ライフサイエンスコーパス: wart

1 sia of grade 2 or higher [CIN2+], or genital warts).

2 rs with between 2 and 50 external anogenital warts.

3 than placebo in the treatment of anogenital warts.

4 and other atopic disease had higher odds of 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 es of abnormal cervical cytology and genital warts.

14 action of local hyperthermia to treat viral warts.

15 which in turn promotes growth by inhibiting Warts.

16 illoma virus cervical cell lines and genital warts.

17 the absence of hypogammaglobulinemia and/or warts.

18 ted nontuberculous mycobacterial disease and warts.

19 ment option for both simple and recalcitrant warts.

20 n investigated as alternative treatments for warts.

21 ate by regulating the activity of the kinase Warts.

22 age 75% reduction in the number of cutaneous warts.

23 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

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

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

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

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

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

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

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

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

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

33 nctional importance of their localization to Warts activation.

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

35 resolution of recalcitrant and disseminated warts after vaccination.

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

37 rends in the annual prevalence of anogenital warts (AGW) from 2010-2016 were described by sex and by

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 Condylomata acuminata (anogenital warts [AGWs]) are prevalent in human immunodeficiency vi

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

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 reduce the number of diagnoses of anogenital warts and cervical intraepithelial neoplasia of grade 2

53 reduce the number of diagnoses of anogenital warts and cervical intraepithelial neoplasia of grade 2

54 wide, and persistent HPV infection can cause warts and even cancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 a traditional medicine for the management of warts and tumors for many decades.

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

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

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

76 ies: 23 for HPV infection, 29 for anogenital warts, and 13 for CIN2+.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 /18 infection, approximately 90% for genital warts, approximately 45% for low-grade cytological cervi

93 Anogenital warts are a common disorder associated with significant

94 Approximately 90% of genital warts are caused by human papillomavirus (HPV) types 6 a

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

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

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

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

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

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

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

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

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

104 Cutaneous wart biopsy specimens from HIV-positive patients harbore

105 , and thrombocytopenia were ameliorated, the wart burden and frequency of infection declined, human p

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

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

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

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

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

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

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

113 % (RR 0.32, 95% CI 0.19-0.52) and anogenital warts decreased significantly by 61% (0.39, 0.22-0.71) i

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

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

116 Among boys aged 15-19 years anogenital wart diagnoses decreased significantly by 48% (RR 0.52,

117 Anogenital wart diagnoses decreased significantly by 67% (RR 0.33,

118 papillomavirus on HPV infections, anogenital wart diagnoses, and cervical intraepithelial neoplasia g

119 endpoint (genital HPV infections, anogenital wart diagnoses, or histologically confirmed CIN2+) betwe

120 N2+ among girls and women, and on anogenital warts diagnoses among girls, women, boys, and men.

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

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

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

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

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

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

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

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

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

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

131 Genital wart (GW) incidence is high among men.

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

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

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

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

136 wide, real-world data on the risk of genital warts (GWs) after <3 vaccine doses.

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

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

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

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

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

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

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

144 ruit latex, when applied on HPV-induced skin warts, has shown potential as a possible cure for this v

145 Similar hyperabsorptive warts have evolved repeatedly in lineages colonised by f

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

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

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

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

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

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

152 Herein, we noted that the Hippo/Salvador-Warts-Hippo signaling pathway, which controls organ size

153 petitor' cells with mutation in the Salvador-Warts-Hippo tumour suppressor pathway or expressing elev

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

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

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

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

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

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

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

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

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

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

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

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

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

167 WHIM syndrome (warts, hypogammaglobulinemia, infections, and myelokathe

168 Warts, hypogammaglobulinemia, infections, and myelokathe

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

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

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

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

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

174 Warts, hypogammaglobulinemia, infections, and myelokathe

175 Warts, hypogammaglobulinemia, infections, and myelokathe

176 Warts, hypogammaglobulinemia, infections, and myelokathe

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

178 MYD88 and CXCR4 warts, hypogammaglobulinemia, infections, myelokathexis

179 WHIM (warts, hypogammaglobulinemia, infections, myelokathexis)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 major regulatory input provided by the Hippo-Warts kinase cascade.

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

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

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

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

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

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

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

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

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

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

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

212 disease characterized by a hard dome-like or wart-like nodule which is solitary and does not fuse.

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

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

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

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

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

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

219 ly and exclusively fertilise hyperabsorptive warts on the inner walls of plant-formed structures (dom

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 al inhibitory input independent of the Hippo-Warts pathway.

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

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

237 Instead, Warts phosphorylates and inhibits the actin regulator En

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

239 djacent PPXY motifs at the C-terminus of the Warts polypeptide and additional WW domains bind unoccup

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

241 WW domains interactions with the full-length Warts PPXY domain, and numerous PPXY motif variants of W

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

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

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

245 pendent modifier loci had smaller effects on wart resistance.

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

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

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

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

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

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

252 domain, and numerous PPXY motif variants of Warts show that the two proteins assemble via binding of

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

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

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

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

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

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

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

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

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

262 Melted represses warts transcription to disrupt Hippo pathway activity an

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

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

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

266 the Yorkie transcription coactivator and the Warts tumor suppressor.

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

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

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

270 s 1.0/100PY (95% CI, 0.3-2.6) and of genital warts was 1.0/100PY (95% CI, 0.3-2.5).

271 e interval [CI], 1.1-4.1), and IR of genital warts was 2.3/100PY (95% CI, 1.2-4.1).

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

273 Warts were also associated with increased odds of all ex

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

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

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

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

278 8 reported cases of disseminated, recurrent warts with resolution after quadrivalent HPV vaccination

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 w that CRL4Mahj forms a protein complex with Warts (Wts/large tumor suppressor [Lats]), a kinase of t

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