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Tsc1 is involved in regulation of interactive network between the cilium and the TOR pathway.
The mTOR (show FRAP1 Proteins)-dependent, epithelial phenotype of TSC (show SLC12A3 Proteins) astrocytes suggests TSC1/2 and mTOR (show FRAP1 Proteins) tune the phosphorylation level of catenin delta-1 (show CTNND1 Proteins) by controlling PKCe (show PRKCE Proteins) activity, thereby regulating the mesenchymal-epithelial-transition (MET)
We conditionally ablated the tuberous sclerosis complex 1 (Tsc1) gene, an mTOR (show FRAP1 Proteins) inhibitor, in the rods of the Pde6b (show PDE6B Proteins)(H620Q/H620Q) preclinical RP mouse model and observed, functionally and morphologically, an improvement in the survival of rods and cones at early and late disease stages.
TSC1 mutations leading to tuberous sclerosis in Chinese children.
Our results indicate that TSC2 and less commonly TSC1 alterations are the primary essential driver event in angiomyolipoma/Lymphangioleiomyomatosis, whereas other somatic mutations are rare and likely do not contribute to tumor development.
brain somatic mutations in TSC1 and TSC2 cause focal cortical dysplasia
TSC1 expression is reduced in two subsets of clear-cell renal cell carcinomas, those with monoallelic VHL (show VHL Proteins) gene inactivation and those with concurrent low HIF-1alpha (show HIF1A Proteins) and high HIF-2alpha (show EPAS1 Proteins) expression.
Repression of TSC1/TSC2 mediated by MeCP2 (show MECP2 Proteins) regulates human embryo lung fibroblast cell differentiation and proliferation.
TSC1 mutation is associated in patients, diagnosed with tuberous sclerosis associated vascular malformation.
Novel TSC1 mutations in Chinese patients with tuberous sclerosis.
Gene expression level of TSC1 is significantly higher in AD patients when compared to normal controls.
suppression of AKT (show AKT1 Proteins) by hyperactivation of mTORC1, inhibition on nuclear ERalpha (show ESR1 Proteins) signaling, and down-regulation of cell-cycle-driving proteins play important roles in the retarded mammary development induced by Tsc1 deletion.
TSC1 knockout mice are lean, glucose intolerant with a decreased activation of protein kinase B (Akt/PKB (show AKT1 Proteins)) targets that regulate glucose transporters in skeletal muscle.
a pivotal role for Tsc1 in regulating various aspects of visual-pathway development, is reported.
PAK2 (show PAK2 Proteins) is a direct effector of TSC1-TSC2-RHEB (show RHEB Proteins) signaling and a new target for rational drug therapy in TSC (show SLC12A3 Proteins).
Tsc1 plays a critical role in regulating macrophage survival, function and polarization via inhibition of mTORC1 activity.
TSC1-KO results in the accumulation of transitional-1 B cells and progressive losses of B cells as they mature beyond the T1 stage. However, Peyer's patch germinal centers are unimpaired in TSC1-KO mice.
TSC1 deletion led to enhanced mTORC1 signaling in neural crest derived bones and the increase in bone formation is responsible for the aberrantly increased bone mass.
Results describe the development of new vascular mouse model with a conditional knockout allele of Tsc1 with a Darpp32 (show PPP1R1B Proteins)-Cre allele. This mouse displayed accelerated formation of both kidney cystadenomas and paw hemangiosarcomas.
PLK1 protein levels are increased in hamartin and tuberin deficient cells and Lymphangioleiomyomatosis patient-derived specimens, and that this increase is rapamycin-sensitive.
This gene encodes a growth inhibitory protein thought to play a role in the stabilization of tuberin. Mutations in this gene have been associated with tuberous sclerosis. Alternative splicing results in multiple transcript variants.
tuberous sclerosis 1 protein
, tuberous sclerosis 1
, tumor suppressor
, tuberous sclerosis 1 protein homolog
, chromosome 9 TSC1