ライフサイエンスコーパス: tuberous

1 ity, but only in the more irregularly firing tuberous afferents a synchrony code is established, wher

2 nd comparing neuronal response properties in tuberous and ampullary electroreceptor afferents of the

3 ition, and monolayers sporadically generated tuberous foci, a phenotype blocked by the mTOR inhibitor

4 selection linked to the domestication of the tuberous morphotypes, turnip (B. rapa) and kohlrabi (B.

5 Thus, studying the molecular mechanism of tuberous root development and storage is very important.

6 In addition, the tuberous roots of all three species of Decalepis possess

7 The medicinally important fleshy tuberous roots of Decalepis hamiltonii are traded as sub

8 the pathological manifestations observed in tuberous sclerosis (TS) and in pulmonary lymphangioleiom

9 Tuberous sclerosis (TS) is a multi-organ autosomal domin

10 Tuberous Sclerosis (TSC) also known as Bourneville disea

11 LAM cells bear mutations in tuberous sclerosis (TSC) genes.

12 Tuberous sclerosis (TSC) is a benign tumour syndrome cau

13 Tuberous sclerosis (TSC) is a hamartoma syndrome attribu

14 Tuberous sclerosis (TSC) is a hamartoma syndrome caused

15 Tuberous sclerosis (TSC) is a tumor suppressor gene synd

16 Tuberous sclerosis (TSC) is an autosomal dominant diseas

17 Tuberous sclerosis (TSC) is an autosomally dominant neur

18 Tuberous sclerosis (TSC) is an inherited syndrome in whi

19 ions of the TSC1/TSC2 complex (TSC1/2) cause tuberous sclerosis (TSC), a hereditary syndrome with neu

20 In tuberous sclerosis (TSC), elevation of mammalian target

21 cal trials are underway for the treatment of tuberous sclerosis (TSC)-associated tumours using mTOR i

22 rome, neurofibromatosis (NF-1), and possibly tuberous sclerosis (TSC).

23 also found in brain lesions associated with tuberous sclerosis (TSC).

24 We report here that tuberous sclerosis (TSC)1 is critical for T-cell anergy.

25 bumin (Alb)-Cre mice, we selectively deleted tuberous sclerosis (Tsc)1, a negative regulator of Ras h

26 ivity via ablation of its negative regulator tuberous sclerosis 1 (Tsc1) impaired DC development in v

27 The tumor suppressor tuberous sclerosis 1 (TSC1) is an important negative reg

28 We report in this study that the tuberous sclerosis 1 (TSC1), a negative regulator of mTO

29 We describe here that tuberous sclerosis 1 (Tsc1), a regulator of mTOR signali

30 cell-specific deletion of the gene encoding tuberous sclerosis 1 (TSC1), an upstream negative regula

31 chloride intracellular channel 4 (CLIC4) and tuberous sclerosis 1 (TSC1), important innate immunity r

32 lular vesicles such as exosomes derived from tuberous sclerosis 1 (Tsc1)-null cells transform phenoty

33 ulating one of its core negative regulators, tuberous sclerosis 1 (Tsc1).

34 The tuberous sclerosis 1 (TSC1)/TSC2 complex negatively regu

35 The tuberous sclerosis 1 (TSC1)/TSC2 tumor suppressor comple

36 ed protein kinase 2 and on the inhibition of tuberous sclerosis 1 and 2, a negative regulatory comple

37 phosphatase and tensin homologue (PTEN), and tuberous sclerosis 1 promotes ON regeneration.

38 We find that liver-specific loss of TSC1 (tuberous sclerosis 1), an mTORC1 inhibitor, leads to a f

39 ction in phosphorylation of the Akt1 target, tuberous sclerosis 2 (TSC2) at Ser-939.

40 bryonic fibroblasts with genetic ablation of tuberous sclerosis 2 (TSC2) gene.

41 metabolism, we examined the function of the tuberous sclerosis 2 (Tsc2) protein, a key target import

42 macrophages by deletion of the gene encoding tuberous sclerosis 2 (Tsc2) was sufficient to induce hyp

43 beta, proline-rich Akt substrate 40 kDa and tuberous sclerosis 2 (TSC2)) and a kinase assay, was not

44 ents, Myc directly affected transcription of tuberous sclerosis 2 (TSC2), as shown by quantitative mR

45 or AKT phosphorylation of the mTOR regulator Tuberous Sclerosis 2 (TSC2).

46 t Thr 172, acetyl-CoA carboxylase at Ser 79, tuberous sclerosis 2 at Thr 1462 and eukaryotic translat

47 Tuberous sclerosis affected three of these patients.

48 ty College of Dentistry, with a diagnosis of tuberous sclerosis and a chief complaint of gingival enl

49 Even individuals with tuberous sclerosis and a normal intelligence quotient (a

50 ractivity and predispose individuals to both tuberous sclerosis and lymphangioleiomyomatosis.

51 ome (54%), Cornelia de Lange syndrome (43%), tuberous sclerosis complex (36%), Angelman's syndrome (3

52 ogenic yields were highest for children with tuberous sclerosis complex (9 of 11 [81.8%]), metabolic

53 have mutations in the tumor suppressor genes tuberous sclerosis complex (TSC) 1 or 2 and have the cap

54 Genetic studies have shown that the tuberous sclerosis complex (TSC) 1-TSC2-mammalian target

55 t renal angiomyolipomas in which the loss of tuberous sclerosis complex (TSC) 1/2 function gave rise

56 associated with reversible nitrosylation of tuberous sclerosis complex (TSC) 2, and inhibited dimeri

57 Neurological symptoms in tuberous sclerosis complex (TSC) and associated brain le

58 The most common neurological symptom of tuberous sclerosis complex (TSC) and focal cortical dysp

59 T) are of value as a diagnostic criterion of tuberous sclerosis complex (TSC) and in the differentiat

60 bearing fibroblasts from a patient with both tuberous sclerosis complex (TSC) and LAM (TSC-LAM) into

61 genes give rise to the neoplastic disorders tuberous sclerosis complex (TSC) and lymphangioleiomyoma

62 cancer-associated genetic disorders, such as tuberous sclerosis complex (TSC) and sporadic lymphangio

63 cancer as well as genetic disorders such as tuberous sclerosis complex (TSC) and sporadic lymphangio

64 Mutations in the tuberous sclerosis complex (TSC) are associated with var

65 Rett syndrome (RTT) and tuberous sclerosis complex (TSC) are both Mendelian diso

66 Seizure development in tuberous sclerosis complex (TSC) correlates with the pre

67 Patients with tuberous sclerosis complex (TSC) develop hamartomas cont

68 Patients with tuberous sclerosis complex (TSC) frequently develop coll

69 Cells lacking the tuberous sclerosis complex (TSC) gene products are a mod

70 TS pathology is caused by mutations in tuberous sclerosis complex (TSC) genes and is associated

71 cells results, in part, from dysfunction in tuberous sclerosis complex (TSC) genes TSC1 (hamartin) a

72 markers, harbor mTOR-activating mutations in tuberous sclerosis complex (TSC) genes, and recruit abun

73 with inactivating mutations of either of the tuberous sclerosis complex (TSC) genes, Tsc1 and Tsc2.

74 ween the polycystic kidney disease (PKD) and tuberous sclerosis complex (TSC) genes.

75 es including exosomes in the pathogenesis of tuberous sclerosis complex (TSC) have not yet been studi

76 Cells lacking a functional tuberous sclerosis complex (TSC) heterodimer are sensiti

77 Tuberous sclerosis complex (TSC) is a disorder arising f

78 Tuberous sclerosis complex (TSC) is a dominantly inherit

79 Tuberous sclerosis complex (TSC) is a genetic disease as

80 Tuberous sclerosis complex (TSC) is a genetic disease th

81 Tuberous sclerosis complex (TSC) is a genetic disorder c

82 Tuberous sclerosis complex (TSC) is a genetic disorder c

83 Tuberous sclerosis complex (TSC) is a genetic disorder l

84 Tuberous sclerosis complex (TSC) is a genetic disorder w

85 Tuberous sclerosis complex (TSC) is a genetic disorder w

86 Tuberous sclerosis complex (TSC) is a genetic multiorgan

87 Tuberous sclerosis complex (TSC) is a leading genetic ca

88 Tuberous sclerosis complex (TSC) is a multiorgan genetic

89 Tuberous sclerosis complex (TSC) is a multiorgan genetic

90 Tuberous sclerosis complex (TSC) is a multisystem geneti

91 Tuberous sclerosis complex (TSC) is a multisystem geneti

92 Tuberous sclerosis complex (TSC) is a neurodevelopmental

93 Tuberous sclerosis complex (TSC) is a neurodevelopmental

94 Tuberous sclerosis complex (TSC) is a neurogenetic disor

95 Tuberous sclerosis complex (TSC) is a pediatric disorder

96 Tuberous sclerosis complex (TSC) is a rare autosomal dom

97 Tuberous sclerosis complex (TSC) is a rare genetic disea

98 Tuberous Sclerosis Complex (TSC) is a rare genetic disor

99 Tuberous sclerosis complex (TSC) is a relatively rare au

100 Tuberous sclerosis complex (TSC) is a tumor suppressor g

101 Tuberous sclerosis complex (TSC) is a tumor suppressor g

102 Tuberous sclerosis complex (TSC) is a tumor suppressor s

103 Tuberous sclerosis complex (TSC) is an autosomal dominan

104 Tuberous sclerosis complex (TSC) is an autosomal dominan

105 Tuberous sclerosis complex (TSC) is an autosomal dominan

106 Tuberous sclerosis complex (TSC) is an autosomal dominan

107 Tuberous sclerosis complex (TSC) is an autosomally inher

108 Tuberous sclerosis complex (TSC) is associated with tumo

109 Tuberous sclerosis complex (TSC) is caused by heterozygo

110 The autism spectrum disorder tuberous sclerosis complex (TSC) is caused by mutations

111 Tuberous sclerosis complex (TSC) is caused by mutations

112 Tuberous sclerosis complex (TSC) is characterized by the

113 Tuberous sclerosis complex (TSC) is one such genetic dis

114 ferentiation abnormalities are a hallmark of tuberous sclerosis complex (TSC) manifestations; however

115 protein filamin A (FLNA) is overexpressed in tuberous sclerosis complex (TSC) mice, a PI3K-mTOR model

116 Prompted by kidney cyst formation in tuberous sclerosis complex (TSC) patients and rodent mod

117 We demonstrate in this paper that the tuberous sclerosis complex (TSC) plays a critical role i

118 The tuberous sclerosis complex (TSC) proteins TSC1 and TSC2

119 studies identified Pam to be associated with tuberous sclerosis complex (TSC) proteins, ubiquitinatin

120 Tuberous sclerosis complex (TSC) represents one of the m

121 Genetic loss of TSC1/TSC2 function in tuberous sclerosis complex (TSC) results in overactivati

122 o acids, is independent of growth factor and tuberous sclerosis complex (TSC) signaling, is driven by

123 ntile spasms, are often seen in infants with tuberous sclerosis complex (TSC) soon after birth.

124 Clinical similarities between BHD and tuberous sclerosis complex (TSC) suggest that the BHD an

125 , and renal cell carcinoma can also occur in tuberous sclerosis complex (TSC) suggests that the BHD a

126 Somatic or germline mutations in the tuberous sclerosis complex (TSC) tumor suppressor genes

127 The tuberous sclerosis complex (TSC) tumor suppressors form

128 Loss of the tuberous sclerosis complex (TSC) tumor suppressors resul

129 sion is suppressed in cells with loss of the tuberous sclerosis complex (TSC) tumor suppressors, whic

130 TSC2 are two genes, mutations in which cause tuberous sclerosis complex (TSC), a disease characterize

131 Germline TSC1 or TSC2 mutations cause tuberous sclerosis complex (TSC), a hamartoma syndrome w

132 nation, oligodendrocyte-specific deletion of tuberous sclerosis complex (TSC), a major upstream inhib

133 The tumor suppressors Tsc1 and Tsc2 form the tuberous sclerosis complex (TSC), a regulator of mTOR ac

134 d TSC2, the two tumor suppressors underlying tuberous sclerosis complex (TSC), and generated a SS/L n

135 l inactivation of neurofibromatosis-1 (NF1), tuberous sclerosis complex (TSC), and PTEN genes is asso

136 Tuberous sclerosis complex (TSC), caused by dominant mut

137 alian target of rapamycin (mTOR)-suppressing tuberous sclerosis complex (TSC), comprised of TSC1 and

138 In the tuberous sclerosis complex (TSC), hamartomas develop in

139 dvances in the neuroimaging of patients with tuberous sclerosis complex (TSC), highlighting its appli

140 R) pathway, most notably those affecting the tuberous sclerosis complex (TSC), lead to aberrant activ

141 reveal new interactions between R2TP and the tuberous sclerosis complex (TSC), pointing to a potentia

142 utations in either of the genes encoding the tuberous sclerosis complex (TSC), TSC1 and TSC2, result

143 These genes encode the proteins tuberous sclerosis complex (TSC)-1 and TSC2, which are d

144 The tuberous sclerosis complex (TSC)-mammalian target of rap

145 Here, we examine the function of the tuberous sclerosis complex (TSC)-mTOR signaling pathway,

146 n autism spectrum disorders (ASD), including tuberous sclerosis complex (TSC).

147 Epilepsy is a major manifestation of tuberous sclerosis complex (TSC).

148 ge of neurodevelopmental disorders including tuberous sclerosis complex (TSC).

149 ases with sirolimus treatment in adults with tuberous sclerosis complex (TSC).

150 2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC).

151 cell growth that is aberrantly activated in tuberous sclerosis complex (TSC).

152 common brain lesions found in patients with tuberous sclerosis complex (TSC).

153 (PP2A) or AMP-activated protein kinase AMPK-tuberous sclerosis complex (TSC).

154 tumors, including hamartomas associated with tuberous sclerosis complex (TSC).

155 ystic lung disease affecting some women with tuberous sclerosis complex (TSC).

156 Here, we report that the progrowth Ras/tuberous sclerosis complex (TSC)/mTORC1 signaling pathwa

157 with mutations in the tumor suppressor genes tuberous sclerosis complex (TSC)1 or TSC2.

158 The status of the tuberous sclerosis complex (TSC-1/TSC-2) was significant

159 alian target of rapamycin (mTOR) through the tuberous sclerosis complex (TSC1/2 complex), as a new mo

160 Tuberous sclerosis complex 1 (TSC1) and TSC2 are suppres

161 otein kinase (AMPK), liver kinase B1 (LKB1), tuberous sclerosis complex 1 (TSC1) and tuberous scleros

162 We conditionally ablated the tuberous sclerosis complex 1 (Tsc1) gene, an mTOR inhibi

163 perinatal neural progenitor cells (NPCs) of tuberous sclerosis complex 1 (Tsc1) heterozygote mice le

164 rt in this article that the tumor suppressor tuberous sclerosis complex 1 (TSC1) is a critical regula

165 The tuberous sclerosis complex 1 (TSC1) is a tumor suppresso

166 as a result of loss-of-function mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 genes, cause

167 and colleagues (2485-2495) show that without Tuberous Sclerosis Complex 1 (Tsc1) or Tsc2, molecules l

168 thelium by a conditional genetic deletion of tuberous sclerosis complex 1 (Tsc1), a potent negative r

169 involving I kappaB kinases beta (IKK beta), tuberous sclerosis complex 1 (TSC1), and mammalian targe

170 ic overactivation of mTORC1, via ablation of tuberous sclerosis complex 1 (TSC1), causes hypomyelinat

171 negatively regulated by the tumor suppressor tuberous sclerosis complex 1 (TSC1).

172 The tuberous sclerosis complex 1 and 2 (TSC1/2) proteins and

173 otypic feature common to fragile X syndrome, tuberous sclerosis complex 1 and 2, neurofibromatosis 1,

174 We found that the product of the tuberous sclerosis complex 1 gene (TSC1), hamartin, is s

175 ons was a loss-of-function mutation in TSC1 (tuberous sclerosis complex 1), a regulator of mTOR pathw

176 ting this pathway by conditional knockout of tuberous sclerosis complex 1, another negative regulator

177 site optical recordings from neurons lacking tuberous sclerosis complex 1, Tsc1, in a mouse model of

178 The tuberous sclerosis complex 1/2 (TSC1/2) is an endogenous

179 mTOR is negatively controlled by the tuberous sclerosis complex 1/2 (TSC1/2), and activation

180 The importance of tuberous sclerosis complex 1/2-mammalian target of rapam

181 Knockdown of tuberous sclerosis complex 1a (tsc1a), which encodes an

182 To test this, we used cells lacking tuberous sclerosis complex 2 (TSC2(-/-) cells), which sh

183 Tuberous sclerosis complex 2 (TSC2) and phosphatase and

184 e mTORC1 activity through phosphorylation of tuberous sclerosis complex 2 (TSC2) and PRAS40, both neg

185 beta1 integrin-protein phosphatase 2A (PP2A)-tuberous sclerosis complex 2 (TSC2) complex that repress

186 ational inactivation of the tumor suppressor tuberous sclerosis complex 2 (TSC2) constitutively activ

187 The tuberous sclerosis complex 2 (TSC2) gene encodes the pro

188 Inactivating mutations in the tuberous sclerosis complex 2 (TSC2) gene, which encodes

189 p-regulation of mTOR activity by deletion of tuberous sclerosis complex 2 (TSC2) in DRGs is sufficien

190 Mutational inactivation of tumor suppressor tuberous sclerosis complex 2 (TSC2) in LAM constitutivel

191 itutive activation of mTORC1 by depletion of tuberous sclerosis complex 2 (TSC2) inhibits lipophagy i

192 ng mTORC1 by deleting its negative regulator tuberous sclerosis complex 2 (TSC2) leads to hypersensit

193 LAM is typically caused by tuberous sclerosis complex 2 (TSC2) mutations resulting

194 ular kinase Akt, yet directly phosphorylates tuberous sclerosis complex 2 (TSC2) on the same sites as

195 Deguelin inhibited survivin expression in tuberous sclerosis complex 2 (TSC2) wild-type mouse embr

196 Levels of tuberous sclerosis complex 2 (TSC2), a negative regulato

197 oinositide 3-kinase typical of cells lacking tuberous sclerosis complex 2 (TSC2), a tumor suppressor

198 B1), tuberous sclerosis complex 1 (TSC1) and tuberous sclerosis complex 2 (TSC2), leads to uncontroll

199 e encoding the negative regulator of mTORC1, tuberous sclerosis complex 2 (TSC2), resulted in the gen

200 ular kinase Akt to phosphorylate and repress tuberous sclerosis complex 2 (TSC2), resulting in the ac

201 P-mediated degradation of the mTOR inhibitor tuberous sclerosis complex 2 (TSC2).

202 specific sites of mTOR inhibitors raptor and tuberous sclerosis complex 2 (TSC2).

203 ctivated protein kinase and tumor suppressor tuberous sclerosis complex 2 and inhibited mammalian tar

204 induced by the MAPK pathway are dependent on tuberous sclerosis complex 2 but demonstrate a lesser de

205 arget of the GTPase-activating domain of the tuberous sclerosis complex 2 gene product tuberin.

206 of Hsp70 mRNA is deficient in cells lacking tuberous sclerosis complex 2.

207 rotein kinase (AMPK) activity, activation of tuberous sclerosis complex 2/mammalian target of rapamyc

208 ligible patients had a definite diagnosis of tuberous sclerosis complex and at least one lesion with

209 Tuberous sclerosis complex and fragile X syndrome are ge

210 options and who need continued treatment for tuberous sclerosis complex and its varied manifestations

211 ycin (mTOR), and are common in patients with tuberous sclerosis complex and sporadic lymphangioleiomy

212 ze of neoplastic growths in animal models of tuberous sclerosis complex and to reduce the size of ang

213 ofile compared with placebo in patients with tuberous sclerosis complex and treatment-resistant seizu

214 tudy, eligible patients aged 2-65 years with tuberous sclerosis complex and treatment-resistant seizu

215 The Tuberous Sclerosis Complex component, TSC1, functions as

216 LAM cells have biallelic loss of either tuberous sclerosis complex gene (but predominantly TSC-2

217 Loss of the tuberous sclerosis complex genes (TSC1 or TSC2) leads to

218 LAM is caused by mutations in the tuberous sclerosis complex genes (TSC1 or TSC2), resulti

219 ermline or somatic inactivating mutations in tuberous sclerosis complex genes (TSC1 or TSC2).

220 iant cell astrocytoma (SEGA) associated with tuberous sclerosis complex had at least 50% reduction in

221 Tuberous sclerosis complex is a disease caused by mutati

222 Tuberous sclerosis complex is a genetic disorder leading

223 Neither step requires intact tuberous sclerosis complex of proteins to activate mTORC

224 Angiomyolipomas in patients with the tuberous sclerosis complex or sporadic lymphangioleiomyo

225 e angiomyolipoma volume in patients with the tuberous sclerosis complex or sporadic lymphangioleiomyo

226 ameliorative treatment in patients with the tuberous sclerosis complex or sporadic lymphangioleiomyo

227 eport that in murine models, deletion of the tuberous sclerosis complex protein 1 (Tsc1) in renal pro

228 tivate mTORC1 by binding to and antagonizing tuberous sclerosis complex protein 2 (TSC2).

229 Mutation of TSC (encoding tuberous sclerosis complex protein) and activation of ma

230 Recent clinical trials using rapalogues in tuberous sclerosis complex show regression in volume of

231 scle-like cells with mutations in one of the tuberous sclerosis complex tumor-suppressor genes (TSC1/

232 tic activation of mTORC1 through loss of the tuberous sclerosis complex tumour suppressors, TSC1 or T

233 Systemic tuberous sclerosis complex was present in 8 patients (19

234 d, placebo-controlled study in patients with tuberous sclerosis complex who had SEGA that was growing

235 liver kinase B1/AMP-activated protein kinase/tuberous sclerosis complex, and F12-protein binding.

236 and suggest a link between genes involved in Tuberous Sclerosis Complex, Fragile X syndrome, Angelman

237 the induction of REDD1 and activation of the tuberous sclerosis complex, prevents the DNA damage-indu

238 Tuberous sclerosis complex-1 or 2 (TSC1/2) mutations cau

239 ssociated with changes in phosphorylation of tuberous sclerosis complex-2 (TSC2) and targeting of mTO

240 or CRISPR/Cas9-mediated genetic knock-out of tuberous sclerosis complex-2 (Tsc2) blocked the IL-4-dep

241 Our data demonstrate that tuberous sclerosis complex-mammalian target of rapamycin

242 The tuberous sclerosis complex-Ras homologue enriched in bra

243 Tuberous sclerosis complex-related connective tissue nev

244 ays and implicate EMT in the pathogenesis of tuberous sclerosis complex-related diseases.

245 ymal giant cell astrocytomas associated with tuberous sclerosis complex.

246 n the trunk and extremities of patients with tuberous sclerosis complex.

247 gle-center study of 4 patients (8 eyes) with tuberous sclerosis complex.

248 ng PEComas to other neoplasms related to the tuberous sclerosis complex.

249 RCC), such as Von Hippel-Lindau syndrome and tuberous sclerosis complex.

250 giant-cell astrocytomas in patients with the tuberous sclerosis complex.

251 n regulated by gene products involved in the tuberous sclerosis complex.

252 ibitors prevent epilepsy in a mouse model of tuberous sclerosis complex.

253 ough phosphorylation and inactivation of the tuberous sclerosis complex.

254 d for various benign tumours associated with tuberous sclerosis complex.

255 treatment-resistant focal-onset seizures in tuberous sclerosis complex.

256 ch is turned off in response to AMPK via the tuberous sclerosis complex.

257 lly, primary fibroblasts from a patient with tuberous sclerosis exhibited increased mTORC1 activity a

258 Cells mutant for the tuberous sclerosis gene Tsc2 also had extra cilia and di

259 omyomatosis are associated with mutations in tuberous sclerosis genes resulting in constitutive activ

260 LAM is caused by mutations in the tuberous sclerosis genes, resulting in activation of the

261 Studies of murine models of tuberous sclerosis have found defects in cognition and l

262 Tuberous sclerosis is a developmental genetic disorder c

263 Tuberous sclerosis is a single-gene disorder caused by h

264 Tuberous sclerosis is an autosomal-dominant inherited di

265 l cerebral O2 consumption in the brains of a tuberous sclerosis model (Eker rat).

266 Fragile X and tuberous sclerosis offer paradigms for the development o

267 ical assessment) and a definite diagnosis of tuberous sclerosis or sporadic lymphangioleiomyomatosis

268 on everolimus with placebo in patients with tuberous sclerosis or sporadic lymphanioleiomyomatosis-a

269 e profile of deregulated mRNA translation in tuberous sclerosis pathology.

270 Analysis of 15 tuberous sclerosis patient samples in which deletions in

271 diet is used as anti-seizure therapy i.a. in tuberous sclerosis patients, but its impact on concomita

272 suggest that the thalamus may be affected in tuberous sclerosis patients, but this has not been exper

273 pomas, benign renal neoplasms often found in tuberous sclerosis patients, we found evidence of Notch

274 The tuberous sclerosis proteins TSC1 and TSC2 are key integr

275 Cell, Ozcan et al. show that the loss of the tuberous sclerosis tumor suppressor complex induces endo

276 Genetic studies have shown the tuberous sclerosis tumor suppressors TSC1/2 and the REDD

277 mic chemotherapy in the treatment of various tuberous sclerosis tumors.

278 highly comorbid with autism - fragile X and tuberous sclerosis types 1 and 2 syndromes.

279 he second patient was a 52-year-old man with tuberous sclerosis who was a recipient of a living relat

280 The report presents a case of tuberous sclerosis with gingival enlargement histologica

281 les linked to the autosomal dominant disease tuberous sclerosis, an increase in the activity of the t

282 me of the cognitive deficits associated with tuberous sclerosis, and they show that treatment with mT

283 with histology correlation or a diagnosis of tuberous sclerosis, and to determine which characteristi

284 Born with tuberous sclerosis, Deborah never learned to speak and l

285 he former lead to clinical syndromes such as tuberous sclerosis, Peutz-Jeghers syndrome, and Cowden's

286 are features with the archetypal mTORopathy, tuberous sclerosis, raising the possibility of therapies

287 ctrum Disorder (ASD), Fragile X Syndrome and Tuberous Sclerosis, the role of other mGluRs and their a

288 e models of the familial hamartoma syndrome, tuberous sclerosis, we show here that Raptor-mTOR and S6

289 might be a novel candidate for treatment of tuberous sclerosis-mediated tumor growth.

290 ronal morphogenesis as seen in patients with tuberous sclerosis.

291 ase-modifying treatment for other aspects of tuberous sclerosis.

292 ymal giant cell astrocytomas associated with tuberous sclerosis.

293 reatment for angiomyolipomas associated with tuberous sclerosis.

294 ymal giant cell astrocytomas associated with tuberous sclerosis.

295 and 3) histologic diagnosis or diagnosis of tuberous sclerosis.

296 behavioral deficits in this animal model of tuberous sclerosis.

297 ature associated with oral manifestations of tuberous sclerosis.

298 ent with the characteristic angiofibromas of tuberous sclerosis.

299 its associations with Fragile X syndrome and tuberous sclerosis.

300 anism that contributes to hypomyelination in tuberous sclerosis.