ライフサイエンスコーパス: tuberous sclerosis

1 , and mutations in them underlie the disease tuberous sclerosis.

2 ronal morphogenesis as seen in patients with tuberous sclerosis.

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

4 ymal giant cell astrocytomas associated with tuberous sclerosis.

5 reatment for angiomyolipomas associated with tuberous sclerosis.

6 ymal giant cell astrocytomas associated with tuberous sclerosis.

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

8 behavioral deficits in this animal model of tuberous sclerosis.

9 ature associated with oral manifestations of tuberous sclerosis.

10 anism that contributes to hypomyelination in tuberous sclerosis.

11 amine mice with RPE-specific deletion of the tuberous sclerosis 1 (Tsc1) gene which encodes an upstre

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

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

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

24 Lastly, mRNA from tuberous sclerosis-1/2-null mice brain tissue exhibiting

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

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

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

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

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

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

31 Tuberous sclerosis affected three of these patients.

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

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

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

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

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

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

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

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

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

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

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

43 ly other mTORopathies.SIGNIFICANCE STATEMENT Tuberous sclerosis complex (TSC) and focal cortical dysp

44 Tuberous sclerosis complex (TSC) and focal cortical dysp

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

46 lepsy develops in 70 to 90% of children with tuberous sclerosis complex (TSC) and is often resistant

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

48 Tuberous Sclerosis Complex (TSC) and Lymphangioleiomyoma

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

50 nd sufficient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) and other genetic disor

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

52 cancer-associated 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 Here, we show that conditional loss of the Tuberous Sclerosis Complex (TSC) gene, Tsc1, which inhib

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

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

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

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

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

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

65 Tuberous Sclerosis Complex (TSC) is a complex and hetero

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 neurodevelopmental

85 Tuberous sclerosis complex (TSC) is a neurogenetic disor

86 Tuberous sclerosis complex (TSC) is a pediatric disorder

87 Tuberous sclerosis complex (TSC) is a potent inhibitor o

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

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

90 Tuberous Sclerosis Complex (TSC) is a rare genetic disea

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

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

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

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

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

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

97 Tuberous sclerosis complex (TSC) is an autosomal dominan

98 Tuberous sclerosis complex (TSC) is an autosomal dominan

99 Tuberous sclerosis complex (TSC) is an autosomal dominan

100 Tuberous sclerosis complex (TSC) is an autosomal dominan

101 Tuberous sclerosis complex (TSC) is an autosomal dominan

102 Tuberous Sclerosis Complex (TSC) is an autosomal dominan

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 autosomally inher

106 Tuberous sclerosis complex (TSC) is associated with tumo

107 Tuberous sclerosis complex (TSC) is caused by heterozygo

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

109 Tuberous Sclerosis Complex (TSC) is caused by mutations

110 Tuberous sclerosis complex (TSC) is caused by mutations

111 Tuberous sclerosis complex (TSC) is characterized by the

112 Tuberous sclerosis complex (TSC) is characterized by tum

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 conditions in ex vivo rat hippocampus and in tuberous sclerosis complex (TSC) patient-derived astrocy

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

118 The Tuberous Sclerosis Complex (TSC) protein complex (TSCC),

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

126 The tuberous sclerosis complex (TSC) tumor suppressors form

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

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

129 limus for seizure reduction in patients with tuberous sclerosis complex (TSC), a disease with overact

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 n applied to alleviate epileptic seizures in tuberous sclerosis complex (TSC).

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

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

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

150 ysplasia (FCD), hemimegalencephaly (HME) and tuberous sclerosis complex (TSC).

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

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

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

154 2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC).

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

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

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

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

159 due to bi-allelic inactivating mutations in tuberous sclerosis complex (TSC1/TSC2) genes coding for

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 Loss of the tumor suppressor tuberous sclerosis complex 1 (Tsc1) in the liver promote

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

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

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

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

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

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

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

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

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

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

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

176 e-specific Raptor KO, and adipocyte-specific tuberous sclerosis complex 1 KO mice by crossing floxed

177 ipocyte-specific mTOR nor adipocyte-specific tuberous sclerosis complex 1 KO mice exhibited similar d

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

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

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

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

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

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

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

185 Tuberous sclerosis complex 2 (TSC2) and phosphatase and

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

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

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

189 t CDK4 blockade decreased phosphorylation of tuberous sclerosis complex 2 (TSC2) enhancing EGFR signa

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

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

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

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

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

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

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 cells with two, one, or no functional TSC2 (tuberous sclerosis complex 2) alleles and found that los

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 ctive-age women associated with mutations in tuberous sclerosis complex genes.

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

222 Tuberous sclerosis complex is a disease caused by mutati

223 Tuberous sclerosis complex is a genetic disorder leading

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

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

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

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

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

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

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

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

232 constitutive Rheb activation through loss of tuberous sclerosis complex subunit 2 (TSC2) exploit the

233 atients with ADPKD or in older children with tuberous sclerosis complex to evaluate both kidney cysts

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

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

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

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

238 HNF1B nephropathy, various ciliopathies, and tuberous sclerosis complex), and fewer patients have sim

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

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

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

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

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

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

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

246 The tuberous sclerosis complex-Ras homologue enriched in bra

247 Tuberous sclerosis complex-related connective tissue nev

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

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

250 ymal giant cell astrocytomas associated with tuberous sclerosis complex.

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

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

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

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

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

256 ene expression to cells lacking a functional tuberous sclerosis complex.

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

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

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

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

261 os syndrome, alpha-1 antitrypsin deficiency, tuberous sclerosis complex/lymphangioleiomyomatosis, Loe

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

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

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

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

266 mTORopathies (for example, mutations in the tuberous sclerosis genes TSC1 or TSC2) are due to hypera

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

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

269 Tuberous sclerosis is a developmental genetic disorder c

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

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

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

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

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

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

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

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

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

279 The tuberous sclerosis proteins TSC1 and TSC2 are key integr

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

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

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

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

284 Tuberous Sclerosis (TSC) also known as Bourneville disea

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

286 Tuberous sclerosis (TSC) is a hamartoma syndrome attribu

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

288 Tuberous sclerosis (TSC) is an autosomal dominant diseas

289 Tuberous sclerosis (TSC) is an autosomally dominant neur

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

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

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

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

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

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

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

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

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

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

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

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