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1 nt process, where it acts upstream of JNK in LE cells.
2 Dpp fails to be expressed in shark(1) mutant LE cells.
3 gnaling pathway leading to Dpp expression in LE cells.
4 f the siphon, which does not cause firing of LE cells.
5 tion assay for 10-day clonal growth of mouse LE cells.
6 cally and dynamically distinct from those of LE cells.
7 the regulation of integrin- and FAK-mediated LE cell adhesion during lens development.
8  for 5-bromo-2'-deoxyuridine (BrdU) in mouse LE cells after 2-week osmotic pump delivery of BrdU.
9 to be required for interactions both between LE cells and between LE and LF cells.
10 s of JNK-dependent expression of dpp mRNA in LE cells, and decreased epidermal F-actin staining and L
11                           To explore whether LE cells are specified in response to early dorsoventral
12                                          How LE cells are specified remains unclear.
13 ll-matrix junctions between lens epithelial (LE) cells, between lens fiber (LF) cells, and between th
14                     Through a bioinformatics-led cell biological screen, we have identified Orai1 as
15 ound of dpp expression is also restricted to LE cells but Dpp signaling specifies the repression of t
16                                Dpp and other LE cell-derived signaling molecules stimulate the bilate
17 nd defined glandular and luminal epithelium (LE) cell differentiation trajectories.
18                                  Because the LE cells display increasing discharge to increasing pres
19 and dorsal ectoderm genetically, and assayed LE cell fate.
20 feration capacity of murine lens epithelial (LE) cells in vitro and in vivo.
21         Instead, increased CDC25B expression led cells into senescence.
22 nificantly reduced proliferative capacity of LE cells is associated with increased age of mice and is
23                                          The LE cell line, HLE-B3, was sensitive to Fas-dependent apo
24 s were then targeted to the lox sites of the LES cell lines.
25                Our results indicate that the LE cells make a substantial contribution to the evoked r
26 her pinching or pinning the siphon decreases LE cell mechanosensory threshold and enhances soma excit
27                                              LE cells play a crucial role in the morphogenetic proces
28 Crim1 mouse mutants originate from defective LE cell polarity, proliferation and cell adhesion.
29 nsfection assays utilizing ovine endometrial LE cells, progesterone increased transcriptional activit
30  caloric restriction mediates its effects on LE cell proliferation remains to be investigated further
31                                              LE cell sensitization has effects, resembling hyperalges
32 ses have been made of the responses of these LE cells to mechanical stimulation of the tightly pinned
33 ng) and dorsal suturing of the leading edge (LE) cells to enclose the viscera.
34         Here we use Drosophila leading-edge (LE) cells to explore how Diaphanous (Dia)-related formin
35 ection with an HRG expression construct that led cells to acquire estrogen independence and metastasi
36         Paradoxically, this anabolic program led cells to apoptosis during chronic ER stress in a man
37 ls, began within seconds of NO exposure, and led cells to construct sGC heterodimers and thus increas
38                               Contraction of LES cells was reduced by the alpha beta gamma pseudosubs
39  siphon movements often fail to activate the LE cells when the siphon is unrestrained.
40                   We show that Crim1 acts in LE cells, where it colocalizes with and regulates the le