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1 ufficient to redirect the PVD dendrites onto seam cells.
2 d elt-6 as Wnt pathway targets in the larval seam cells.
3 as it is virtually undetectable in nonfusing seam cells.
4 uences necessary for expression in vulval or seam cells.
5 expression in the developing vulva and adult seam cells.
6 elopment of the lateral epidermal cells, the seam cells.
7 and -6 repress elt-3 expression in wild-type seam cells.
8 ts attachment to the vulva and the epidermal seam cells.
9 or the terminal differentiation of epidermal seam cells.
10     Two deficiencies result in multinucleate seam cells.
11 of the three major epidermal cell types, the seam cells.
12 on of the stem cell-like lateral hypodermal (seam) cells.
13 essed exclusively in the lateral hypodermal (seam) cells.
14                              We use here the seam cells, a population of epidermal stem cells in Caen
15 inactivate the LIN-28 pluripotency factor in seam cells, a stem-like cell type in Caenorhabditis eleg
16 ind that during differentiation of stem-like seam cells, a typical UPR target, the Caenorhabditis ele
17 ired in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva f
18 lization and severe disorganization over the seam cells after NHR-23 depletion, while the expression
19 the anchor cell does not fuse to the uterine seam cell and, instead, remains at the apex of the vulva
20 ectopic Ptbx-2::gfp expression in hypodermal seam cells and gut.
21           elt-5 and -6 are both expressed in seam cells and many other cells, and are apparently func
22 e differences in gene expression between the seam cells and the hypodermis.
23 he major hypodermal cells except the lateral seam cells, and expression is initiated immediately afte
24 2 is expressed in the posterior gut, cuticle seam cells, and spermatheca, the first two of which are
25                               The C. elegans seam cells are lateral epithelial cells arrayed in a sin
26                         Furthermore, because seam cells as well as pharyngeal cells secrete their gly
27 ditis elegans epidermal stem cells, known as seam cells, as a readout.
28 teins are expressed in neurons and epidermal seam cells, as well as in other cells.
29                       We show that in larval seam cell asymmetric divisions, EGL-18 is expressed stro
30  Wnt asymmetry pathway already exist between seam cells at 20 degrees and this may sensitize cells to
31 r level of let-7 gfp transgene expression in seam cells at L3 stage.
32 LINK) between the uterine utse and epidermal seam cell BMs in Caenorhabditis elegans that supports th
33 (DTC), intestine, and the lateral hypodermal seam cells but not in the main body hypodermal syncytium
34 nic mutations that enhance LIT-1 activity in seam cells can simultaneously also enhance the opposing,
35 coordinate development of the vulval-uterine-seam cell connection.
36 ell must fuse with the multinucleate uterine seam cell, derived from uterine cells that adopt a (pi)
37                                              Seam cell development has mostly been studied so far in
38  protein that is required for proper uterine seam cell development in Caenorhabditis elegans.
39 coding GATA factors essential for viability, seam cell development, and vulval development in Caenorh
40 6 is sufficient to modify Wnt signalling and seam cell development, highlighting that natural variati
41 ranscription and chromatin factors acting in seam cell development.
42 hroughout C. elegans development to regulate seam cell differentiation and cell fusion.
43  that puf-9 and let-7 may mediate hypodermal seam cell differentiation by regulating common targets.
44 hat regulates a late-stage aspect of uterine seam cell differentiation that specifically affects anch
45  described herein cause delays in vulval and seam cell differentiation, indicating a role for lin-66
46 ule fluorescence hybridisation, we find that seam cell division and differentiation patterns are most
47  last larval stage (L4), following the final seam cell division, which occurs during the L3-to-L4 mol
48 n-23 mutants the phenotypes of supernumerary seam cell divisions, defective alae formation, and the a
49 l growth, molting, and the proper pattern of seam-cell divisions.
50 al differentiation of the lateral hypodermal seam cells during the larval-to-adult molt.
51 vitro, and this site is necessary for robust seam cell expression in vivo.
52 th larval stage, leading to the retention of seam cell fate in both daughter cells.
53 cription factor egl-18, which is involved in seam cell fate maintenance, is more tolerated in the CB4
54 al cryptic genetic variation that reinforces seam cell fate through potentiating Wnt signalling.
55 am cell specification, and for hypodermal to seam cell fate transformations induced by ectopic Wnt pa
56 ains through symmetric divisions towards the seam cell fate were observed at low frequency.
57 on causes the precocious expression of adult seam cell fates.
58  abnormalities in vulval lineage and uterine seam-cell formation.
59 hat specifically affects anchor cell-uterine seam cell fusion.
60 aughter cells following division, as well as seam cell gains through symmetric divisions towards the
61 s, a row of epidermal precursor cells called seam cells generates a pattern of cuticular alae in ante
62                                              Seam cells go through a reproducible pattern of asymmetr
63  of driving extra cell divisions, leading to seam cell hyperplasia.
64 were expressed exclusively in the intestine, seam cells, hypodermal cells of the main body syncytium,
65                                              Seam cells in affected animals do not differentiate prop
66                                              Seam cells in affected animals often undergo inappropria
67 isms involved, we studied the stem cell-like seam cells in the Caenorhabditis elegans epidermis.
68 nts, all epidermal cells, except the lateral seam cells, inappropriately fuse into a single large syn
69 find that OSM-11 is secreted from hypodermal seam cells into the pseudocoelomic body cavity and acts
70            Ectopic expression of LECT-2 from seam cells is sufficient to redirect the PVD dendrites o
71 rees introduces variability in the wild-type seam cell lineage, with a proportion of animals showing
72  specificity of cell fates in the hypodermal seam cell lineages.
73 f-renewing and proliferative behavior in the seam cell lineages.
74 , we used the postembryonic epithelial stem (seam) cell lineages of Caenorhabditis elegans.
75 remains unchanged when nmy-2 is inactivated, seam cell loss occurs through inappropriate terminal dif
76                                Nevertheless, seam cell losses due to the inappropriate differentiatio
77 al 23 deficiencies blocked expression of the seam cell marker, in some cases without preventing cell
78     Here, we report that a gene required for seam cell maturation is also required for specification
79 ng polarised growth of vulval precursors and seam cells, migrations of neuroblasts and axons, and the
80 e earliest detectable LIN-29 accumulation in seam cell nuclei is during the last larval stage (L4), f
81 uring development, which affect the terminal seam cell number in opposing directions.
82  culture temperature, although their average seam cell number is comparable at 20 degrees .
83 null mutation in the fusogen eff-1 increases seam cell number variability.
84 -helix (bHLH) transcription factor, increase seam cell number variability.
85 proportion of animals showing an increase in seam cell number.
86 g, and symmetric divisions that increase the seam cell number.
87 ermis, is often ectopically expressed in the seam cells of affected animals, demonstrating that ELT-5
88 pparatus occurring exclusively in hypodermal seam cells, pharyngeal cells, and spermatheca.
89 e main hypodermal syncytium, indicating that seam cells play the major role in secreting surface coat
90 otypic variability in the normally invariant seam cell population.
91 ress pal-1 and in the neighboring hypodermal seam cell precursors, which do not, as well as in poster
92 seven deficiencies had no apparent effect on seam cell production, 21 were found to result in subnorm
93                                          How seam cell progenitors differ transcriptionally from the
94 d that rnt-1 is a rate-limiting regulator of seam cell proliferation in C. elegans, as overexpression
95 e is that all are expressed most strongly in seam cells, rather than in the main hypodermal syncytium
96 ar level, whereas low nuclear POP-1 promotes seam cell self-renewal.
97  isolates of C. elegans display variation in seam cell sensitivity to increased culture temperature,
98 ting the continuity of the seam and changing seam cell shape, highlighting the role of tissue homeost
99  that two GATA factors that are required for seam cell specification in the embryo independently of W
100 iously been shown to be required for initial seam cell specification in the embryo.
101    egl-18 and elt-6 are necessary for larval seam cell specification, and for hypodermal to seam cell
102 lin-4, the lin-58 mutations cause precocious seam cell terminal differentiation and thus define a new
103                        The let-7 miRNA times seam cell terminal differentiation in C. elegans.
104 -29 specify the timing of lateral hypodermal seam cell terminal differentiation in Caenorhabditis ele
105  mutations also restore other aspects of the seam cell terminal differentiation program that are defe
106 because of mutation of lin-4, which prevents seam cell terminal differentiation.
107                NCX-9 functions in hypodermal seam cells that secrete the axon guidance cue UNC-129/BM
108 al development and upregulated in developing seam cells upon heat stress and during the stress-resist
109 ne controls gene expression in the epidermal seam cells, uterus and vulva, and may help to coordinate
110 ns uterine anchor cell (AC) with the uterine-seam cell (utse) is an excellent model system for studyi
111           The Caenorhabditis elegans uterine seam cell (utse) is an H-shaped syncytium that connects
112 egans, six lateral epidermal stem cells, the seam cells V1-V6, are located in a row along the anterio
113                                     Anterior seam cells (V1-V4) undergo a fairly simple sequence of s
114                                    Posterior seam cells (V5 and V6) undergo a more complicated sequen
115 Hox gene mab-5 is required for two posterior seam cells, V5 and V6, to generate rays.
116 d during the last larval stage in hypodermal seam cells which is transcriptionally regulated by hbl-1
117  We address this question by focusing on the seam cells, which display stem cell properties in the ep
118 nuclei of which are largely generated by the seam cells, which exhibit stem cell-like behaviour durin
119 here on a population of epidermal cells, the seam cells, which show stem cell-like behaviour and divi
120 hormone receptor daf-12 is a let-7 target in seam cells, while the forkhead transcription factor pha-
121 g larval development can cause fusion of all seam cells with the surrounding syncytia and pronounced
122 vestigate the translational potential of the SEAM, cells within it that resemble ocular-surface epith

 
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