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1 ymal giant cell astrocytomas associated with tuberous sclerosis complex.
2 gle-center study of 4 patients (8 eyes) 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 ene expression to cells lacking a functional tuberous sclerosis complex.
10 n the trunk and extremities of patients with tuberous sclerosis complex.
11 d for various benign tumours associated with tuberous sclerosis complex.
12 treatment-resistant focal-onset seizures in tuberous sclerosis complex.
13 ch is turned off in response to AMPK via the tuberous sclerosis complex.
17 otein kinase (AMPK), liver kinase B1 (LKB1), tuberous sclerosis complex 1 (TSC1) and tuberous scleros
19 perinatal neural progenitor cells (NPCs) of tuberous sclerosis complex 1 (Tsc1) heterozygote mice le
21 rt in this article that the tumor suppressor tuberous sclerosis complex 1 (TSC1) is a critical regula
23 as a result of loss-of-function mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 genes, cause
24 and colleagues (2485-2495) show that without Tuberous Sclerosis Complex 1 (Tsc1) or Tsc2, molecules l
25 thelium by a conditional genetic deletion of tuberous sclerosis complex 1 (Tsc1), a potent negative r
26 involving I kappaB kinases beta (IKK beta), tuberous sclerosis complex 1 (TSC1), and mammalian targe
27 ic overactivation of mTORC1, via ablation of tuberous sclerosis complex 1 (TSC1), causes hypomyelinat
30 otypic feature common to fragile X syndrome, tuberous sclerosis complex 1 and 2, neurofibromatosis 1,
32 e-specific Raptor KO, and adipocyte-specific tuberous sclerosis complex 1 KO mice by crossing floxed
33 ipocyte-specific mTOR nor adipocyte-specific tuberous sclerosis complex 1 KO mice exhibited similar d
34 ons was a loss-of-function mutation in TSC1 (tuberous sclerosis complex 1), a regulator of mTOR pathw
35 ting this pathway by conditional knockout of tuberous sclerosis complex 1, another negative regulator
36 site optical recordings from neurons lacking tuberous sclerosis complex 1, Tsc1, in a mouse model of
40 on of insulin receptor substrate (IRS)-1 and tuberous sclerosis complex-1 by siRNAs failed to abrogat
43 sing rats carrying a germ-line defect in the tuberous sclerosis complex 2 (Tsc-2) tumor-suppressor ge
46 e mTORC1 activity through phosphorylation of tuberous sclerosis complex 2 (TSC2) and PRAS40, both neg
47 beta1 integrin-protein phosphatase 2A (PP2A)-tuberous sclerosis complex 2 (TSC2) complex that repress
48 ational inactivation of the tumor suppressor tuberous sclerosis complex 2 (TSC2) constitutively activ
49 t CDK4 blockade decreased phosphorylation of tuberous sclerosis complex 2 (TSC2) enhancing EGFR signa
50 tes and thereby targets the tumor suppressor tuberous sclerosis complex 2 (TSC2) for degradation, lea
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
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 Deguelin inhibited survivin expression in tuberous sclerosis complex 2 (TSC2) wild-type mouse embr
62 oinositide 3-kinase typical of cells lacking tuberous sclerosis complex 2 (TSC2), a tumor suppressor
63 tion of Erk and the tumor suppressor protein tuberous sclerosis complex 2 (TSC2), an upstream regulat
64 B1), tuberous sclerosis complex 1 (TSC1) and tuberous sclerosis complex 2 (TSC2), leads to uncontroll
65 e encoding the negative regulator of mTORC1, tuberous sclerosis complex 2 (TSC2), resulted in the gen
66 ular kinase Akt to phosphorylate and repress tuberous sclerosis complex 2 (TSC2), resulting in the ac
67 via direct phosphorylation and inhibition of tuberous sclerosis complex 2 (TSC2), which is a negative
71 phosphorylation of its cytosolic substrates tuberous sclerosis complex 2 and BAD by epidermal growth
72 ctivated protein kinase and tumor suppressor tuberous sclerosis complex 2 and inhibited mammalian tar
73 induced by the MAPK pathway are dependent on tuberous sclerosis complex 2 but demonstrate a lesser de
76 cells with two, one, or no functional TSC2 (tuberous sclerosis complex 2) alleles and found that los
77 ed amino acid stimulation while knockdown of tuberous sclerosis complex 2, a negative regulator of TO
81 rotein kinase (AMPK) activity, activation of tuberous sclerosis complex 2/mammalian target of rapamyc
82 ribosomal S6 kinase pathways and subsequent tuberous sclerosis complex 2/tuberin inactivation or by
83 ssociated with changes in phosphorylation of tuberous sclerosis complex-2 (TSC2) and targeting of mTO
84 or CRISPR/Cas9-mediated genetic knock-out of tuberous sclerosis complex-2 (Tsc2) blocked the IL-4-dep
85 ome (54%), Cornelia de Lange syndrome (43%), tuberous sclerosis complex (36%), Angelman's syndrome (3
86 ogenic yields were highest for children with tuberous sclerosis complex (9 of 11 [81.8%]), metabolic
87 death is inhibited by shRNAs targeting TSC2 (tuberous sclerosis complex), a protein with which RTP801
88 Mutation in the TSC2 tumor suppressor causes tuberous sclerosis complex, a disease characterized by h
90 ligible patients had a definite diagnosis of tuberous sclerosis complex and at least one lesion with
92 options and who need continued treatment for tuberous sclerosis complex and its varied manifestations
93 iabetes and obesity), tumor syndromes (e.g., tuberous sclerosis complex and Peutz-Jegher's syndrome),
94 ycin (mTOR), and are common in patients with tuberous sclerosis complex and sporadic lymphangioleiomy
95 ze of neoplastic growths in animal models of tuberous sclerosis complex and to reduce the size of ang
96 ofile compared with placebo in patients with tuberous sclerosis complex and treatment-resistant seizu
97 tudy, eligible patients aged 2-65 years with tuberous sclerosis complex and treatment-resistant seizu
98 HNF1B nephropathy, various ciliopathies, and tuberous sclerosis complex), and fewer patients have sim
99 liver kinase B1/AMP-activated protein kinase/tuberous sclerosis complex, and F12-protein binding.
100 TSC2, two tumor suppressor genes involved in tuberous sclerosis complex, as regulators of the mammali
101 priate phosphorylation, which is specific to tuberous sclerosis complex-associated brain lesions.
103 and suggest a link between genes involved in Tuberous Sclerosis Complex, Fragile X syndrome, Angelman
105 LAM cells have biallelic loss of either tuberous sclerosis complex gene (but predominantly TSC-2
111 iant cell astrocytoma (SEGA) associated with tuberous sclerosis complex had at least 50% reduction in
117 os syndrome, alpha-1 antitrypsin deficiency, tuberous sclerosis complex/lymphangioleiomyomatosis, Loe
122 e angiomyolipoma volume in patients with the tuberous sclerosis complex or sporadic lymphangioleiomyo
123 ameliorative treatment in patients with the tuberous sclerosis complex or sporadic lymphangioleiomyo
124 the induction of REDD1 and activation of the tuberous sclerosis complex, prevents the DNA damage-indu
125 eport that in murine models, deletion of the tuberous sclerosis complex protein 1 (Tsc1) in renal pro
126 in pathway, the AMP-activated protein kinase-tuberous sclerosis complex protein 1/tuberous sclerosis
128 kinase-tuberous sclerosis complex protein 1/tuberous sclerosis complex protein 2-Rheb pathway, and t
131 l size regulation, but it does not depend on tuberous sclerosis complex/Ras homolog enriched in brain
134 Recent clinical trials using rapalogues in tuberous sclerosis complex show regression in volume of
135 constitutive Rheb activation through loss of tuberous sclerosis complex subunit 2 (TSC2) exploit the
136 with several hamartoma syndromes, including tuberous sclerosis complex, the PTEN-related hamartoma s
137 atients with ADPKD or in older children with tuberous sclerosis complex to evaluate both kidney cysts
139 have mutations in the tumor suppressor genes tuberous sclerosis complex (TSC) 1 or 2 and have the cap
141 t renal angiomyolipomas in which the loss of tuberous sclerosis complex (TSC) 1/2 function gave rise
142 associated with reversible nitrosylation of tuberous sclerosis complex (TSC) 2, and inhibited dimeri
144 The most common neurological symptom of tuberous sclerosis complex (TSC) and focal cortical dysp
145 ly other mTORopathies.SIGNIFICANCE STATEMENT Tuberous sclerosis complex (TSC) and focal cortical dysp
147 T) are of value as a diagnostic criterion of tuberous sclerosis complex (TSC) and in the differentiat
148 lepsy develops in 70 to 90% of children with tuberous sclerosis complex (TSC) and is often resistant
149 bearing fibroblasts from a patient with both tuberous sclerosis complex (TSC) and LAM (TSC-LAM) into
150 genes give rise to the neoplastic disorders tuberous sclerosis complex (TSC) and lymphangioleiomyoma
152 nd sufficient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) and other genetic disor
154 cancer-associated genetic disorders, such as tuberous sclerosis complex (TSC) and sporadic lymphangio
155 cancer as well as genetic disorders such as tuberous sclerosis complex (TSC) and sporadic lymphangio
165 Here, we show that conditional loss of the Tuberous Sclerosis Complex (TSC) gene, Tsc1, which inhib
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.
172 es including exosomes in the pathogenesis of tuberous sclerosis complex (TSC) have not yet been studi
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 conditions in ex vivo rat hippocampus and in tuberous sclerosis complex (TSC) patient-derived astrocy
241 studies identified Pam to be associated with tuberous sclerosis complex (TSC) proteins, ubiquitinatin
244 (FCD) and giant cells (GCs) in tubers of the tuberous sclerosis complex (TSC) share phenotypic simila
246 o acids, is independent of growth factor and tuberous sclerosis complex (TSC) signaling, is driven by
249 , and renal cell carcinoma can also occur in tuberous sclerosis complex (TSC) suggests that the BHD a
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 limus for seizure reduction in patients with tuberous sclerosis complex (TSC), a disease with overact
257 TSC1 or TSC2 tumor suppressor genes lead to tuberous sclerosis complex (TSC), a dominant hamartomato
259 nation, oligodendrocyte-specific deletion of tuberous sclerosis complex (TSC), a major upstream inhib
260 The tumor suppressors Tsc1 and Tsc2 form the tuberous sclerosis complex (TSC), a regulator of mTOR ac
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
264 alian target of rapamycin (mTOR)-suppressing tuberous sclerosis complex (TSC), comprised of TSC1 and
266 dvances in the neuroimaging of patients with tuberous sclerosis complex (TSC), highlighting its appli
267 R) pathway, most notably those affecting the tuberous sclerosis complex (TSC), lead to aberrant activ
268 reveal new interactions between R2TP and the tuberous sclerosis complex (TSC), pointing to a potentia
269 utations in either of the genes encoding the tuberous sclerosis complex (TSC), TSC1 and TSC2, result
271 tion (eIF4G) pathways in the pathogenesis of tuberous sclerosis complex (TSC)-associated cortical tub
272 stress response REDD1 gene as a mediator of tuberous sclerosis complex (TSC)-dependent mTOR regulati
292 alian target of rapamycin (mTOR) through the tuberous sclerosis complex (TSC1/2 complex), as a new mo
293 due to bi-allelic inactivating mutations in tuberous sclerosis complex (TSC1/TSC2) genes coding for
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
300 d, placebo-controlled study in patients with tuberous sclerosis complex who had SEGA that was growing