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 e hypothesised that the bulbous, cormous and tuberous habits promote diversification, but this had ye

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

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

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

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

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

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

11 Tuberous Sclerosis (TSC) also known as Bourneville disea

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

13 Tuberous sclerosis (TSC) is a hamartoma syndrome attribu

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

15 Tuberous sclerosis (TSC) is an autosomally dominant neur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Tuberous sclerosis affected three of these patients.

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

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

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

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

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

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

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

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

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

51 Tuberous sclerosis complex (TSC) and focal cortical dysp

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

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

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

55 Tuberous Sclerosis Complex (TSC) and Lymphangioleiomyoma

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

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

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

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

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

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

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

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

64 Here, we show that conditional loss of the Tuberous Sclerosis Complex (TSC) gene, Tsc1, which inhib

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

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

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

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

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

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

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

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

73 Tuberous sclerosis complex (TSC) is a dominantly inherit

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

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

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

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

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

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

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

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

82 Tuberous sclerosis complex (TSC) is a genetic multiorgan

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

84 Tuberous sclerosis complex (TSC) is a multiorgan genetic

85 Tuberous sclerosis complex (TSC) is a multiorgan genetic

86 Tuberous sclerosis complex (TSC) is a multisystem geneti

87 Tuberous sclerosis complex (TSC) is a multisystem geneti

88 Tuberous sclerosis complex (TSC) is a neurodevelopmental

89 Tuberous sclerosis complex (TSC) is a neurodevelopmental

90 Tuberous Sclerosis Complex (TSC) is a neurodevelopmental

91 Tuberous sclerosis complex (TSC) is a neurogenetic disor

92 Tuberous sclerosis complex (TSC) is a pediatric disorder

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

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

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

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

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 s

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 autosomal dominan

106 Tuberous sclerosis complex (TSC) is an autosomal dominan

107 Tuberous Sclerosis Complex (TSC) is an autosomal dominan

108 Tuberous sclerosis complex (TSC) is an autosomal dominan

109 Tuberous sclerosis complex (TSC) is an autosomally inher

110 Tuberous sclerosis complex (TSC) is associated with tumo

111 Tuberous sclerosis complex (TSC) is caused by heterozygo

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

113 Tuberous Sclerosis Complex (TSC) is caused by mutations

114 Tuberous sclerosis complex (TSC) is caused by mutations

115 Tuberous sclerosis complex (TSC) is characterized by the

116 Tuberous sclerosis complex (TSC) is characterized by tum

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

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

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

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

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

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

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

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

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

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

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

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

129 The tuberous sclerosis complex (TSC) tumor suppressors form

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 n applied to alleviate epileptic seizures in 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 ysplasia (FCD), hemimegalencephaly (HME) and tuberous sclerosis complex (TSC).

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

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

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

157 2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 Tuberous sclerosis complex 2 (TSC2) and phosphatase and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 Tuberous sclerosis complex and fragile X syndrome are ge

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

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

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

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

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

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

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

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

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

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

223 Tuberous sclerosis complex is a disease caused by mutati

224 Tuberous sclerosis complex is a genetic disorder leading

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 The tuberous sclerosis complex-Ras homologue enriched in bra

248 Tuberous sclerosis complex-related connective tissue nev

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

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

251 ymal giant cell astrocytomas associated with tuberous sclerosis complex.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 The tuberous sclerosis proteins TSC1 and TSC2 are key integr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

292 ronal morphogenesis as seen in patients with tuberous sclerosis.

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

294 ymal giant cell astrocytomas associated with tuberous sclerosis.

295 reatment for angiomyolipomas associated with tuberous sclerosis.

296 ymal giant cell astrocytomas associated with tuberous sclerosis.

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

298 behavioral deficits in this animal model of tuberous sclerosis.

299 anism that contributes to hypomyelination in tuberous sclerosis.

300 of diversification for bulbous, cormous and tuberous taxa compared with rhizomatous and nongeophytic