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1 es Dictyostelium amoebae to differentiate as prestalk cells.
2 ecule DIF-1 that causes differentiation into prestalk cells.
3 ) null slugs have twice the normal number of prestalk cells.
4 s in a significantly increased proportion of prestalk cells.
5 e greatly enriched in prespore compared with prestalk cells.
6 duce DIF-1 at more than 20 times the rate of prestalk cells.
7 t results from an inability to properly sort prestalk cells.
8 cting region that prevents expression in the prestalk cells.
9 produce the classic, apical pattern of ecmAO prestalk cells.
10 and the fbxA mRNA is highly enriched in the prestalk cells.
11 ent of myb+ cells, mybC is expressed only in prestalk cells.
12 o the prestalk zone or to differentiate into prestalk cells.
13 hat sporulate in the absence of signals from prestalk cells.
14 e cells, both are required for expression in prestalk cells.
15 s and appears to have a defect in sorting of prestalk cells.
16 bility to signal terminal differentiation in prestalk cells.
17 usively in prespore cells and is absent from prestalk cells.
18 results in an abnormally high percentage of prestalk cells.
19 gests that it is preferentially expressed in prestalk cells.
20 tern, with cAR2 being expressed on anterior, prestalk cells and cAR3 present in the rest of the organ
21 The ecmA gene is specifically expressed in prestalk cells and its transcription is induced by the c
22 indicates that prespore cells divide before prestalk cells and later encapsulate as G1-arrested spor
23 P receptor present on a restricted subset of prestalk cells and whose expression does not respond typ
24 r with wild-type cells still produced excess prestalk cells and wild-type cells carrying the ecmA::la
26 cell-cycle phase at the time of starvation: prestalk cells are derived from cells which, are the tim
28 egation and then appears to be restricted to prestalk cells as a consequence of rapid turnover in pre
42 n Dictyostelium, we observed that GFP-tagged prestalk cells (ecmAO-expressing cells) moved independen
43 During normal development, apically situated prestalk cells express the ecmB gene just as they commit
45 ially and temporally distinct cues may guide prestalk cells first to an initial cluster and then late
52 lls are undergoing terminal differentiation, prestalk cells in tipA mutants form very small clumps, m
53 when Dictyostelium cells are exposed to the prestalk cell inducer Differentiation inducing factor 1
57 ls have RhT activity, but during development prestalk cells lose RhT activity while prespore cells re
58 xpressed, there is increased expression of a prestalk cell marker at the slug posterior, a phenocopy
62 tagA(-) cells become overrepresented in the prestalk cell population, suggesting that this phenotype
63 eating in D. discoideum because defecting on prestalk cell production results in an even greater redu
66 P-dependent protein kinase (PKA) activity in prestalk cells reduced stalk gene induction by c-di-GMP,
67 P-expressing crlA(-) mutants in the anterior prestalk cell region of chimeric organisms supports a ce
69 tagA mutant aggregates elaborate multiple prestalk cell regions during development and produce spo
71 velopmental life cycle is a process by which prestalk cells sort to form the anterior region of the m
72 age were first expressed as the prespore and prestalk cells sorted out in aggregates, some were found
73 cluster in tip protrusion, we examined ecmAO prestalk-cell sorting in a myosin II regulatory light ch
75 relatively highly expressed in the subset of prestalk cells that coats the prestalk zone, but in slug
77 vely maintained within the sub-population of prestalk cells that form the tip, the organizing center
78 t is not detectably expressed in the band of prestalk cells that lies behind the tip (the pstO cells)
79 nto two specialized cell types, prespore and prestalk cells, that continue to signal each other in co
82 ntric wave territory containing prespore and prestalk cell types can undergo "dislocation": a wave fi
83 null strain revealed that differentiation of prestalk cell types was delayed and maintenance of prest
86 cmA::lacZ construct formed normal numbers of prestalk cells when developed together with an equal num
88 differentiation and precocious induction of prestalk cells, which were reminiscent of cells lacking
89 a direct activator of cudA transcription in prestalk cells, while a protein with a DNA binding speci
90 equires a number of specialized sub-types of prestalk cell whose nature and function are not well und
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