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1 cyte, we found that exopher removal requires hypodermal actin and Arp2/3, and the hypodermal plasma m
3 sisted for weeks after infection, regulating hypodermal adipocyte expansion and production of the adi
7 ion and quantification method for infectious hypodermal and hematopoietic necrosis virus (IHHNV), a s
9 berrant expression of SKN-1 causes a loss of hypodermal and neuronal tissue and an excess of pharynge
11 nt ages but generally had reduced dermal and hypodermal areas compared with age-matched controls.
12 osed skin histology revealed highly inflamed hypodermal areas with infiltrated immune cells at 6 and
14 duced in size by different proportions, with hypodermal blast cell size most closely proportional to
15 the inappropriate deaths of many of the Pn.p hypodermal blast cells and prevent the surviving Pn.p ce
16 patterns were observed, either intestinal or hypodermal, but no gross RNAi phenotypes were found poss
17 al ovule development in maize, only a single hypodermal cell develops into an archesporial cell and t
18 shown that ELT-3 is not essential for either hypodermal cell differentiation or the viability of the
21 ot suppress defects in two different ventral hypodermal cell fate decisions in hermaphrodites and mal
24 er transcription factor that is required for hypodermal cell terminal differentiation and proper vulv
25 he heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the fina
30 he mutants had abnormal-shaped epidermal and hypodermal cells and showed an unusual arrangement of sm
32 in transgene is expressed in lateral rows of hypodermal cells and these cells fail to properly change
33 in the adult stage with strong expression in hypodermal cells and weaker expression in gut cells.
34 nt bundles at the adherens junctions between hypodermal cells and, thereby, transmit the force of bun
36 endently of immediately adjacent neighboring hypodermal cells because dorsal intercalation is not blo
38 pecify and/or maintain the fates not only of hypodermal cells but also of all other non-neuronal ecto
44 plays an important role in the switch of the hypodermal cells from the vegetative pathway to the meio
45 plays an important role in the switch of the hypodermal cells from the vegetative to the meiotic (spo
46 les, LECT-2 decorates neuronal processes and hypodermal cells in a pattern similar to the cell adhesi
48 eir direction of migration; posterior dorsal hypodermal cells in die-1(w34) mutants appear to extend
50 aphrodites at the L2 stage there are 11 Pn.p hypodermal cells in the ventral midline arrayed along th
51 o drive expression of a seam marker in other hypodermal cells in wild-type animals, and in anterior h
52 est a model in which postembryonic growth of hypodermal cells is regulated by TGFbeta-related signali
55 ed exclusively in the intestine, seam cells, hypodermal cells of the main body syncytium, and the exc
57 cZ) is widely expressed in the intestine and hypodermal cells of transgenic worms, while the fusion p
58 e progenitors for either half of the lateral hypodermal cells or the posterior half of the dorsal hyp
61 insight into how NHR-23 acts in the seam and hypodermal cells to coordinate aECM regeneration during
62 ositional cues from muscle are transduced to hypodermal cells to direct sensory dendrite outgrowth.
67 ls (including various muscle, intestinal and hypodermal cells) in high-resolution images of adult C.e
68 elongate properly, abnormal contacts between hypodermal cells, and failure of the pharynx to attach t
69 EGL-15 indicate that EGL-15 is expressed in hypodermal cells, and hypodermal promoters can drive ful
71 les in the intercalation of posterior dorsal hypodermal cells, in muscle cell positioning and in inte
72 eporter, which is localized to boundaries of hypodermal cells, shows that hypodermis is disorganized
73 neurons, the posterior intestine cells, tail hypodermal cells, the T cells and specific T-cell descen
74 d the dense body to the hemidesmosome on the hypodermal cells, which in turn instructed the SAX-7 str
93 nesis associated with increased fibulin-2 in hypodermal connective tissues and decreased fibulin-5 at
95 esting this gene is required for maintaining hypodermal-cuticle attachment as the animal grows in siz
96 the head cells and spermatheca is constant, hypodermal daf-9::GFP expression is modulated by multipl
98 oral discoordination between the accelerated hypodermal development and normally timed somatic gonada
99 lin-28, a central heterochronic regulator of hypodermal development, causes reduced fertility associa
100 ression pattern suggests a role for ELT-3 in hypodermal development, no functional studies have yet b
101 ct downstream of lin-28 in the regulation of hypodermal developmental timing also act downstream of l
102 ryonic blastomeres, to activate a program of hypodermal differentiation even in blastomeres that are
106 ssue-specific promoter studies indicate that hypodermal expression of ptc-3 is required for normal de
107 ent protein gene (gfp) and demonstrated that hypodermal expression of the fusion gene is adult-specif
110 , a GATA transcription factor that specifies hypodermal fate in the embryo, as a regulator of sperm-s
112 pmental program, while its repression in the hypodermal-fated cells requires a transcriptional regula
113 cells in wild-type animals, and in anterior hypodermal-fated daughters in a Wnt pathway-sensitized b
114 -1 structure from mutant Tsk fibrillin cause hypodermal fibrosis and associated changes in dermal gen
116 t the conclusion that mup-4 is essential for hypodermal function and that this function is necessary
117 ealed a previously unknown role for mab-9 in hypodermal function and we suggest that MAB-9 is require
119 T-1 and that, conversely, ELT-1 can activate hypodermal gene expression in the absence of ELT-3.
120 ithin the mantle, instead of the specialised hypodermal glands in the second antennular segment as re
127 ctive tissues and decreased fibulin-5 at the hypodermal M-CT interface suggest that these proteins me
128 phages in tissue remodeling, we examined the hypodermal macrophages (HDMs) and their impact on host s
129 tion of hypodermal cells and expression of a hypodermal marker in hbl-1(RNAi) animals suggests that m
131 utants, cell migrations are defective during hypodermal morphogenesis, QL neuroblast migration, and t
132 mup-4 is essential in embryonic epithelial (hypodermal) morphogenesis and maintenance of muscle posi
133 ayer found normally at the interface between hypodermal muscle and connective tissue was absent from
139 ntrast and fluorescence imaging of embryonic hypodermal nuclear migration events were used to charact
141 enesis of the Caenorhabditis elegans embryo, hypodermal (or epidermal) cells migrate to enclose the e
145 In Caenorhabditis elegans larvae, failure of hypodermal P-cell nuclear migration results in uncoordin
146 form the hermaphrodite vulva, a specialized hypodermal passageway used for egg laying and sperm entr
147 into numerous smaller vesicles that acquire hypodermal phagosome maturation markers, with vesicular
148 equires hypodermal actin and Arp2/3, and the hypodermal plasma membrane adjacent to newly formed exop
149 , resulting in a deformed vulva, and the P12 hypodermal precursor often differentiates into a second
151 EGL-15 is expressed in hypodermal cells, and hypodermal promoters can drive full clr-1 and egl-15 res
153 suggesting that puf-9 and let-7 may mediate hypodermal seam cell differentiation by regulating commo
155 ls that express pal-1 and in the neighboring hypodermal seam cell precursors, which do not, as well a
156 28, and lin-29 specify the timing of lateral hypodermal seam cell terminal differentiation in Caenorh
158 l tip cell (DTC), intestine, and the lateral hypodermal seam cells but not in the main body hypoderma
159 the terminal differentiation of the lateral hypodermal seam cells during the larval-to-adult molt.
162 upregulated during the last larval stage in hypodermal seam cells which is transcriptionally regulat
163 lutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-t
164 the Golgi apparatus occurring exclusively in hypodermal seam cells, pharyngeal cells, and spermatheca
168 To investigate myotactin's role in muscle-hypodermal signaling, we characterized the myotactin loc
169 ns in C. elegans are engulfed by surrounding hypodermal skin cells and are then broken up into numero
170 lar signaling pathway in which intestinal or hypodermal SPHK-1 signals through the neuronal G protein
172 podermal seam cells but not in the main body hypodermal syncytium (hyp7) that underlies, synthesizes,
173 ective in the anchoring of nuclei within the hypodermal syncytium and in the migrations of the two di
174 hat lin-35 activity is required in the major hypodermal syncytium and not in the VPCs to inhibit vulv
178 ongly in seam cells, rather than in the main hypodermal syncytium, indicating that seam cells play th
179 Most of the epidermis consists of the hyp7 hypodermal syncytium, the nuclei of which are largely ge
181 tion of the heterochronic gene lin-42 causes hypodermal terminal differentiation to occur precociousl
183 that heme homeostasis in the extraintestinal hypodermal tissue was facilitated by the transmembrane p
184 ers showed that CeRh1 is mainly expressed in hypodermal tissue, although it is also in other cell typ
185 tion at defined locations in the surrounding hypodermal tissue, whereas DMA-1 acts as the cognate rec
188 pathway that communicates from intestinal or hypodermal tissues to neurons to promote aversive learni
190 for larval seam cell specification, and for hypodermal to seam cell fate transformations induced by