ライフサイエンスコーパス: tuberous sclerosis complex

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

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

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

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

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

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

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

8 ough phosphorylation and inactivation of the tuberous sclerosis complex.

9 C2 tumor suppressor gene are responsible for Tuberous Sclerosis Complex.

10 onsible for the inherited genetic disease of tuberous sclerosis complex.

11 growths develop resulting in the syndrome of tuberous sclerosis complex.

12 tial contributions to epileptogenesis in the tuberous sclerosis complex.

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

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

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

16 ymal giant cell astrocytomas associated with tuberous sclerosis complex.

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

18 Tuberous sclerosis complex 1 (TSC1) and TSC2 tumor suppr

19 Furthermore, tuberous sclerosis complex 1 (TSC1) and TSC2, which are

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

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

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

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

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

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

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

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

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

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

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

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

32 otein products of the tumor suppressor genes tuberous sclerosis complex 1 and 2 form a protein comple

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

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

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

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

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

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

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

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

41 on of insulin receptor substrate (IRS)-1 and tuberous sclerosis complex-1 by siRNAs failed to abrogat

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

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

44 sing rats carrying a germ-line defect in the tuberous sclerosis complex 2 (Tsc-2) tumor-suppressor ge

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

46 Tuberous sclerosis complex 2 (TSC2) and phosphatase and

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

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

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

50 tes and thereby targets the tumor suppressor tuberous sclerosis complex 2 (TSC2) for degradation, lea

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

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

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

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

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

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

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

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

59 ly activated and the mTOR negative regulator tuberous sclerosis complex 2 (TSC2) protein fails to fun

60 Recently the tuberous sclerosis complex 2 (TSC2) tumor suppressor gen

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

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

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

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

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

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

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

68 via direct phosphorylation and inhibition of tuberous sclerosis complex 2 (TSC2), which is a negative

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

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

71 tes growth by phosphorylating and inhibiting tuberous sclerosis complex 2 (TSC2).

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

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

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

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

76 ing events and mutations associated with the tuberous sclerosis complex 2 gene product tuberin.

77 Tuberin, the product of the tuberous sclerosis complex 2 tumor suppressor gene, is a

78 ed amino acid stimulation while knockdown of tuberous sclerosis complex 2, a negative regulator of TO

79 Three genetic diseases including tuberous sclerosis complex 2, neurofibromatosis type 1,

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

81 teins of the TOR signaling pathway, TOR, and tuberous sclerosis complex 2.

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

83 ribosomal S6 kinase pathways and subsequent tuberous sclerosis complex 2/tuberin inactivation or by

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

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

86 t, which carries a germ-line mutation in the tuberous sclerosis complex-2 (Tsc2) tumor suppressor gen

87 This approach identifies the tuberous sclerosis complex-2 gene product, tuberin, as a

88 site for the tumor suppressor gene tuberin (tuberous sclerosis complex-2).

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

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

91 death is inhibited by shRNAs targeting TSC2 (tuberous sclerosis complex), a protein with which RTP801

92 Mutation in the TSC2 tumor suppressor causes tuberous sclerosis complex, a disease characterized by h

93 Tuberous sclerosis complex, an autosomal dominant diseas

94 Mutations in either TSC1 or TSC2 cause tuberous sclerosis complex, an autosomal dominant disord

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

96 Tuberous sclerosis complex and fragile X syndrome are ge

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

98 iabetes and obesity), tumor syndromes (e.g., tuberous sclerosis complex and Peutz-Jegher's syndrome),

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

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

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

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

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

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

105 priate phosphorylation, which is specific to tuberous sclerosis complex-associated brain lesions.

106 The Tuberous Sclerosis Complex component, TSC1, functions as

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

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

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

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

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

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

113 In Drosophila, TSC1 and TSC2 (tuberous sclerosis complex genes 1 and 2) act together t

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

115 Tuberous sclerosis complex is a disease caused by mutati

116 Tuberous sclerosis complex is a genetic disorder leading

117 Although tuberous sclerosis complex is a tumor suppressor gene sy

118 Tuberous sclerosis complex is a tumor suppressor gene sy

119 Tuberous sclerosis complex is a tumor suppressor syndrom

120 Tuberous sclerosis complex is caused by mutations in tum

121 of epileptogenesis in cortical tubers in the tuberous sclerosis complex is unknown.

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

123 The tuberous sclerosis complex-mammalian target of rapamycin

124 clinical findings and molecular advances in tuberous sclerosis complex, neurofibromatosis type 1, Bl

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

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

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

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

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

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

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

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

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

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

135 The tuberous sclerosis complex-Ras homologue enriched in bra

136 l size regulation, but it does not depend on tuberous sclerosis complex/Ras homolog enriched in brain

137 Tuberous sclerosis complex-related connective tissue nev

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

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

140 with several hamartoma syndromes, including tuberous sclerosis complex, the PTEN-related hamartoma s

141 cell astrocytoma (SEGA; n = 6) specimens in tuberous sclerosis complex to define the developmental p

142 Tuberous sclerosis complex (TSC) 1 and TSC2 are thought

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

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

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

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

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

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

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

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

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

152 Tuberous sclerosis complex (TSC) and Peutz-Jeghers syndr

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

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

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

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

157 Tubers in the tuberous sclerosis complex (TSC) are characterized histo

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

159 Persons affected with tuberous sclerosis complex (TSC) develop a wide range of

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

161 Patients with tuberous sclerosis complex (TSC) develop hamartomatous t

162 The most exciting advances in the tuberous sclerosis complex (TSC) field occurred in 1993

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

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

165 Tuberous sclerosis complex (TSC) gene products negativel

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

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

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

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

170 y loss of heterozygosity (LOH) of one of the tuberous sclerosis complex (TSC) genes.

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

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

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

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

175 Tuberous sclerosis complex (TSC) is a dominantly inherit

176 Tuberous sclerosis complex (TSC) is a familial hamartoma

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

178 Tuberous sclerosis complex (TSC) is a genetic disease ca

179 Tuberous sclerosis complex (TSC) is a genetic disease ca

180 Tuberous sclerosis complex (TSC) is a genetic disease ca

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

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

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

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

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

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

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

188 Tuberous Sclerosis Complex (TSC) is a genetic disorder t

189 The tuberous sclerosis complex (TSC) is a genetic disorder t

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

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

192 Tuberous sclerosis complex (TSC) is a genetic multiorgan

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

194 Tuberous sclerosis complex (TSC) is a multiorgan genetic

195 Tuberous sclerosis complex (TSC) is a multiorgan genetic

196 Tuberous sclerosis complex (TSC) is a multisystem geneti

197 Tuberous sclerosis complex (TSC) is a multisystem geneti

198 Tuberous sclerosis complex (TSC) is a neurodevelopmental

199 Tuberous sclerosis complex (TSC) is a neurodevelopmental

200 Tuberous sclerosis complex (TSC) is a neurogenetic disor

201 Tuberous sclerosis complex (TSC) is a pediatric disorder

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

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

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

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

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

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

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

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

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

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

212 Tuberous sclerosis complex (TSC) is an autosomal dominan

213 Tuberous sclerosis complex (TSC) is an autosomal dominan

214 Tuberous sclerosis complex (TSC) is an autosomal dominan

215 Tuberous sclerosis complex (TSC) is an autosomal dominan

216 Tuberous sclerosis complex (TSC) is an autosomal dominan

217 Tuberous sclerosis complex (TSC) is an autosomal dominan

218 Tuberous sclerosis complex (TSC) is an autosomal dominan

219 Tuberous Sclerosis Complex (TSC) is an autosomal dominan

220 Tuberous sclerosis complex (TSC) is an autosomal dominan

221 Tuberous sclerosis complex (TSC) is an autosomal dominan

222 Tuberous sclerosis complex (TSC) is an autosomal dominan

223 Tuberous sclerosis complex (TSC) is an autosomal dominan

224 Tuberous sclerosis complex (TSC) is an autosomal-dominan

225 Tuberous sclerosis complex (TSC) is an autosomally inher

226 Tuberous sclerosis complex (TSC) is associated with tumo

227 Tuberous sclerosis complex (TSC) is caused by heterozygo

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

229 Tuberous sclerosis complex (TSC) is caused by mutations

230 Tuberous sclerosis complex (TSC) is characterized by the

231 Tuberous sclerosis complex (TSC) is characterized by the

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

233 phangioleiomyomatosis (LAM) in patients with tuberous sclerosis complex (TSC) is unknown.

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

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

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

237 Here we demonstrate that primary tumors from tuberous sclerosis complex (TSC) patients and the Eker r

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

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

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

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

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

243 (FCD) and giant cells (GCs) in tubers of the tuberous sclerosis complex (TSC) share phenotypic simila

244 The pathology associated with tuberous sclerosis complex (TSC) shows diverse phenotype

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

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

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

248 Excessive astrocytosis in cortical tubers in tuberous sclerosis complex (TSC) suggests that astrocyte

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

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

251 The tuberous sclerosis complex (TSC) tumor suppressors form

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

253 0 ribosomal S6 kinase-signaling targets, the tuberous sclerosis complex (TSC) tumor suppressors TSC1

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

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

256 TSC1 or TSC2 tumor suppressor genes lead to tuberous sclerosis complex (TSC), a dominant hamartomato

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

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

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

260 Tuberous sclerosis complex (TSC), an autosomal dominant

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

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

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

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

265 cted pulmonary LAM cells from a patient with tuberous sclerosis complex (TSC), demonstrating for the

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

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

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

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

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

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

272 tion (eIF4G) pathways in the pathogenesis of tuberous sclerosis complex (TSC)-associated cortical tub

273 stress response REDD1 gene as a mediator of tuberous sclerosis complex (TSC)-dependent mTOR regulati

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

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

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

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

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

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

280 2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC).

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

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

283 pulmonary lymphangiomyomatosis (LAM), and in tuberous sclerosis complex (TSC).

284 g of the chest on 23 asymptomatic women with tuberous sclerosis complex (TSC).

285 sorder (sporadic LAM) or in association with tuberous sclerosis complex (TSC).

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

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

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

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

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

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

292 The tuberous sclerosis complex (TSC1-2) suppresses cell grow

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

294 The two genes that underlie tuberous sclerosis complex, tuberin and hamartin, lie at

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

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

297 cycle and proliferation were associated with tuberous sclerosis complex type 2 or neurofibromatosis t

298 Tuberous sclerosis complex was present in 14.8% of subje

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

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