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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 ic removal of the five MMPs expressed during anchor cell (AC) invasion in C. elegans, we find that MM
15                           Using the model of anchor cell (AC) invasion in C. elegans, we have previou
16 genetically and visually accessible model of anchor cell (AC) invasion in C. elegans, we have recentl
17  through their juxtaposed BMs at the site of anchor cell (AC) invasion in C. elegans.
18       Using the ATP sensor PercevalHR during anchor cell (AC) invasion in Caenorhabditis elegans, we
19 sing an RNAi screen and live-cell imaging of anchor cell (AC) invasion in Caenorhabditis elegans, we
20 veloping live-cell imaging methods to follow anchor cell (AC) invasion in Caenorhabditis elegans, we
21                                   C. elegans anchor cell (AC) invasion is a genetically tractable in
22  as a precisely regulated requirement of the anchor cell (AC) invasion program.
23 -specific RNAi during Caenorhabditis elegans anchor cell (AC) invasion, we demonstrate that the lipog
24 eening for defects in Caenorhabditis elegans anchor cell (AC) invasion, we found that UNC-6(netrin)/U
25 stereotyped timing of Caenorhabditis elegans anchor cell (AC) invasion, we generated an AC transcript
26                          The presence of the anchor cell (AC) nucleus within the utse is necessary fo
27 in directing development and function of the anchor cell (AC) of the gonad, the critical organizer of
28 fusion of the Caenorhabditis elegans uterine anchor cell (AC) with the uterine-seam cell (utse) is an
29 ell in the Caenorhabditis elegans gonad, the anchor cell (AC), initiates uterine-vulval contact throu
30 ion, the daughters of the VPC closest to the anchor cell (AC), P6.p, are induced by the AC.
31 naling activity of a gonadal cell called the anchor cell (AC).
32 3 promote expression in vulval cells and the anchor cell (AC).
33                During the naturally variable anchor cell (AC)/ventral uterine precursor cell (VU) dec
34 al lineages and in the LIN-12/Notch-mediated anchor cell (AC)/ventral uterine precursor cell (VU) dec
35 egans hermaphrodite vulva, a signal from the anchor cell activates the LET-23 epidermal growth factor
36                           A single cell, the anchor cell, acts to induce and to organize specializati
37 in-1 (TAG-1), a glycosylphosphatidylinositol-anchored cell adhesion molecule.
38 TN3-6), a group of glycophosphatidylinositol-anchored cell adhesion molecules involved in the wiring
39              IgLONs are a family of four GPI-anchored cell adhesion molecules that regulate neurite o
40 ontaining glycosylphosphatidylinositol (GPI)-anchored cell adhesion molecules, as a candidate TSG in
41      Suppression of ZmHb2 induces PCD in the anchoring cells, allowing the embryos to develop further
42 s abnormal, the utse failed to fuse with the anchor cell and a functional uterine-vulval connection w
43                    fos-1 is expressed in the anchor cell and controls invasion cell autonomously.
44  around the same time by an induction by the anchor cell and lateral signaling between the vulva prec
45 ne lin-11 expression responds to the uterine anchor cell and the lin-12-encoded receptor.
46 t cell behaviors: the post-mitotic, invasive anchor cell and the neighboring proliferative, non-invas
47 t utse development: the uterine toroids, the anchor cell and the sex myoblasts.
48 fects in the generation of distal tip cells, anchor cells, and spermatheca; three of the five tissues
49 sequent induction of the pi cell fate by the anchor cell are mediated by the lin-12 gene.
50          Two types of mutants with defective anchor cell behavior reveal that anchor cell invasion of
51                     They not only physically anchor cells, but also critically integrate signaling be
52                        In cog-2 mutants, the anchor cell does not fuse to the uterine seam cell and,
53       Both the initial selection of a single anchor cell during the anchor cell vs. ventral uterine p
54                In fos-1 mutants, the gonadal anchor cell extends cellular processes normally toward v
55  ventral uterine pi-cell differentiation and anchor cell fusion.
56 h pre-exposed and non-exposed to agents; non-anchored cell-gels were then incubated with agents for v
57    In wild-type animals, the somatic gonadal anchor cell generates the LIN-3/EGF ligand to induce vul
58                                    After the anchor cell has induced specialized uterine intermediate
59                                    After the anchor cell has induced the vulva, it stretches toward t
60                        The cell fates of the anchor cell in hermaphrodites and the linker cells in th
61 rane cation-dependent heterodimers that both anchor cells in position and transduce signals into and
62 sup-17 activity causes the production of two anchor cells in the hermaphrodite gonad, instead of one-
63                      Expansion of purged GPI-anchor+ cells in the Mut lines and analyses using aeroly
64                   Adhesions are critical for anchoring cells in their environment, as signaling platf
65  Our work supports a model in which AdamTS-A anchors cells in place and preserves CNS architecture by
66 ditis elegans hermaphrodite development, the anchor cell induces the vulva and the uterine pi cells w
67                                          The anchor cell induces the vulva from ventral epithelial ce
68  imaging of the DCC orthologue UNC-40 during anchor cell invasion in Caenorhabditis elegans, we have
69 h defective anchor cell behavior reveal that anchor cell invasion of the vulva is important for formi
70 g an in vivo model of Caenorhabditis elegans anchor cell invasion, we characterize the gene regulator
71  multichannel time-lapse confocal imaging of anchor-cell invasion in live Caenorhabditis elegans.
72 , we genetically dissect this process during anchor-cell invasion into the vulval epithelium in C. el
73                                          The anchor cell is initially specified in a stochastic cell
74 ypeptide growth factor activation of MAPK in anchored cells is far more effective than in cells maint
75                                uPAR is a GPI-anchored cell membrane receptor that shows increased exp
76 or cell invasion, the Caenorhabditis elegans anchor cell migrates through basement membranes towards
77 nvade past basement membrane, the C. elegans anchor cell must cease dividing before differentiating a
78 ection between the vulva and the uterus, the anchor cell must fuse with the multinucleate uterine sea
79  to respond to the inductive signal from the anchor cell of the somatic gonad.
80                                              Anchored cells of the basal epidermis constantly undergo
81 signated positions and directly transfer the anchored cells onto various substrates.
82 vulval precursor cells further away from the anchor cell (P3.p, P4.p, and P8.p).
83  in the vulval precursor cell closest to the anchor cell (P6.p) prevents induction of vulval precurso
84                                          The anchor cell plays a central role in organizing the repro
85                 A new study reveals that the anchor cell polarity network can break symmetry and osci
86                           In C. elegans, the anchor cell signal induces Pn.p cells to form the vulva
87  that mpk-1 may transduce most or all of the anchor cell signal.
88     LIN-39 activity is also regulated by the anchor cell signal/let-23 receptor tyrosine kinase/let-6
89 (encodes an Ets transcription factor) in the anchor cell signaling pathway.
90 erless) and nhr-67 (NR2E1/TLX), that mediate anchor cell specification and/or invasive behavior.
91        In the different monodelphic species, anchor cell specification is biased, or fully fixed, to
92                                    Following anchor cell specification, egl-43, hlh-2 and nhr-67 func
93 ription factor interactions before and after anchor cell specification.
94 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens.
95 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens.
96 e and a glycosylphosphatidylinositol- (GPI-) anchored cell surface coreceptor, either GDNF family rec
97 pression of ART2.1, but not ART2.2, as a GPI-anchored cell surface ectoenzyme.
98 se (ADPRT) is a glycosylphosphatidylinositol-anchored cell surface enzyme on CTL.
99 eport that the glycosyl phosphatidylinositol-anchored cell surface glycoprotein T-cadherin (encoded b
100 are a family of glycosylphosphatidylinositol-anchored cell surface heparan sulfate proteoglycans impl
101 llular matrix ligand (laminin) or a membrane-anchored cell surface ligand (ADAM 2).
102 bsence of glycosylphosphatidylinositol (GPI)-anchored cell surface membrane proteins in affected hema
103 ow that the folate-receptor 1 (FolR1), a GPI-anchored cell surface molecule, specifically marks mesDA
104              The mechanism by which membrane-anchored cell surface proteases utilize these putative a
105 ndings are likely relevant to other membrane-anchored cell surface proteases.
106 s use the glycosylphosphatidylinositol (GPI)-anchored cell surface protein hyaluronidase 2 (Hyal2) as
107 gen (PSCA) is a glycosylphosphatidylinositol-anchored cell surface protein that is expressed in norma
108 While it is widely assumed that CSP is a GPI-anchored cell surface protein, compelling biochemical ev
109  displayed properties of a glycophospholipid-anchored cell surface protein.
110 encode putative glycosylphosphatidylinositol-anchored cell surface proteins of the opportunistic fung
111             Here we describe a family of GPI-anchored cell surface proteins that function as ligands
112 ily members are cysteine-rich, generally GPI-anchored cell surface proteins, which have definite or p
113 , glycosylphosphatidylinositol-anchored (GPI-anchored) cell surface glycoprotein.
114 hich is a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein and is required for insuli
115       PSCA is a glycosylphosphatidylinositol-anchored cell-surface protein belonging to the Ly-6/Thy-
116 YAL2) encodes a glycosylphosphatidylinositol-anchored cell-surface protein that serves as an entry re
117     Second, the glycosylphosphatidylinositol-anchored cell-surface protein Thy-1 significantly partit
118 ctually a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein.
119 emonstrate that glycosylphosphatidylinositol-anchored cell-surface receptors of the Nogo Receptor fam
120  is a family of glycosylphosphatidylinositol-anchored, cell-surface heparan sulfate proteoglycans.
121  to a family of glycosylphosphatidylinositol-anchored, cell-surface heparan sulfate proteoglycans.
122 w the DDR2-ECD, when expressed as a membrane-anchored, cell-surface protein, affects collagen fibrill
123 evelopment is initiated by a signal from the anchor cell that is transduced by a receptor tyrosine ki
124 sive migration of the Caenorhabditis elegans anchor cell through a basement membrane barrier during d
125 ly protein, is first produced by the gonadal anchor cell to induce vulval precursor cells to generate
126 ferentiation within a tissue by mechanically anchoring cells to their neighbors.
127 ley et al. (2019) reveal that the C. elegans anchor cell uses physical force to breach basement membr
128 ll differentiation that specifically affects anchor cell-uterine seam cell fusion.
129                                          The anchor cell/ventral uterine precursor cell (AC/VU) decis
130                                       In the anchor cell/ventral uterine precursor cell (AC/VU) fate
131 f sel-5 activity can suppress defects in the anchor cell/ventral uterine precursor cell fate decision
132 selection of a single anchor cell during the anchor cell vs. ventral uterine precursor cell decision
133           Escherichia coli Spr is a membrane-anchored cell wall hydrolase.
134 ration in bacteria can be driven by membrane-anchored cell wall hydrolases.
135  to adhere to host tissue is mediated by GPI-anchored cell wall proteins (GPI-CWPs); the correspondin
136           Glycosylphosphatidylinositol (GPI)-anchored cell wall proteins play an important role in th
137 the class of yeast serine/threonine-rich GPI-anchored cell wall proteins.
138 the class of yeast serine/threonine-rich GPI-anchored cell wall proteins.
139  and release of glycosylphosphatidylinositol-anchored cell wall proteins.
140 (FMGX) inhibits glycosylphosphatidylinositol anchored cell wall transfer protein 1, essential for anc
141         This study demonstrates that sortase-anchored cell wall-associated proteins are responsible f
142  molecules, glycerophosphoinositide membrane anchors, cell wall pectic noncellulosic polysaccharides,
143 aa renders them equally likely to become the anchor cell, which links the uterus to the vulva.

 
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