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1 tes in a pattern centered around the gonadal anchor cell.
2 the uterine-vulval interface, fuses with the anchor cell.
3 ription of lin-3 in the vulva but not in the anchor cell.
4 un kinase (JNK) was also much more robust in anchored cells.
5 tides were required for maximal apoptosis of anchored cells.
6                                     Data for anchor cell ablation fix the parameters needed to define
7                  Replacement regulation upon anchor cell ablation is conserved in some species, but l
8 gh coordinated signaling between the uterine anchor cell (AC) and a ventral uterine (VU) cell.
9 granddaughters attach to the somatic gonadal anchor cell (AC) and generate four vulF cells, while the
10 ment, LIN-12 (Notch) signaling specifies the anchor cell (AC) and ventral uterine precursor cell (VU)
11    During C. elegans vulval development, the anchor cell (AC) in the somatic gonad expresses lin-3, a
12            A cell fate decision in which the anchor cell (AC) induces adjacent ventral uterine interm
13                                  The uterine anchor cell (AC) induces the vulva through LIN-3/epiderm
14                           Using the model of anchor cell (AC) invasion in C. elegans, we have previou
15 genetically and visually accessible model of anchor cell (AC) invasion in C. elegans, we have recentl
16  through their juxtaposed BMs at the site of anchor cell (AC) invasion in C. elegans.
17 sing an RNAi screen and live-cell imaging of anchor cell (AC) invasion in Caenorhabditis elegans, we
18 veloping live-cell imaging methods to follow anchor cell (AC) invasion in Caenorhabditis elegans, we
19                                   C. elegans anchor cell (AC) invasion is a genetically tractable in
20  as a precisely regulated requirement of the anchor cell (AC) invasion program.
21 eening for defects in Caenorhabditis elegans anchor cell (AC) invasion, we found that UNC-6(netrin)/U
22                          The presence of the anchor cell (AC) nucleus within the utse is necessary fo
23 in directing development and function of the anchor cell (AC) of the gonad, the critical organizer of
24 fusion of the Caenorhabditis elegans uterine anchor cell (AC) with the uterine-seam cell (utse) is an
25 ell in the Caenorhabditis elegans gonad, the anchor cell (AC), initiates uterine-vulval contact throu
26 ion, the daughters of the VPC closest to the anchor cell (AC), P6.p, are induced by the AC.
27 naling activity of a gonadal cell called the anchor cell (AC).
28 3 promote expression in vulval cells and the anchor cell (AC).
29 al lineages and in the LIN-12/Notch-mediated anchor cell (AC)/ventral uterine precursor cell (VU) dec
30                During the naturally variable anchor cell (AC)/ventral uterine precursor cell (VU) dec
31 egans hermaphrodite vulva, a signal from the anchor cell activates the LET-23 epidermal growth factor
32                           A single cell, the anchor cell, acts to induce and to organize specializati
33 in-1 (TAG-1), a glycosylphosphatidylinositol-anchored cell adhesion molecule.
34 TN3-6), a group of glycophosphatidylinositol-anchored cell adhesion molecules involved in the wiring
35              IgLONs are a family of four GPI-anchored cell adhesion molecules that regulate neurite o
36 ontaining glycosylphosphatidylinositol (GPI)-anchored cell adhesion molecules, as a candidate TSG in
37      Suppression of ZmHb2 induces PCD in the anchoring cells, allowing the embryos to develop further
38 s abnormal, the utse failed to fuse with the anchor cell and a functional uterine-vulval connection w
39                    fos-1 is expressed in the anchor cell and controls invasion cell autonomously.
40  around the same time by an induction by the anchor cell and lateral signaling between the vulva prec
41 ne lin-11 expression responds to the uterine anchor cell and the lin-12-encoded receptor.
42 t utse development: the uterine toroids, the anchor cell and the sex myoblasts.
43 fects in the generation of distal tip cells, anchor cells, and spermatheca; three of the five tissues
44 sequent induction of the pi cell fate by the anchor cell are mediated by the lin-12 gene.
45          Two types of mutants with defective anchor cell behavior reveal that anchor cell invasion of
46                        In cog-2 mutants, the anchor cell does not fuse to the uterine seam cell and,
47       Both the initial selection of a single anchor cell during the anchor cell vs. ventral uterine p
48                In fos-1 mutants, the gonadal anchor cell extends cellular processes normally toward v
49  ventral uterine pi-cell differentiation and anchor cell fusion.
50 h pre-exposed and non-exposed to agents; non-anchored cell-gels were then incubated with agents for v
51    In wild-type animals, the somatic gonadal anchor cell generates the LIN-3/EGF ligand to induce vul
52                                    After the anchor cell has induced specialized uterine intermediate
53                                    After the anchor cell has induced the vulva, it stretches toward t
54                        The cell fates of the anchor cell in hermaphrodites and the linker cells in th
55 rane cation-dependent heterodimers that both anchor cells in position and transduce signals into and
56 sup-17 activity causes the production of two anchor cells in the hermaphrodite gonad, instead of one-
57                      Expansion of purged GPI-anchor+ cells in the Mut lines and analyses using aeroly
58  Our work supports a model in which AdamTS-A anchors cells in place and preserves CNS architecture by
59 ditis elegans hermaphrodite development, the anchor cell induces the vulva and the uterine pi cells w
60                                          The anchor cell induces the vulva from ventral epithelial ce
61  imaging of the DCC orthologue UNC-40 during anchor cell invasion in Caenorhabditis elegans, we have
62 h defective anchor cell behavior reveal that anchor cell invasion of the vulva is important for formi
63  multichannel time-lapse confocal imaging of anchor-cell invasion in live Caenorhabditis elegans.
64 , we genetically dissect this process during anchor-cell invasion into the vulval epithelium in C. el
65 ypeptide growth factor activation of MAPK in anchored cells is far more effective than in cells maint
66 or cell invasion, the Caenorhabditis elegans anchor cell migrates through basement membranes towards
67 nvade past basement membrane, the C. elegans anchor cell must cease dividing before differentiating a
68 ection between the vulva and the uterus, the anchor cell must fuse with the multinucleate uterine sea
69  to respond to the inductive signal from the anchor cell of the somatic gonad.
70 signated positions and directly transfer the anchored cells onto various substrates.
71 vulval precursor cells further away from the anchor cell (P3.p, P4.p, and P8.p).
72  in the vulval precursor cell closest to the anchor cell (P6.p) prevents induction of vulval precurso
73                                          The anchor cell plays a central role in organizing the repro
74                 A new study reveals that the anchor cell polarity network can break symmetry and osci
75                           In C. elegans, the anchor cell signal induces Pn.p cells to form the vulva
76  that mpk-1 may transduce most or all of the anchor cell signal.
77     LIN-39 activity is also regulated by the anchor cell signal/let-23 receptor tyrosine kinase/let-6
78 (encodes an Ets transcription factor) in the anchor cell signaling pathway.
79        In the different monodelphic species, anchor cell specification is biased, or fully fixed, to
80 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens.
81 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens.
82 e and a glycosylphosphatidylinositol- (GPI-) anchored cell surface coreceptor, either GDNF family rec
83 pression of ART2.1, but not ART2.2, as a GPI-anchored cell surface ectoenzyme.
84 se (ADPRT) is a glycosylphosphatidylinositol-anchored cell surface enzyme on CTL.
85 eport that the glycosyl phosphatidylinositol-anchored cell surface glycoprotein T-cadherin (encoded b
86 are a family of glycosylphosphatidylinositol-anchored cell surface heparan sulfate proteoglycans impl
87 llular matrix ligand (laminin) or a membrane-anchored cell surface ligand (ADAM 2).
88 bsence of glycosylphosphatidylinositol (GPI)-anchored cell surface membrane proteins in affected hema
89 ow that the folate-receptor 1 (FolR1), a GPI-anchored cell surface molecule, specifically marks mesDA
90              The mechanism by which membrane-anchored cell surface proteases utilize these putative a
91 ndings are likely relevant to other membrane-anchored cell surface proteases.
92 s use the glycosylphosphatidylinositol (GPI)-anchored cell surface protein hyaluronidase 2 (Hyal2) as
93 gen (PSCA) is a glycosylphosphatidylinositol-anchored cell surface protein that is expressed in norma
94  displayed properties of a glycophospholipid-anchored cell surface protein.
95 encode putative glycosylphosphatidylinositol-anchored cell surface proteins of the opportunistic fung
96             Here we describe a family of GPI-anchored cell surface proteins that function as ligands
97 ily members are cysteine-rich, generally GPI-anchored cell surface proteins, which have definite or p
98 , glycosylphosphatidylinositol-anchored (GPI-anchored) cell surface glycoprotein.
99       PSCA is a glycosylphosphatidylinositol-anchored cell-surface protein belonging to the Ly-6/Thy-
100 YAL2) encodes a glycosylphosphatidylinositol-anchored cell-surface protein that serves as an entry re
101     Second, the glycosylphosphatidylinositol-anchored cell-surface protein Thy-1 significantly partit
102 ctually a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein.
103 emonstrate that glycosylphosphatidylinositol-anchored cell-surface receptors of the Nogo Receptor fam
104  is a family of glycosylphosphatidylinositol-anchored, cell-surface heparan sulfate proteoglycans.
105  to a family of glycosylphosphatidylinositol-anchored, cell-surface heparan sulfate proteoglycans.
106 w the DDR2-ECD, when expressed as a membrane-anchored, cell-surface protein, affects collagen fibrill
107 evelopment is initiated by a signal from the anchor cell that is transduced by a receptor tyrosine ki
108 ly protein, is first produced by the gonadal anchor cell to induce vulval precursor cells to generate
109 ferentiation within a tissue by mechanically anchoring cells to their neighbors.
110 ll differentiation that specifically affects anchor cell-uterine seam cell fusion.
111                                          The anchor cell/ventral uterine precursor cell (AC/VU) decis
112 f sel-5 activity can suppress defects in the anchor cell/ventral uterine precursor cell fate decision
113 selection of a single anchor cell during the anchor cell vs. ventral uterine precursor cell decision
114           Escherichia coli Spr is a membrane-anchored cell wall hydrolase.
115 ration in bacteria can be driven by membrane-anchored cell wall hydrolases.
116           Glycosylphosphatidylinositol (GPI)-anchored cell wall proteins play an important role in th
117 the class of yeast serine/threonine-rich GPI-anchored cell wall proteins.
118  and release of glycosylphosphatidylinositol-anchored cell wall proteins.
119 the class of yeast serine/threonine-rich GPI-anchored cell wall proteins.
120         This study demonstrates that sortase-anchored cell wall-associated proteins are responsible f
121  molecules, glycerophosphoinositide membrane anchors, cell wall pectic noncellulosic polysaccharides,
122 aa renders them equally likely to become the anchor cell, which links the uterus to the vulva.

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