ライフサイエンスコーパス: vulva

1 e named these genes sqv-1 to sqv-8 (squashed vulva).

2 elvic malignancies (prostate, cervix, penis, vulva).

3 e specification in the posterior half of the vulva.

4 in inhibiting LIN-12/Notch signalling in the vulva.

5 of egl-18/elt-6 function specifically in the vulva.

6 ulate cell fate patterning in the C. elegans vulva.

7 the pharynx in the hypodermis, hindgut, and vulva.

8 es have feminized gonads and often develop a vulva.

9 neurons, body wall muscle, spermatheca, and vulva.

10 with abnormal somatic gonad, germ line, and vulva.

11 e tail before the spicule tips penetrate the vulva.

12 on if a previous thrust failed to breach the vulva.

13 ulval cells helps determine the shape of the vulva.

14 ulval primordium and are essential to form a vulva.

15 ns nervous system and also in the developing vulva.

16 mid-body region, leading to formation of the vulva.

17 rity protein PAR-1 in the development of the vulva.

18 y shown to promote formation of a functional vulva.

19 ining pA-D is required for expression in the vulva.

20 in the mechanisms that pattern the nematode vulva.

21 the anterior and the posterior sides of the vulva.

22 cells, which also connect the uterus to the vulva.

23 uv1 cells), which connect the uterus to the vulva.

24 es several tissues, including the uterus and vulva.

25 osterior structures are induced instead of a vulva.

26 s in the central body region to generate the vulva.

27 that mediates induction of the hermaphrodite vulva.

28 stead, a protrusion forms at the site of the vulva.

29 the induction of the Caenorhabditis elegans vulva.

30 e anchor cell, which links the uterus to the vulva.

31 ke the connection between the uterus and the vulva.

32 uterine cell fates, the AC also induces the vulva.

33 mal cells that are competent to generate the vulva.

34 eotyped series of cell divisions to form the vulva.

35 hen male reproductive structures contact the vulva.

36 ed women with squamous cell carcinoma of the vulva.

37 as of the cervix, ovary, uterus, vagina, and vulva.

38 search of the hermaphrodite surface for the vulva.

39 penis, prostate, rectum, testis, vagina, and vulva.

40 e contractions during attempts to breach the vulva.

41 mple taken from the lesion and contralateral vulva.

42 ent difficulty in locating the hermaphrodite vulva.

43 atory infiltrate was found in the cervix and vulva.

44 posite orientations in the two halves of the vulva.

45 tation displayed in the anterior half of the vulva.

46 cancers of the cervix (3.3%), vagina (8.3%), vulva (1.5%), and penis (8.3%).

47 As a model, we used the nematode vulva, a highly conserved, essential organ, the developm

48 ced RAS signalling and engendered protruding vulva, a phenotype previously linked to the RASopathy-ca

49 of the Caenorhabditis elegans hermaphrodite vulva, a signal from the anchor cell activates the LET-2

50 lyzing the cells that form the hermaphrodite vulva, a specialized hypodermal passageway used for egg

51 ck layer of vulval tissue at the apex of the vulva and a physical blockage of the exit to the vulva f

52 sufficient for expression in the developing vulva and adult seam cells.

53 re essential for the proper organogenesis of vulva and appear to be temporally regulated, the mechani

54 s of cell fates and fusion in the developing vulva and are apparent direct transcriptional targets of

55 of the heart, haemorrhages, prenatal death, vulva and clitoral defects and keratoconjunctivitis sicc

56 Because human SCCs of the vulva and head and neck exhibited hallmarks of B cell in

57 e expression by RNAi suppressed the aberrant vulva and hypodermis development phenotypes of let-7(n28

58 SQV-4 is expressed in the vulva and in oocytes, among many other cells, and SQV-4

59 SQV-1 and SQV-7 are both expressed in the vulva and in oocytes, where they likely act in vulval mo

60 ted with chief complaints of pruritis in the vulva and insomnia due to frequent urination during the

61 s hermaphrodites requires development of the vulva and its precise connection with the uterus.

62 germline proliferation, the formation of the vulva and male tail, and the metaphase to anaphase trans

63 rrest showed mutant phenotypes such as burst vulva and molting defects.

64 igration defects, the AC fails to invade the vulva and no lumen is formed in vulF.

65 men should have a thorough inspection of the vulva and perianal region, and women with abnormalities-

66 red with more radical surgical approaches in vulva and possibly vaginal melanomas.

67 chanically sense passage of eggs through the vulva and release tyramine to inhibit egg laying, in par

68 pmental arrest, morphological defects of the vulva and tail, and reduced fecundity.

69 The Caenorhabditis elegans vulva and the Drosophila eye are two classic paradigms f

70 l called the utse, and its attachment to the vulva and the epidermal seam cells.

71 ite development, the anchor cell induces the vulva and the uterine pi cells whose daughters connect t

72 lack of temporal synchronization between the vulva and the uterus is not due to precocious or acceler

73 To form a functional connection between the vulva and the uterus, the anchor cell must fuse with the

74 Development of the vulva and the ventral uterus is coordinated by the induc

75 velops with a temporal delay relative to the vulva and, thus, is not present when the connection norm

76 1 cervical carcinoma, 1 Bowen disease of the vulva, and 1 multiple Epstein-Barr virus(+) leiomyosarco

77 s, such as erosions on the lips, eye mucosa, vulva, and blisters on the trunk appeared, and SJS was t

78 basement membranes between the gonad and the vulva, and in mutants in unc-6 netrin or its receptor un

79 elatinous mass that covers the hermaphrodite vulva, and its deposition decreases the mating success o

80 pment of the excretory system, hermaphrodite vulva, and male spicules.

81 sion in the epidermal seam cells, uterus and vulva, and may help to coordinate the terminal developme

82 een in HPV-related precursors of the vagina, vulva, and penis further support the notion that junctio

83 dividual sites of the genital tract (cervix, vulva, and rectum) with that from one swab with secretio

84 y, timing developmental events in the gonad, vulva, and sex myoblasts, in addition to its well-establ

85 es vulval cell fate, resulting in a deformed vulva, and the P12 hypodermal precursor often differenti

86 those in cellular sampling of the cervix and vulva, and their correlation with rigorously confirmed c

87 The primary tumor was limited to the vulva, and there were no groin lymph nodes that were cli

88 sis and management of cancers of the cervix, vulva, and vagina are reviewed.

89 anules in oocytes, with the uterine wall and vulva, and with membrane systems in the spermathecal val

90 The cell lineages that form each half of the vulva are identical, except that they occur in opposite

91 Heritability estimates of VS traits, vulva area (VA), height (VH), and width (VW) measurement

92 The status of the vulva as an overachiever is in part due to its inherent

93 cation events in the epithelial cells of the vulva as well as the mesodermal cells in the uterus of t

94 pharynx in cells surrounding the rectum and vulva, as well as in the germ line.

95 they do not perform the subsequent steps of vulva attachment via spicule insertion and sperm transfe

96 ell and, instead, remains at the apex of the vulva, blocking the connection between the vulval and ut

97 necessary for transcription of lin-3 in the vulva but not in the anchor cell.

98 als, three VPCs are induced to form a single vulva, but, in fog; fbf mutants, four or five VPCs are t

99 r cell signal induces Pn.p cells to form the vulva by activating a conserved receptor tyrosine kinase

100 r displayed a long-term efficacy against the vulva carcinoma cell line A431, there was a notable in-e

101 ecordings of fluorescent keratin 13 in human vulva carcinoma-derived A431 cells.

102 tors assemble on the apical surfaces of each vulva cell type, with clear distinctions seen between Ra

103 e expressed differentially in the developing vulva cells, providing a potential readout for different

104 ale tail presses against the hermaphrodite's vulva, cholinergic and glutamatergic reciprocal innervat

105 imerization partner, RB-like, E2F, and multi-vulva class B (DREAM) transcriptional repressor complex,

106 The mature vulva comprises seven cell types (vulA, vulB1, vulB2, vu

107 estricts repetitive intromission attempts to vulva cues was unclear.

108 Ventral cord and vulva development are analyzed in a large sample of nema

109 Comparative studies of vulva development between Caenorhabditis elegans and oth

110 number and directionality of changes in the vulva development characters.

111 s, vulva development is similar to wild-type vulva development except that it occurs precociously, in

112 ctivated protein kinase pathway required for vulva development in Caenorhabditis elegans.

113 Recent studies of vulva development in the nematode Pristionchus pacificus

114 In lin-28 mutants, vulva development is similar to wild-type vulva developm

115 Caenorhabditis elegans vulva development provides an in vivo model to genetical

116 pe voltage-gated calcium channels to promote vulva development, and acts downstream or parallel to LE

117 we analyzed more than 40 characteristics of vulva development, including cell fates, fate induction,

118 During nematode vulva development, precursor cells acquire one of three

119 n several developmental processes, including vulva development, somatic gonad development, and male t

120 nc-62 are also required for several steps in vulva development.

121 d lin-2, lin-7, and lin-10) are required for vulva development.

122 vulval epithelium, a step crucial for proper vulva development.

123 interaction between ceMIB and lin-18/RYK in vulva development.

124 The vulva develops from a subset of ectodermal vulval precur

125 The Caenorhabditis elegans vulva develops from the progeny of three vulval precurso

126 necessary for sensation of the hermaphrodite vulva during mating.

127 ail and insert them into the hermaphrodite's vulva during mating.

128 ian tubes, uterus, cervix, and the vagina or vulva; each tissue of origin presenting unique signature

129 o that the male can respond to hermaphrodite vulva efficiently.

130 Panagrolaimidae, the number of cells in the vulva equivalence group is limited by apoptosis and decr

131 of twelve ventral epidermal cells form the 'vulva equivalence group'; although all six cells are com

132 multiple mutants in which the uterus and the vulva fail to make a functional connection, resulting in

133 ts were isolated in which the uterus and the vulva fail to make a proper connection.

134 vulval muscle contraction and opening of the vulva for efficient egg laying.

135 nt patient with an invasive carcinoma of the vulva for which postoperative inguinopelvic radiotherapy

136 teral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying.

137 cells, adjacent to the vulva, for wild-type vulva formation and egg laying.

138 any non-hypodermal cells with known roles in vulva formation or egg laying.

139 Vulva formation requires the heterochronic gene lin-29,

140 lated by Hox gene lin-39: cell migration and vulva formation.

141 t cell lineages in the posterior half of the vulva from a default orientation displayed in the anteri

142 a and a physical blockage of the exit to the vulva from the uterus.

143 The anchor cell induces the vulva from ventral epithelial cells via the LIN-3 growth

144 Mutations in C. elegans sqv (squashed vulva) genes affect both vulval morphogenesis and embryo

145 sqv (squashed vulva) genes comprise a set of eight independent loci in

146 f eight Caenorhabditis elegans sqv (squashed vulva) genes, the vulval extracellular space fails to ex

147 g surgery [grade 3]; recurrent cancer of the vulva [grade 4]) and six serious adverse events were rep

148 rait they produce does not, and the nematode vulva has become a model organ for detecting such "devel

149 The Caenorhabditis elegans vulva has been a paradigm for understanding many aspects

150 The Caenorhabditis elegans vulva has been a valuable paradigm for defining componen

151 f only 22 nuclei, the Caenorhabditis elegans vulva has done very well for itself.

152 epleting PAR-1 during the development of the vulva has no detectable effect on fate specification or

153 uamous cell carcinoma (SCC) of the cervix or vulva have limited therapeutic options, and the potentia

154 n biological roles of Cb-glp-1, e.g., in the vulva, have diverged from those of Ce-glp-1 and Cr-glp-1

155 Development of the vulva in C. elegans is mediated by the combinatorial act

156 k-1 MAP kinase signaling pathway induces the vulva in C. elegans.

157 h sensory functions and the uv1 cells of the vulva in hermaphrodites.

158 l precursor cells (VPCs), which generate the vulva in the hermaphrodite.

159 t of a connection between the uterus and the vulva in the nematode Caenorhabditis elegans requires sp

160 s by the LIN-3/EGF morphogen gradient during vulva induction in Caenorhabditis elegans.

161 negative regulator of EGFR signaling during vulva induction.

162 males inject sperm through the hermaphrodite vulva into the uterus.

163 ple, mirror-image symmetry of the C. elegans vulva is achieved by the opposite division orientation o

164 The Caenorhabditis elegans vulva is an elegant model for dissecting a gene regulato

165 The Caenorhabditis elegans vulva is an important paradigm for cell-cell interaction

166 6 reporter gene expression in the developing vulva is attenuated in lin-39(rf) mutants, and overexpre

167 The Caenorhabditis elegans vulva is comprised of highly similar anterior and poster

168 The pathogenesis of carcinoma of the vulva is diverse and includes both human papilloma virus

169 inement of spicule insertion attempts to the vulva is facilitated by D2-like receptor modulation of g

170 A precocious vulva is formed by essentially normal cell lineage patte

171 ke Caenorhabditis elegans and relatives, the vulva is formed from the four precursor cells P(5-8).p o

172 o maximize the probability that a functional vulva is formed.

173 vior reveal that anchor cell invasion of the vulva is important for forming the toroidal shape of the

174 fter vulval induction and that the 1 degrees vulva is necessary to induce the uv1 uterine cell fate.

175 The hermaphrodite vulva is not required for the cue.

176 The formation of the nematode vulva is one tractable system for such evolutionary deve

177 The C. elegans vulva is patterned by epidermal growth factor (EGF) acti

178 After the anchor cell has induced the vulva, it stretches toward the induced vulval cells.

179 causes these cells to form ectopic, anterior vulva-like invaginations.

180 We demonstrate that male vulva location behavior and expression of lov-1 and pkd-

181 rays, hook and head, which mediate response, vulva location, and potentially chemotaxis to hermaphrod

182 luding response to hermaphrodite contact and vulva location, but they do not perform the subsequent s

183 everal substeps: response, backing, turning, vulva location, spicule insertion and sperm transfer.

184 esponse to hermaphrodites, backing, turning, vulva location, spicule insertion, and sperm transfer, c

185 ves the steps of response, backing, turning, vulva location, spicule insertion, and sperm transfer.

186 ns HOA and HOB are specifically required for vulva location.

187 or two male sensory behaviours: response and vulva location.

188 ific sensory cilia required for response and vulva-location mating behaviors.

189 Here we describe the vulva luminal matrix, which contains chondroitin proteog

190 pithelial attachments, including the rectum, vulva, mechanosensory neurons, and excretory duct/pore.

191 mal cell terminal differentiation and proper vulva morphogenesis.

192 roductive system is due to feedback from the vulva muscles that reports ongoing reproduction to the n

193 n anogenital malignancies (1.6%) were found: vulva (n=6), cervix (n=5), and anus (n=5).

194 The small-cell carcinomas of the vagina and vulva need to be distinguished from Merkel cell cancers.

195 are involved in gene regulation outside the vulva, negatively regulating the expression of the Delta

196 sion patterns of the cells in the developing vulva of nT1 mutants, we demonstrate that egl-18/elt-6 p

197 tations that perturb the invagination of the vulva of the Caenorhabditis elegans hermaphrodite, we ha

198 ments continue until the male shifts off the vulva or genital penetration is accomplished.

199 = 107), ovary (n = 64), cervix (n = 30), and vulva or vagina (n = 14).

200 lopment of various cancers including penile, vulva, oropharyngeal and cervical cancers.

201 rminal bulb, the rectal epithelial cells and vulva; pB directs expression in the motor neurone PDA, t

202 ted with ulcers, plaques, and nodules in the vulva, perineum, inguinal creases, and left axilla.

203 NA interference of PAR-1 causes a protruding vulva phenotype.

204 ve activity upon lin-45 Raf and induce multi-vulva phenotypes in C.elegans.

205 for patterns of nucleotide polymorphism and vulva precursor cell lineage, and conduct a series of hy

206 frequency in African C. elegans for the P3.p vulva precursor cell, and in African C. briggsae for P4.

207 is elegans, the fates of the six multipotent vulva precursor cells (VPCs) are specified by extracellu

208 In vulva precursor cells (VPCs), a pathway of heterochronic

209 port on the fastest evolving cell fate among vulva precursor cells in Caenorhabditis nematodes, that

210 nchor cell and lateral signaling between the vulva precursor cells.

211 The Caenorhabditis elegans vulva provides a simple model for the genetic analysis o

212 equent grade 3 and 4 events were pain in the vulva, pruritus, fatigue, and headache.

213 netic screen for mutants having a protruding-vulva (Pvl) mutant phenotype.

214 he development of the Caenorhabditis elegans vulva requires the involution of epithelial cells and pr

215 , from the Caenorhabditis elegans developing vulva requires the lipoprotein receptor-related proteins

216 e hermaphrodite's surface for the vulva (the vulva search).

217 Development of the Caenorhabditis elegans vulva serves as a paradigm for intercellular signaling d

218 In the vulva, sex myoblasts, and hypodermis, lin-42 activity pr

219 Recent results indicated that vulva size (VS) may be predictive of reproductive perfor

220 tissue chromophores both in the superficial vulva skin for epidermal water content and the deeper la

221 METT-10 also promotes vulva, somatic gonad, and embryo development and ensures

222 tion together in a single complex to repress vulva-specific gene transcription.

223 e of Ras signaling by selectively activating vulva-specific genes.

224 Mutations in eight squashed vulva (sqv) genes in Caenorhabditis elegans cause defect

225 ordinated activation of uv1 cells across the vulva, suggesting mechanical stimulation of one uv1 cell

226 all ages and is characterized by pain at the vulva that is present during sexual and/or non-sexual si

227 l neoplasia is a skin disorder affecting the vulva that, if left untreated, can become cancerous.

228 e we identify a gene, lov-1 (for location of vulva), that is required for two male sensory behaviours

229 earch of the hermaphrodite's surface for the vulva (the vulva search).

230 When the spicule tips penetrate the vulva, the protractors undergo prolonged contraction to

231 oductive system, cells that give rise to the vulva, the vulval precursor cells (VPCs), remain quiesce

232 rine pi cells whose daughters connect to the vulva, thereby organizing the uterine-vulval connection.

233 The uterine anchor cell (AC) induces the vulva through LIN-3/epidermal growth factor (EGF) signal

234 es over the past twenty years have shown the vulva to be a microcosm for organogenesis and a model fo

235 integrity of the embryo is monitored by the vulva to detect damage and initiate an organismal protec

236 re of the two mirror-symmetric halves of the vulva to join into a single, coherent organ.

237 ing in vulval lineages, establishment of the vulva-uterine connection, development and function of th

238 ous cell carcinomas of the oropharynx, anus, vulva, vagina or penis, or cervical carcinoma.

239 ed for carcinomas and premalignancies of the vulva, vagina, anus, and oropharynx.

240 lly type 16) can cause cancer of the cervix, vulva, vagina, anus, penis, and oropharynx.

241 , site-by-site, for primary melanomas of the vulva, vagina, urethra, ovary, and the uterine cervix.

242 high-risk types to be first detected in the vulva/vagina (P = .03).

243 tions were more likely to be detected in the vulva/vagina than in the cervix (odds ratio, 4.38 [95% c

244 d, the AC induces patterned proliferation of vulva via expression of LIN-3 (EGF) and then invades int

245 ch the number of precursor cells forming the vulva was reduced from four to two.

246 ulent discharge from mucous membranes of the vulva were observed.

247 s arising from genital skin (penis, scrotum, vulva) were higher in women (0.54) than in men (0.30).

248 precocious phenotypes in the hypodermis and vulva when expressed from multicopy arrays.

249 to allow the vaginal opening to form in the vulva, whereas in males and in females with CAH, androge

250 il, but typically HSNs were located near the vulva, which also varies in anterior-posterior position

251 gonadal cells organize the alignment of the vulva with the sex myoblasts, the progenitors of the egg

252 Sixty-four Gy IMRT was prescribed to the vulva, with 50-64 Gy delivered to the groins/low pelvis.

253 The Caenorhabditis elegans vulva, with its invariant cell lineage and interaction o

254 describe chronic burning and/or pain in the vulva without objective physical findings to explain the