression.
122          The endocycle represents a modified mitotic cell cycle that in plants is often coupled to ce
123 daughter cells switch synchronously from the mitotic cell cycle to endoreduplication.
124 njury, quiescent hepatocytes can reenter the mitotic cell cycle to restore tissue homeostasis.
125 evealed that MeJA delays the switch from the mitotic cell cycle to the endoreduplication cycle, which
126 , multiple genes involved in maintaining the mitotic cell cycle were rapidly down-regulated and senes
127 ed with centromeres during all stages of the mitotic cell cycle, except from metaphase to mid-anaphas
128                                   During the mitotic cell cycle, Geminin can act both as a promoter a
129  kleisin, recombination 8 (Rec8), during the mitotic cell cycle, instead of its paralog, Scc1.
130 veloped a novel computational model of human mitotic cell cycle, integrating diverse cellular mechani
131 B(S) classifier, including those involved in mitotic cell cycle, microtubule organization, and chromo
132 cohesin dissociation from DNA throughout the mitotic cell cycle, modulating sister chromatid cohesion
133  cells progressing synchronously through the mitotic cell cycle, while preserving the coupling of cel
134 ulation of cytokinesis," "G1/S transition of mitotic cell cycle," "DNA recombination," and "telomere
135 clin with the CDK protein Cdc2 can drive the mitotic cell cycle.
136 r this particular KRP as an activator of the mitotic cell cycle.
137 eiosis and suggest a similar function in the mitotic cell cycle.
138 quence of a block in the G(2)/M stage of the mitotic cell cycle.
139 cells in early, mid, and late S phase of the mitotic cell cycle.
140  TTP/HuR mRNA ratios and was involved in the mitotic cell cycle.
141                        Thus, while the major mitotic cell-cycle activity is blocked after DNA damage,
142                      Moreover, TTP augmented mitotic cell-cycle arrest as demonstrated by flow cytome
143                                     Although mitotic cell cycles can take place in the absence of cen
144 of which p57 is essential for switching from mitotic cell cycles to endocycles.
145 ut not p27, the CDK inhibitor that regulates mitotic cell cycles.
146 depletion resulted in a dramatic increase in mitotic cell death upon challenge with spindle poisons.
147   Furthermore, delayed mitosis and increased mitotic cell death was observed following TH588 treatmen
148 on prolonged mitotic progression and induced mitotic cell death, both of which are indicative of mito
149 amics, prometaphase arrest, tetraploidy, and mitotic cell death.
150 ily member, Noxa, is a critical initiator of mitotic cell death.
151 ubule dynamics and mitotic abnormalities and mitotic cell death.
152 ation-induced centrosome overduplication and mitotic cell death.
153 d cells are a specialized population of post-mitotic cells decorated with dozens of motile cilia that
154 e demonstrate that CME can be 'restarted' in mitotic cells despite high membrane tension, by allowing
155            Yet, how tissue tension elongates mitotic cells despite those cells undergoing mitotic rou
156                                     However, mitotic cells display no detectable recruitment of the E
157 ces neurogenesis and increases the number of mitotic cells dividing away from the ventricular surface
158 matogonial stem cells into spermatocytes via mitotic cell division and the production of haploid sper
159 tion is correlated with the decision to exit mitotic cell division and to enter cell expansion, which
160 ividual chromosome segregation errors during mitotic cell division are sufficient to drive extensive
161 helming down-regulation of genes involved in mitotic cell division but an up-regulation of genes invo
162                                              Mitotic cell division is controlled by cyclin-dependent
163                           How BRCA2 controls mitotic cell division is debated.
164                      Finally, we report that mitotic cell division is not required for genomic reprog
165 te SMC2 transcription as a key player in the mitotic cell division machinery.
166 ynchronous mitotic domains leads to aberrant mitotic cell division orientations.
167 requires a tightly controlled orientation of mitotic cell division relative to the apical polarity ax
168                      Successful execution of mitotic cell division requires the tight synchronisation
169           We find that convergent-extension, mitotic cell division, and daughter cell rearrangement d
170  arise from defects in DNA recombination and mitotic cell division, respectively.
171  of an event on the concerted process of the mitotic cell division.
172 dle assembly and microtubule dynamics during mitotic cell division.
173 tages of female meiotic cell development and mitotic cell division.
174 ng female mouse meiotic cell development and mitotic cell division.
175 scriptional repression is propagated through mitotic cell divisions remains a key unresolved question
176 n chromosome organization during meiotic and mitotic cell divisions.
177 between lipogenesis and protein synthesis in mitotic cell divisions.
178 ution of genetic material during meiotic and mitotic cell divisions.
179                                           In mitotic cells, DNA damage induces temporary G2 arrest vi
180                                           In mitotic cells, double HJs are primarily dissolved by the
181  Sugt1 both disrupts kinetochore assembly in mitotic cells due to the mislocalization of two componen
182 n 2 (MLC2) in the contractile ring region of mitotic cells during cytokinesis.
183 ctivation only ensuing when a DSB-containing mitotic cell enters G1.
184         Indeed, Rad51 foci do not persist in mitotic cells even after G2 checkpoint suppression, sugg
185 in the transition from cell division to post-mitotic cell expansion and concomitant petal maturation.
186 egulation of cell-cycle progression and post-mitotic cell expansion that together sculpt organ form.
187                                   While most mitotic cells express two AURK isoforms (AURKA and AURKB
188                                              Mitotic cells facilitate this process by generating intr
189                                          How mitotic cell fate is regulated in the developing mammali
190 , the functional importance of the spherical mitotic cell for the success of cell division has been t
191 n caused by depletion of endogenous Rad21 in mitotic cells, further indicating the physiological sign
192    Here, we show that in maize (Zea mays L.) mitotic cells, H3T3ph is concentrated at pericentromeric
193 protein (APC) and its binding partner EB1 in mitotic cells has come from siRNA studies.
194                                              Mitotic cells have a distinctive intranuclear heterochro
195 hanical properties of symmetrically dividing mitotic cells have been well characterized, whereas the
196             Using different methods to limit mitotic cell height, we show that a failure to round up
197          O. tauri cultures were enriched for mitotic cells, high-pressure frozen, and then imaged in
198 nd transactivating capacity of HSF1, leaving mitotic cells highly susceptible to proteotoxicity.
199 sient inactivation of ATM and DNA-PK renders mitotic cells hypersensitive to DSB-inducing agents.
200  any effector in precise proportions of post-mitotic cells in Drosophila.
201 ble in mature postmitotic neurons as well as mitotic cells in mice brain by combining CRISPR-Cas9-med
202 omous effects on the differentiation of post-mitotic cells in the bristle lineage.
203  stem cells maintain a proliferative pool of mitotic cells in the Caenorhabditis elegans gonad.
204 increases the numbers of enteroendocrine and mitotic cells in the gut of uninfected larvae, and infec
205                              For labeling of mitotic cells in the hippocampus, bromodeoxyuridine was
206 oriented centrosomes in a rare population of mitotic cells in the mutant retinas.
207    Loss of eIF4A-1 reduces the proportion of mitotic cells in the root meristem and perturbs the rela
208 protocols, FACS separation of interphase and mitotic cells, including mitotic subphases, can be combi
209  and Spr28 colocalize with Cdc3 and Cdc10 in mitotic cells, indicating that incorporation requires a
210 s ability involves dedifferentiation of post-mitotic cells into progenitors that in turn form new str
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 o assess the impact of autonomous changes in mitotic cell mechanics within a stretched monolayer.
216                                           In mitotic cells, membrane tension is increased and this in
217                   EBP50 is not necessary for mitotic cell microvilli, and PKC activation causes a rea
218  the division site by localising Gef2 to the mitotic cell middle.
219                                           In mitotic cells, mitotic centromere associated kinesin (MC
220 rge-scale screening data sets on nuclear and mitotic cell morphologies demonstrates that CellCognitio
221                                              Mitotic cells must form a single nucleus during telophas
222                           As long-lived post-mitotic cells, neurons employ unique strategies to resis
223 a medium containing ON 01910.Na, accumulated mitotic cell number with a peak from 10 to 14 hours and
224 ions accumulate over the life course in post-mitotic cells of many species.
225 y mitophagy during degenerative loss of post-mitotic cells of ocular tissue.
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 al body patterning in land plants acting via mitotic cell plane positioning.
230  number, while simultaneously producing post-mitotic cells (PMCs).
231  a broadly distributed, abundant, and highly mitotic cell pool.
232  without sT, reveals an orthogonal pH3(S10+) mitotic cell population having higher inactive p4E-BP1(T
233  comprises different phases characterized by mitotic cell proliferation, endoreduplication, the accum
234 hanisms of DDR in great detail; however, how mitotic cells respond to DNA damage remains less defined
235 contrast, mucosal epithelial cells and other mitotic cells responded robustly to type I IFNs and did
236                                  Analysis of mitotic cells reveals that pRB depletion compromises cen
237 ia and mouse pro-B cell lymphoid cell lines, mitotic cells reversibly increase their volume by more t
238                    Little is known about how mitotic cells round against epithelial confinement.
239 hese proteins can contribute functionally to mitotic cell rounding and spindle centralization during
240  PSK1-alpha/beta or PSK2 expression inhibits mitotic cell rounding as well as spindle positioning and
241                              We propose that mitotic cell rounding in columnar epithelia allows cells
242  Rho kinase and Diaphanous, which facilitate mitotic cell rounding in confined cell conditions, are e
243                    Despite the importance of mitotic cell rounding in tissue development and cell pro
244                                              Mitotic cell rounding is accompanied by changes in the a
245 erm fluidization is temporally controlled by mitotic cell rounding-dependent cell-cell contact disass
246  between IKNM and the fundamental process of mitotic cell rounding.
247 ll as the potential consequences of abnormal mitotic cell shape and size on chromosome segregation, t
248 ta reveals mitotic FAs as a key link between mitotic cell shape and spindle orientation, and may have
249                       Finally, we found that mitotic cell shape is also abnormal in the mutant VZ.
250                         Thus, interphase and mitotic cells share similar mechanisms for creating larg
251 ts may be important for spindle integrity in mitotic cells so that tensile forces generated at kineto
252               We present a model in which KV mitotic cells strategically place their cytokinetic brid
253 nmitotic cells to apically constrict through mitotic cell stretching.
254 resently unclear how it is triggered in post-mitotic cells such as cardiac myocytes.
255 (mPT), which is especially important in post-mitotic cells such as cardiomyocytes and neurons.
256 sm may be relevant to other highly polarized mitotic cells, such as mammalian neural progenitors.
257                                           In mitotic cells, TACC3 knockdown substantially affected th
258 Moreover, RSK is likely to be more active in mitotic cells than in interphase cells, as evidenced by
259        Muscle fibres are multinucleated post-mitotic cells that can change dramatically in size durin
260                      We find that ES-derived mitotic cells that have been dorsalized by the sonic hed
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 r understanding of the mechanisms that allow mitotic cells to postpone DSB repair without accumulatin
268   Cellular senescence is a mechanism used by mitotic cells to prevent uncontrolled cell division.
269 e to produce strong pushing forces, allowing mitotic cells to round up; it might also, by lowering cy
270 approach to circumvent the inability of post-mitotic cells to support homologous recombination-based
271  relocalization from the nuclear interior in mitotic cells to the periphery at or proximal to telomer
272                                 Moreover, in mitotic cells, transcription termination of meiotic RNAs
273 matin compaction mediates progenitor to post-mitotic cell transitions and modulates gene expression p
274                           Here, we show that mitotic cells treated with DSB-inducing agents activate
275                  ChIP-seq of highly purified mitotic cells uncovered that key hematopoietic regulator
276 ion, spindle tension was markedly reduced in mitotic cells upon exposure to GF-15.
277 analyses of the microtubular cytoskeleton of mitotic cells using wild-type, mpk6-2 mutant and plants
278               Furthermore, EDD siRNA reduced mitotic cell viability and, in nocodazole-treated cells,
279 nnels to functionally cooperate and regulate mitotic cell volume and tumor progression.
280 , we found that the absence of a full DDR in mitotic cells was associated with the high cyclin-depend
281 nd the number of phospho-histone H3 staining mitotic cells was decreased, consistent with G2/M checkp
282                  The number of Ki67-positive mitotic cells was more than doubled, consistent with the
283                  By tracking oscillations in mitotic cells, we reveal that a robust cell-autonomous,
284                                           In mitotic cells, we show that the ER undergoes both spatia
285 n the vast majority of the previous studies, mitotic cells were chemically fixed at room temperature,
286 1 IRIF could be detected when the irradiated mitotic cells were treated with a CDK1 inhibitor.
287 e transcriptional response to stress also in mitotic cells where the chromatin is tightly compacted.
288 alizes to the cleavage furrow and midbody of mitotic cells, where it is required for the completion o
289 ade around DNA damage sites did not occur in mitotic cells, which explains, at least in part, why BRC
290 removal of Rad51 from undamaged chromatin in mitotic cells, which prevents formation of nonrecombinog
291 ed a distinct population of ITGA6(+)ITGB4(+) mitotic cells, whose offspring further segregated into a
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 y due to the imbalance between the number of mitotic cells with respect to the entire cell population
295 ation of endocytic proteins is maintained in mitotic cells with restored CME, indicating that direct
296 d that DNA-damage signaling is attenuated in mitotic cells, with full DDR activation only ensuing whe
297        Our results indicate that a subset of mitotic cells within a population can experience discret
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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