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1 sterior axis and 6 of these cells become the vulval precursor cells.
2 alize LET-23 to the basal membrane domain of vulval precursor cells.
3 activity, up-regulates lin-39 expression in vulval precursor cells.
4 ents activation of the cell-death program in vulval precursor cells.
5 as/MPK-1 MAP kinase signaling pathway in the vulval precursor cells.
6 diffusion of the inductive signal to distal vulval precursor cells.
7 Analysis of ERK activity over time in the vulval precursor cells, a well-characterized paradigm of
8 partly by promoting cell fusion between the vulval precursor cells and the hypodermal syncytium at a
11 uch as interspecific differences in isolated vulval precursor cell behavior and in spatial regulation
13 etic and molecular experiments show that the vulval precursor cells can integrate the input from the
14 nalysis, we show that let-23 activity in the vulval precursor cell closest to the anchor cell (P6.p)
15 e vulva develops from a subset of ectodermal vulval precursor cells distributed along the anteroposte
16 lin-36 functions in and is expressed in the vulval precursor cells, establishing that the lin-36 pat
17 ns, the epithelial Pn.p cells adopt either a vulval precursor cell fate or fuse with the surrounding
18 Two seemingly conflicting verbal models of vulval precursor cell fate specification have been propo
21 involved in providing a signal that inhibits vulval precursor cells from adopting vulval fates in Cae
22 the anchor cell (P6.p) prevents induction of vulval precursor cells further away from the anchor cell
23 ence of a cell-survival signal acting on the vulval precursor cells in two nematodes, Turbatrix aceti
24 This result suggests that LET-23 in proximal vulval precursor cells might bind and sequester the indu
27 . elegans by repressing transcription in the vulval precursor cells of genes required for the express
28 yonic cells (P3.p-P8.p) that normally become vulval precursor cells often fuse with the surrounding e
29 a let-7 family member, is largely absent in vulval precursor cell P6.p at the time that let-60/RAS s
31 tissue in multivulva animals is generated by vulval precursor cells that in the wild type do not gene
32 nent of the cell junctions of the epithelial vulval precursor cells that is required for signaling by
33 FP fusion gene is expressed in many neurons, vulval precursor cells, the distal tip cell (DTC), intes
35 [4] [5-7], ablation of the gonad causes all vulval precursor cells to adopt a default epidermal fate
38 the gonad in the L1 larval stage caused all vulval precursor cells to undergo programed cell death.
39 C. elegans, the descendants of the 1 degrees vulval precursor cell (VPC) establish a fixed spatial pa
44 The source of the FGF ligand is the primary vulval precursor cell (VPC) P6.p, which controls the ori
45 t-grandprogeny of the Caenorhabditis elegans vulval precursor cells (VPCs) adopt one of the final vul
46 cesses, including cell fate specification by vulval precursor cells (VPCs) and migration of the Q(L)
47 vating the EGF receptor signaling pathway in vulval precursor cells (VPCs) and thereby inducing and p
52 bditis elegans, the fates of the multipotent vulval precursor cells (VPCs) are specified by intercell
53 Activation of EGFR-Ras-MAPK signaling in vulval precursor cells (VPCs) by LIN-3/EGF from the gona
55 ulval induction, each of the six multipotent vulval precursor cells (VPCs) commits to one of three fa
56 by the opposite division orientation of the vulval precursor cells (VPCs) flanking the axis of symme
57 ays occurs during the patterning of a row of vulval precursor cells (VPCs) in Caenorhabditis elegans:
58 ans vulva develops from the progeny of three vulval precursor cells (VPCs) induced to divide and diff
60 accumulates in the perinuclear region of the vulval precursor cells (VPCs) of living hermaphrodites,
62 s also show an increase in the percentage of vulval precursor cells (VPCs) that adopt vulval cell fat
63 ling pathways specify Caenorhabditis elegans vulval precursor cells (VPCs) to adopt a spatial pattern
64 as and Notch signaling pathways causes three vulval precursor cells (VPCs) to adopt induced cell fate
65 lin-28 loss-of-function mutations cause the vulval precursor cells (VPCs) to enter S phase and to di
66 mining the ability of Caenorhabditis elegans vulval precursor cells (VPCs) to respond to the inductiv
67 stem, cells that give rise to the vulva, the vulval precursor cells (VPCs), remain quiescent for two
68 hat has similar developmental origins to the vulval precursor cells (VPCs), which generate the vulva
70 notype is generated by aberrant induction of vulval precursor cells (VPCs): in wild-type animals, thr
71 asolateral membrane domain of the epithelial vulval precursor cells, where it acts through a conserve
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