ライフサイエンスコーパス: tuberous sclerosis

1 ronal morphogenesis as seen in patients with tuberous sclerosis.

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

3 ymal giant cell astrocytomas associated with tuberous sclerosis.

4 reatment for angiomyolipomas associated with tuberous sclerosis.

5 ymal giant cell astrocytomas associated with tuberous sclerosis.

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

7 behavioral deficits in this animal model of tuberous sclerosis.

8 ature associated with oral manifestations of tuberous sclerosis.

9 ent with the characteristic angiofibromas of tuberous sclerosis.

10 its associations with Fragile X syndrome and tuberous sclerosis.

11 anism that contributes to hypomyelination in tuberous sclerosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 Tuberous sclerosis affected three of these patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Tuberous sclerosis complex (TSC) is a dominantly inherit

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

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

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

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

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

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

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

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

76 Tuberous sclerosis complex (TSC) is a genetic multiorgan

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

78 Tuberous sclerosis complex (TSC) is a multiorgan genetic

79 Tuberous sclerosis complex (TSC) is a multiorgan genetic

80 Tuberous sclerosis complex (TSC) is a multisystem geneti

81 Tuberous sclerosis complex (TSC) is a multisystem geneti

82 Tuberous sclerosis complex (TSC) is a neurodevelopmental

83 Tuberous sclerosis complex (TSC) is a neurodevelopmental

84 Tuberous sclerosis complex (TSC) is a neurogenetic disor

85 Tuberous sclerosis complex (TSC) is a pediatric disorder

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

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

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

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

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

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

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

93 Tuberous sclerosis complex (TSC) is an autosomal dominan

94 Tuberous sclerosis complex (TSC) is an autosomal dominan

95 Tuberous sclerosis complex (TSC) is an autosomal dominan

96 Tuberous sclerosis complex (TSC) is an autosomal dominan

97 Tuberous sclerosis complex (TSC) is an autosomally inher

98 Tuberous sclerosis complex (TSC) is associated with tumo

99 Tuberous sclerosis complex (TSC) is caused by heterozygo

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

101 Tuberous sclerosis complex (TSC) is caused by mutations

102 Tuberous sclerosis complex (TSC) is characterized by the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 The tuberous sclerosis complex (TSC) tumor suppressors form

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 Tuberous sclerosis complex 2 (TSC2) and phosphatase and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 tion of Erk and the tumor suppressor protein tuberous sclerosis complex 2 (TSC2), an upstream regulat

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

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

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

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

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

194 phosphorylation of its cytosolic substrates tuberous sclerosis complex 2 and BAD by epidermal growth

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

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

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

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

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

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

201 Tuberous sclerosis complex and fragile X syndrome are ge

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

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

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

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

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

207 The Tuberous Sclerosis Complex component, TSC1, functions as

208 ation and cell size as a result of increased tuberous sclerosis complex function.

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

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

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

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

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

214 Tuberous sclerosis complex is a disease caused by mutati

215 Tuberous sclerosis complex is a genetic disorder leading

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

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

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

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

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

221 in pathway, the AMP-activated protein kinase-tuberous sclerosis complex protein 1/tuberous sclerosis

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

223 kinase-tuberous sclerosis complex protein 1/tuberous sclerosis complex protein 2-Rheb pathway, and t

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

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

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

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

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

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

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

231 TSC2, two tumor suppressor genes involved in tuberous sclerosis complex, as regulators of the mammali

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

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

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

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

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

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

238 The tuberous sclerosis complex-Ras homologue enriched in bra

239 Tuberous sclerosis complex-related connective tissue nev

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

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

242 ymal giant cell astrocytomas associated with tuberous sclerosis complex.

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

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

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

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

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

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

249 ough phosphorylation and inactivation of the tuberous sclerosis complex.

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

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

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

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

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

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

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

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

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

259 Tuberous sclerosis is a developmental genetic disorder c

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

261 Tuberous sclerosis is an autosomal-dominant inherited di

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

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

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

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

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

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

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

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

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

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

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

273 The tuberous sclerosis proteins TSC1 and TSC2 are key integr

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

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

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

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

278 Tuberous Sclerosis (TSC) also known as Bourneville disea

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

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

281 Tuberous sclerosis (TSC) is a hamartoma syndrome attribu

282 Tuberous sclerosis (TSC) is a hamartoma syndrome caused

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

284 Tuberous sclerosis (TSC) is an autosomal dominant diseas

285 Tuberous sclerosis (TSC) is an autosomally dominant neur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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