ライフサイエンスコーパス: wart

1 action of local hyperthermia to treat viral warts.

2 which in turn promotes growth by inhibiting Warts.

3 and other atopic disease had higher odds of warts.

4 the absence of hypogammaglobulinemia and/or warts.

5 and food allergies than those with AD and no warts.

6 cervical cancers (CxCas) and 90% of genital warts.

7 uperficial basal cell carcinoma, and genital warts.

8 types of HPV are associated with anogenital warts.

9 , which cause 90% of the cases of anogenital warts.

10 her pathway components: Expanded, Hippo, and Warts.

11 two HPV types associated with 90% of genital warts.

12 coactivator Yorkie by the kinases Hippo and Warts.

13 nt for approximately 90% of external genital warts.

14 five (20%) OTR SCC and four of 10 (40%) OTR warts.

15 ted nontuberculous mycobacterial disease and warts.

16 ment option for both simple and recalcitrant warts.

17 n investigated as alternative treatments for warts.

18 ate by regulating the activity of the kinase Warts.

19 illoma virus cervical cell lines and genital warts.

20 rs with between 2 and 50 external anogenital warts.

21 than placebo in the treatment of anogenital warts.

22 R 0.50, 95% CI 0.34-0.74]) and in anogenital warts (0.86 [95% CI 0.79-0.94]) occurred in girls younge

23 reated HIV-positive patients with persistent warts, 42 noninfected controls, and 46 HIV-positive cont

24 ary arterial hypertension 9%), dermatologic (warts 53%, panniculitis 30%), neoplastic (human papillom

25 bulin replacement (14; 45%), cutaneous viral warts (7; 24%), short stature (4; 14%), limb lymphoedema

26 R8 cells is determined by the expression of warts, a core pathway kinase, which interacts with the g

27 oop between Melted, a PH-domain protein, and Warts, a kinase in the Hippo growth pathway.

28 olog of Mst1, forms a signaling complex with Warts, a serine/threonine kinase, which in turn stimulat

29 shapen, a distant relative to the prototypic Warts activating kinase Hippo, interacts with and activa

30 ve not been clarified, nor is it known where Warts activation occurs.

31 ra and genetic manipulations, identify where Warts activation occurs: at apical junctions where Expan

32 nctional importance of their localization to Warts activation.

33 multiple Fat pathway phenotypes but regulate Warts activity independently.

34 of the Fat pathway component dachs, whereas warts acts downstream of dachs.

35 mining the rate at which men develop genital warts after infection with alpha genus human papillomavi

36 resolution of recalcitrant and disseminated warts after vaccination.

37 needed to vaccinate to prevent 1 anogential warts (AGW) case or cervical cancer (CC) was similar for

38 Anogenital warts (AGWs) are considered benign lesions caused by low

39 on human papillomavirus (HPV) and anogenital warts (AGWs), a review of the literature was conducted i

40 has been used in the treatment of anogenital warts (AGWs), but it has not been compared with existing

41 In addition, regressing genital viral warts also harbored high G-to-A or C-to-T mutation in HP

42 incidence of clinically ascertained genital warts among women with incident HPV-6 or HPV-11 infectio

43 termine the association between size of anal wart and CD4(+) count and HIV load.

44 Four of the 7 patients had severe warts and 3 had disseminated nontuberculous mycobacteria

45 Children with warts and AD had a higher number of infections than thos

46 omavirus (HPV)-related cutaneous and genital warts and anogenital (pre)cancer.

47 Human papillomaviruses (HPVs) cause genital warts and cancers in men.

48 MSM) have a high lifetime risk of anogenital warts and cancers related to infection with human papill

49 association between size of the largest anal warts and CD4(+) count at baseline; however, this was no

50 association between size of the largest anal warts and CD4(+) count or HIV load over time.

51 association between size of the largest anal warts and CD4(+) count or HIV load over time.

52 ion, or both contribute to susceptibility to warts and extracutaneous infections in children.

53 parate distributions for Salvador, Expanded, Warts and Hippo.

54 These EV-HPVs cause warts and increase the risk of skin carcinomas in otherw

55 phorylation, mediated directly by the kinase Warts and indirectly by upstream tumor suppressors that

56 le for genes controlling cell proliferation (warts and its partner hippo and salvador) and cell growt

57 of HPV-6-related and HPV-11-related genital warts and juvenile-onset recurrent respiratory papilloma

58 is the major etiological agent of anogenital warts and laryngeal papillomas and has been included in

59 HPV11) is an etiological agent of anogenital warts and laryngeal papillomas and is included in the 4-

60 Substantial declines in anogenital warts and male HPV-related cancer incidence are projecte

61 adult color PRs and the bistable loop of the warts and melted tumor suppressor genes that unambiguous

62 DNA viruses causally associated with benign warts and multiple cancers, including cervical and head-

63 w that BEAF-32 is required for expression of warts and repression of melted Furthermore, BEAF-32 play

64 cating that BEAF-32 differentially regulates warts and Rhodopsins.

65 n WTIP and also enhances WTIP binding to the Warts and Salvador homologs LATS and WW45.

66 the skin or sexual intercourse causes benign warts and sometimes cancer.

67 terminally differentiated cells within HPV1 warts and that colocalization between E1circumflexE4 and

68 ng enhances Jub binding to the Yorkie kinase Warts and the adaptor protein Salvador.

69 operate to modulate the Hippo pathway kinase Warts and the growth regulator Melted; two opposing fact

70 nature of the links among Fat, Expanded, and Warts and the significance of these links to growth cont

71 We show that the Hippo pathway components Warts and Yorkie mediate a transition from low- to high-

72 of epithelial cells, leading to both benign (warts) and malignant tumors (cervical cancer).

73 ortance: Cutaneous verruca vulgaris lesions (warts) and oral squamous cell papillomas are common lesi

74 are workers who treat anogenital warts, oral warts, and anogenital intraepithelial neoplasias (eg, ce

75 HPVs also cause genital warts, and are the most common sexually transmitted dise

76 attendance, HPV prevalence, HIV prevalence, warts, and cancer incidence data.

77 history of disseminated varicella, cutaneous warts, and CD4(+) T-cell lymphopenia.

78 f 4vHPV vaccination on infection, anogenital warts, and cervical cancer or precancerous lesions.

79 uba LIM protein and the Hippo pathway kinase Warts, and decreasing the activity of the growth-promoti

80 PVs associated with cervical cancer, genital warts, and epidermodysplasia verruciformis suggests the

81 ations between childhood AD, atopic disease, warts, and extracutaneous infections suggest that barrie

82 -related endpoint: HPV infection, anogenital warts, and high-grade cervical lesions.

83 rceptions regarding cervical cancer, genital warts, and HPV vaccination collected from parents of vac

84 V) leads to the formation of benign lesions, warts, and in some cases, cervical cancer.

85 : Yki both represses its negative regulator, warts, and promotes its positive regulator, melted.

86 ctions, mucocutaneous candidiasis, cutaneous warts, and skin abscesses.

87 wound healing, pain, psoriasis, scleroderma, warts, and skin cancer.

88 es types 6 and 11, the main cause of genital warts, and types 16 and 18, the main cause of cervical c

89 r blockers during the study and a history of warts anywhere on the body were found to protect against

90 /18 infection, approximately 90% for genital warts, approximately 45% for low-grade cytological cervi

91 Anogenital warts are a common disorder associated with significant

92 Benign genital warts are caused principally by the alpha10 viruses HPV6

93 Our results suggest that genital warts are common after HPV-6 or HPV-11 infection in youn

94 Although cutaneous warts are common lesions, full remission is not always a

95 secondary outcomes were reduction in target wart area and safety.

96 Reduction in target wart area, time to clearance, and patient and investigat

97 ceptor to transcription factor and implicate Warts as an integrator of multiple growth control signal

98 and identify the kinases Discs overgrown and Warts as components of a Fat signaling pathway.

99 Cutaneous wart-associated HPV types 1 and 2 were detected in all b

100 on against both cervical cancer- and genital wart-associated types, we produced at high levels in bac

101 n for posttransplantation patients with skin warts because it serves both as an adjunct to the immuno

102 cells and Drosophila, we uncovered that MOB1/Warts binding is essential for tumor suppression, tissue

103 Cutaneous wart biopsy specimens from HIV-positive patients harbore

104 ogens Wingless and Decapentaplegic, suppress Warts by acting via the atypical myosin Dachs to inhibit

105 The ability to minimize and even resolve warts can improve quality of life by reducing risk of sk

106 cancer-inducing high risk HPV-16 and HPV-18, wart-causing low risk HPV-11, and bovine papillomavirus

107 and promising efficacy in preventing genital warts, cervical neoplasia, and cervical cancer.

108 The regulation of Warts conformation by Mats, Fat/Dachsous signaling, and

109 Although the Hpo/Warts core cascade restrains Yki in the optic lobe, it i

110 estricted through phosphorylation by the Hpo/Warts core kinase cascade, but increasing evidence indic

111 % (RR 0.32, 95% CI 0.19-0.52) and anogenital warts decreased significantly by 61% (0.39, 0.22-0.71) i

112 Here, we use Phos-tag gels to characterize Warts-dependent phosphorylation of Yki in vivo, and show

113 ion occurs in vivo through multiple sites of Warts-dependent phosphorylation on Yki.

114 based reports of a marked decline in genital warts diagnoses among young people in Australia after pr

115 ut 1000 fewer hospital admissions involved a warts diagnosis during 2010-2011.

116 The best control of wart disease is the cultivation of resistant varieties.

117 nscriptional coactivator Yorkie (Yki)/YAP by Warts does not mediate the function of this pathway in p

118 Here, we show that warts, encoding large tumor suppressor (Lats) and melted

119 gl), but not Expanded or Fat-is required for Warts expression and activity in R8 to specify Rh6 fate.

120 g (ewg), is autonomously required to inhibit warts expression and to promote melted expression to spe

121 tants express Rh6 in most R8s due to ectopic warts expression.

122 hood AD is associated with increased risk of warts, extracutaneous infections, and other atopic disea

123 BEAF-32 is dispensable for Warts feedback, indicating that BEAF-32 differentially r

124 Cell-level defects leading to wart formation were traced to sites of active cell divis

125 More than 90% of genital warts (GW) cases are caused by human papillomavirus (HPV

126 Diagnoses of genital warts (GW) in genitourinary medicine (GUM) clinics have

127 k of cancer among men and women with genital warts (GW).

128 ohort study, we assessed the risk of genital warts (GWs) according to timing and number of doses of q

129 o 20.8% in new diagnoses of external genital warts (GWs) among women aged <19 years since the nationa

130 f human papillomavirus (HPV)-related genital warts (GWs) in men are sparse.

131 A reduction in the incidence of genital warts (GWs) is one of the first markers of the effective

132 gical agents of approximately 90% of genital warts (GWs).

133 Children with AD with warts had even higher odds of asthma, hay fever, and foo

134 Finally, children with AD and warts had higher odds of ever receiving a diagnosis of a

135 suppressors, including the kinases Hippo and Warts, has recently been linked to the transmembrane tum

136 The Salvador Warts Hippo (SWH) network limits tissue size in Drosophi

137 The Salvador-Warts-Hippo (Hippo) pathway is a conserved regulator of

138 The Salvador-Warts-Hippo (Hippo) pathway is an evolutionarily conserv

139 Thus, the Salvador-Warts-Hippo pathway has a cell-autonomous function to pr

140 th by suppressing activation of the Salvador-Warts-Hippo pathway of tumor suppressors, activation tha

141 ignaling pathway, also known as the Salvador-Warts-Hippo pathway, is a regulator of organ size.

142 The Salvador/Warts/Hippo (Hippo) signaling pathway defines a novel si

143 The Salvador/Warts/Hippo (Hippo) signaling pathway defines a novel si

144 driven growth is dependent upon the Salvador/Warts/Hippo (SWH) pathway and its transcriptional effect

145 We find that Myopic regulates the Salvador/Warts/Hippo (SWH) tumor suppressor pathway: Myopic PPxY

146 Yki activity is regulated primarily by the Warts/Hippo (Wts/Hpo) tumour suppressor pathway, which i

147 cell polarity) and to affect growth via the Warts/Hippo pathway.

148 e engulfment, and also roles for Myc and the Warts/Hippo tumor suppressor pathway.

149 omolog MAP4K4 similarly interacts with LATS (Warts homolog) and promotes inhibition of YAP (Yorkie ho

150 t studies have shown that the Hippo-Salvador-Warts (HSW) pathway restrains tissue growth by phosphory

151 ion truncations of CXCR4 are associated with warts, hypo-gammaglobulinemia, infections, and myelokath

152 d the activating mutation L265P in MYD88 and warts, hypogammaglobulinemia, infection, and myelokathex

153 to be a potentially useful treatment in the warts, hypogammaglobulinemia, infection, and myelokathex

154 frameshift (FS) germline mutations found in warts, hypogammaglobulinemia, infections and myelokathex

155 Warts, hypogammaglobulinemia, infections, and myelokathe

156 d described the presence of the C1013G/CXCR4 warts, hypogammaglobulinemia, infections, and myelokathe

157 Warts, hypogammaglobulinemia, infections, and myelokathe

158 w-dose plerixafor treatment of patients with warts, hypogammaglobulinemia, infections, and myelokathe

159 rder so-named because it is characterized by warts, hypogammaglobulinemia, infections, and myelokathe

160 s of condyloma specimens from a patient with warts, hypogammaglobulinemia, infections, and myelokathe

161 l immunodeficiency disorder characterized by warts, hypogammaglobulinemia, infections, and myelokathe

162 itutively active CXCR4 mutation in zebrafish warts, hypogammaglobulinemia, infections, and myelokathe

163 Warts, hypogammaglobulinemia, infections, and myelokathe

164 Such anomaly is linked to the warts, hypogammaglobulinemia, infections, myelokathexis

165 MYD88 and CXCR4 warts, hypogammaglobulinemia, infections, myelokathexis

166 WHIM (warts, hypogammaglobulinemia, infections, myelokathexis)

167 WHIM(warts, hypogammaglobulinemia, recurrent bacterial infect

168 IV load predict the size of the largest anal warts in 976 HIV-infected women in an ongoing cohort.

169 atment correlated with regression of genital warts in a subset of patients, including at distant site

170 ted with fewer infections and improvement in warts in combination with imiquimod; however, immunoglob

171 rize the HPV types associated with cutaneous warts in HIV-positive patients.

172 n Papillomavirus (HPV) infection and genital warts in men.

173 Anogenital warts in patients who are HIV+ should be evaluated histo

174 w that activity of the Drosophila NDR kinase Warts in the developing wing depends on its transition f

175 ribute to the development and persistence of warts in this condition and would require different trea

176 show that the protocadherin Fat can regulate Warts in two different ways.

177 icum causes tumor-like tissue proliferation (wart) in potato tubers and thereby considerable crop dam

178 The 24-month cumulative genital wart incidence was 57.9% (95% confidence interval [CI],

179 val central nervous system and uncover a Hpo/Warts-independent function for the tumor suppressor kina

180 escued to viability simply by overexpressing Warts, indicating that their essential function is their

181 We also show that Warts inhibits Yki nuclear localization in vivo, and can

182 w that LATS proteins (mammalian orthologs of Warts) interact directly with YAP in mammalian cells and

183 The kinase LATS/WARTS is a tumor suppressor protein conserved in evoluti

184 f immune response on the development of anal warts is warranted in a larger study.

185 l dermatitis (PDD), also known as hairy heel wart, is a growing cause of lameness of cows in the U.S.

186 tion and with abnormal Pap tests and genital warts; it was negatively associated with marriage and wa

187 ous infectious skin diseases such as genital warts, keratosis, and basal cell carcinoma.

188 y by upstream tumor suppressors that promote Warts kinase activity.

189 In budding yeast, the conserved Ndr/warts kinase Cbk1 localizes to the new daughter cell, wh

190 A double negative feedback loop between the Warts kinase of the Hippo pathway and the PH-domain grow

191 ing pathways, is negatively regulated by the Warts kinase.

192 de, which in Drosophila involves the Hpo and Warts kinases that negatively regulate the activity of t

193 the cluster and signal through the Hippo and Warts kinases to polarize actin and promote border cell

194 y components such as Expanded, the Hippo and Warts kinases, and the transcriptional coactivator Yorki

195 her NDR family kinase, the tumour suppressor Warts/Lats (Wts), regulates the maintenance of dendrites

196 (Hpo) pathway comprises the kinases Hpo and Warts/Lats (Wts), the adaptors Salvador (Sav) and Mob1 a

197 ansduction of the core kinases Hippo/Mst and Warts/Lats are relatively well understood, less is known

198 proteins appear to interact with the related Warts/Lats kinase, which functions as a tumor suppressor

199 e cassette consisting of the Hippo (MST1/2), Warts (LATS1/2), and Tricornered (NDR1/2) kinases togeth

200 The Hippo pathway downstream kinase Warts, LATS1-2 in mammals, associates with the ACD modul

201 vo, and the lack of Canoe phosphorylation by Warts leads to failures of Discs Large apical localizati

202 Loss of the core kinases hippo or warts leads to premature nuclear localization of the tra

203 Unlike the small wart-like lesions usually seen in non-Paridae with avian

204 lacking the downstream Hippo pathway kinase Warts, lymph gland cells overproliferated, differentiate

205 kinase complex, which in turn activates the Warts/Mats kinase complex.

206 Warts/Mats kinase phosphorylates and inhibits Yorkie, a

207 ple prior KCs, and suggest that a history of warts may be associated with reduced SCC risk.

208 through which negative regulation of Yki by Warts-mediated phosphorylation occurs, but find that thi

209 r bacterial skin diseases, cellulitis, viral warts, molluscum contagiosum, and non-melanoma skin canc

210 with hypogammaglobulinemia and/or refractory warts of skin and genitalia.

211 We also noted improvement in warts on her fingers during CMX-001 therapy.

212 lity criteria included no history of genital warts or HIV infection.

213 Eligibility included no history of genital warts or human immunodeficiency virus.

214 d or ulcerated lesions commonly mistaken for warts or other benign skin conditions.

215 g for HPV infection in women with anogenital warts or other sexually transmitted diseases, in their s

216 within the past year, no history of genital warts or penile or anal cancer, and no current diagnosis

217 nce of an association with prevalent genital warts (OR, 0.93, 95% CI, 0.65-1.33; 15 studies).

218 n to healthcare workers who treat anogenital warts, oral warts, and anogenital intraepithelial neopla

219 unctions where Expanded, Salvador, Hippo and Warts overlap.

220 tly identified in HIV-positive patients with warts (P = .004); a susceptible haplotype (HLA-B*44, HLA

221 We find that, in viral warts (papillomas) and HPV gene-induced epidermal tumors

222 The findings show that differences in Warts pathway activity can lead to competition and impli

223 tic tumour suppressors in the Hippo-Salvador-Warts pathway and in neoplastic tumour suppressor genes,

224 cuing RpL36 heterozygous cells, mutations in Warts pathway genes were supercompetitors that could eli

225 wth, ex was largely epistatic to ft, and the Warts pathway mutation hippo largely epistatic to ex.

226 t with its activation by Dachsous in the Fat-Warts pathway, and enhance our understanding of the requ

227 ty can lead to competition and implicate the Warts pathway, certain other tumor suppressors, and nove

228 r, mats, and warts, which are members of the Warts pathway, the tumor suppressor fat, and a novel tum

229 est that ft and ex act partially through the Warts pathway.

230 , Tsc2, and components of the hippo/salvador/warts pathway.

231 the basis for signal transduction by Fat and Warts pathways, including the identification of a DNA-bi

232 Instead, Warts phosphorylates and inhibits the actin regulator En

233 signaling, and Dachs appears independent of Warts phosphorylation by Hippo kinase, establishing a pr

234 two (50%) IC SCC, and one of five (20%) OTR warts positive by PCR.

235 , mononucleosis, mumps, hepatitis B, plantar warts, positive tuberculosis test results, strep throat,

236 hosphorylation of Yki in vivo, and show that Warts promotes phosphorylation of Yki at multiple sites.

237 Warts protein coprecipitates with Dachs, and Warts prote

238 Warts protein coprecipitates with Dachs, and Warts protein levels are influenced by fat, dachs and di

239 eir essential function is their influence on Warts rather than reported effects on endocytosis or oth

240 We identify mechanisms promoting Warts relocalization, and using a phospho-specific antis

241 pendent modifier loci had smaller effects on wart resistance.

242 Progeny of a cross between a wart resistant and a susceptible tetraploid breeding clo

243 Multiple reports have described cases of wart resolution following quadrivalent HPV vaccination.

244 way involving two protein kinases, Hippo and Warts, restricts the growth of imaginal discs in Drosoph

245 fluence of individual upstream regulators of Warts reveals that some mutants (e.g. fat) have only par

246 s with complete clinical clearance of target warts; secondary outcomes were reduction in target wart

247 nd MST2 ortholog, Hippo, as well as the Lats/Warts serine/threonine kinase and a protein named Salvad

248 eorganized on Hippo pathway activation, when Warts shifts from associating with its inhibitor Jub to

249 have established the conservation of Fat and Warts signaling from flies to mammals, and have given us

250 The Fat-Hippo-Warts signaling network regulates both transcription and

251 pillomavirus types (P = .002), compared with wart specimens from noninfected controls.

252 he similarly low transcriptional activity in warts suggests this is an underestimate.

253 ts cell proliferation, mammalian homologs of Warts, termed Lats1 and Lats2, may mediate the function

254 ice that initially presented with persistent warts than in those that spontaneously cleared their inf

255 and Expanded can act in parallel to regulate Warts through distinct mechanisms.

256 e, BEAF-32 plays a second role downstream of Warts to induce Rh6 and prevent Rh5 fate.

257 Jub recruits Warts to junctions in a tension-dependent manner.

258 g kinase Hippo, interacts with and activates Warts to negatively regulate the activity of Yorkie and

259 Melted represses warts transcription to disrupt Hippo pathway activity an

260 Simple and recalcitrant nongenital warts treated with lasers show variable response rates (

261 Currently, use of lasers for wart treatment is limited by lack of established treatme

262 implicated in regulating the activity of the Warts tumor suppressor.

263 ed Hippo pathway, and mutations in Hippo and Warts, two kinases in the Hippo kinase cascade.

264 ored common wart types HPV27/57, the unusual wart type HPV7, and an excess of Betapapillomavirus type

265 s from HIV-positive patients harbored common wart types HPV27/57, the unusual wart type HPV7, and an

266 hin phialides and tuberculate hyphae bearing warts up to 3 mum high), confirms these two isolates as

267 The incidence of anal warts was 4.15 cases per 100 person-years (95% confidenc

268 Warts were also associated with increased odds of all ex

269 onally, significant reductions in anogenital warts were also reported in boys younger than 20 years o

270 n 1999-2011 involving a diagnosis of genital warts were obtained from a comprehensive national databa

271 orts involving laser treatment of nongenital warts were retrieved by searching PubMed with no date li

272 ressors expanded, hippo, salvador, mats, and warts, which are members of the Warts pathway, the tumor

273 l complication of immunosuppression is viral warts, which cause significant disfigurement and increas

274 o groups; low-risk HPV subtypes cause benign warts while high-risk HPVs give rise to cervical cancer.

275 8 reported cases of disseminated, recurrent warts with resolution after quadrivalent HPV vaccination

276 uba LIM protein Jub, a negative regulator of Warts within the Hippo pathway.

277 ession between the Hippo pathway kinase LATS/Warts (Wts) and growth regulator Melted generates mutual

278 usly associated with BLJ function, including warts (wts) and roughened eye (roe), which encode a seri

279 , Ajuba LIM proteins/dJub interact with LATS/Warts (Wts) and WW45/Sav to inhibit phosphorylation of Y

280 Knockdown of Hpo, Salvador (Sav), or Warts (Wts) each result in a partial loss of spindle ori

281 The core pathway consists of the Hpo/Warts (Wts) kinase cassette that phosphorylates and inac

282 ents like Mob as tumor suppressor (Mats) and Warts (Wts) protein kinase are activated is poorly under

283 identified the Large tumor suppressor (Lats)/Warts (Wts) protein kinase as a key component of a pathw

284 ndant manner upstream of the Hippo (Hpo) and Warts (Wts) proteins to regulate cell growth and divisio

285 Although the Warts (Wts) tumor suppressor is a critical regulator of

286 Src kinase (d-Csk) is a genetic modifier of warts (wts), a tumor-suppressor gene in the Hippo pathwa

287 PcG proteins and the tumor suppressor kinase Warts (Wts), providing evidence for their cooperation in

288 two serine/threonine kinases Hippo (Hpo) and Warts (Wts), the scaffold proteins Salvador (Sav) and Ma

289 (Mer), two serine/threonine kinases, Hpo and Warts (Wts), the scaffold proteins Salvador (Sav) and Ma

290 Salvador (Sav), phosphorylates and activates Warts (Wts), which in turn phosphorylates and inactivate

291 al regulation effected by the Drosophila Fat-Warts (Wts)-Hippo (Hpo) pathways.

292 enes in Drosophila are tricornered (trc) and warts (wts).

293 The Salvador (Sav)/Warts (Wts)/Hippo (Hpo) (SWH) network controls tissue gr

294 orylation by Hpo increases its affinity with Warts (Wts)/large tumor suppressor (Lats) serine/threoni

295 (Ex), Hippo (Hpo), Salvador (Sav)/Shar-pei, Warts (Wts)/Large tumor suppressor (Lats), and Mob as tu

296 (MST1/2 in mammals) and a downstream kinase Warts (Wts, Lats1/2 in mammals), as well as several scaf

297 kinase Hippo (Hpo) and the NDR family kinase Warts (Wts; also called Lats).

298 eam effector of the Hippo(Hpo)-Salvador(Sav)-Warts(Wts) signaling cascade, recently identified in fli

299 l/Traffic Jam feedforward module-that allows Warts-Yki-Melted to operate as a bistable switch.

300 gether, this work reveals that the Misshapen-Warts-Yorkie pathway acts in enteroblasts to control nic