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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 27 Feb 2015.

Tuberous sclerosis 1

Tumor Suppressor, TSC1
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. [provided by RefSeq, Jun 2009] (from NCBI)
Top mentioned proteins: TSC2, mTOR, CAN, mTORC1, Akt
Papers on Tumor Suppressor
mTORC1 upregulation via ERK-dependent gene expression change confers intrinsic resistance to MEK inhibitors in oncogenic KRas-mutant cancer cells.
Aoki et al., Kyoto, Japan. In Oncogene, 23 Mar 2015
In agreement with this observation, MEKi induced the expression of negative regulators of mTORC1, including TSC1, TSC2 and Deptor, which occurred more significantly in BRaf-mutant cells than in KRas-mutant cells.
The Retinoblastoma Tumor Suppressor Promotes Efficient Human Cytomegalovirus Lytic Replication.
Kalejta et al., Madison, United States. In J Virol, 18 Mar 2015
UNASSIGNED: The retinoblastoma (Rb) tumor suppressor controls cell cycle, DNA damage, apoptotic, and metabolic pathways.
Disruption of the PHRF1 Tumor Suppressor Network by PML-RARα Drives Acute Promyelocytic Leukemia Pathogenesis.
Atfi et al., Paris, France. In Cell Rep, 11 Mar 2015
UNASSIGNED: PHRF1 functions as an essential component of the TGF-β tumor suppressor pathway by triggering degradation of the homeodomain repressor factor TGIF.
14-3-3ζ Turns TGF-β's Function from Tumor Suppressor to Metastasis Promoter in Breast Cancer by Contextual Changes of Smad Partners from p53 to Gli2.
Yu et al., Houston, United States. In Cancer Cell, 09 Mar 2015
Transforming growth factor β (TGF-β) functions as a tumor suppressor in premalignant cells but as a metastasis promoter in cancer cells.
Cancer-Associated Protein Kinase C Mutations Reveal Kinase's Role as Tumor Suppressor.
Newton et al., San Diego, United States. In Cell, 01 Mar 2015
Protein kinase C (PKC) isozymes have remained elusive cancer targets despite the unambiguous tumor promoting function of their potent ligands, phorbol esters, and the prevalence of their mutations.
BRCA1 and p53 Tumor Suppressor Molecules in Alzheimer's Disease.
Matsuda et al., Nara, Japan. In Int J Mol Sci, Dec 2014
UNASSIGNED: Tumor suppressor molecules play a pivotal role in regulating DNA repair, cell proliferation, and cell death, which are also important processes in the pathogenesis of Alzheimer's disease.
Promotion of Ovarian Follicle Growth following mTOR Activation: Synergistic Effects of AKT Stimulators.
Hsueh et al., Stanford, United States. In Plos One, Dec 2014
Recent studies using oocyte- and granulosa cell-specific deletion of mTOR inhibitor genes TSC1 or TSC2 demonstrated the important role of mTOR signaling in the promotion of ovarian follicle development.
Emerging therapeutic targets in bladder cancer.
Giles et al., United States. In Cancer Treat Rev, Dec 2014
mTOR inhibitors for patients with TSC1 mutations and concomitant targeting of PI3K and MEK represent strategies to block PI3K/AKT/mTOR pathway.
Mechanistic Target of Rapamycin (mTOR) in Tuberous Sclerosis Complex-Associated Epilepsy.
Curatolo, Roma, Italy. In Pediatr Neurol, Dec 2014
BACKGROUND: Tuberous sclerosis complex is a multiorgan disease resulting from a mutation of one of two TSC genes.
Rationale and protocol of the MetNET-1 trial, a prospective, single center, phase II study to evaluate the activity and safety of everolimus in combination with octreotide LAR and metformin in patients with advanced pancreatic neuroendocrine tumors.
Buzzoni et al., In Tumori, Nov 2014
Metformin has recently shown some anti-cancer activity in both in vitro and in vivo studies by its indirect properties to decrease insulin and insulin-like growth factor-1 (IGF-1) levels and by its antitumour effect to promote AMPK activation and consequently inhibition to TSC1-2/mTOR complex.
Coordinated regulation of protein synthesis and degradation by mTORC1.
Manning et al., Boston, United States. In Nature, Oct 2014
Genetic activation of mTORC1 through loss of the tuberous sclerosis complex tumour suppressors, TSC1 or TSC2, or physiological activation of mTORC1 in response to growth factors or feeding resulted in increased NRF1 expression in cells and tissues.
Molecular genetics of clear-cell renal cell carcinoma.
Brugarolas, Dallas, United States. In J Clin Oncol, Jul 2014
Several additional tumor suppressor genes have been identified near the VHL gene, within a region that is frequently deleted in ccRCC on chromosome 3p: SETD2, BAP1, and PBRM1.
Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome.
Manning et al., Boston, United States. In Cell, Mar 2014
Insulin activates mTORC1 through the PI3K-Akt pathway, which inhibits the TSC1-TSC2-TBC1D7 complex (the TSC complex) to turn on Rheb, an essential activator of mTORC1.
The neural crest lineage as a driver of disease heterogeneity in Tuberous Sclerosis Complex and Lymphangioleiomyomatosis.
Stanford et al., Ottawa, Canada. In Front Cell Dev Biol, 2013
The pathological basis of LAM is associated with Tuberous Sclerosis Complex (TSC), a multi-system disorder marked by low-grade tumors in the brain, kidneys, heart, eyes, lung and skin, arising from inherited or spontaneous germ-line mutations in either of the TSC1 or TSC2 genes.
Connection between Tumor Suppressor BRCA1 and PTEN in Damaged DNA Repair.
Matsuda et al., Nara, Japan. In Front Oncol, 2013
The tumor suppressor, phosphatase and tensin homolog on chromosome 10 (PTEN), is a dual-specificity phosphatase, which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI3K activity.
Genome sequencing identifies a basis for everolimus sensitivity.
Solit et al., New York City, United States. In Science, 2012
Targeted sequencing revealed TSC1 mutations in about 8% of 109 additional bladder cancers examined, and TSC1 mutation correlated with everolimus sensitivity.
Tuberous sclerosis complex: genotype/phenotype correlation of retinal findings.
Singh et al., Cleveland, United States. In Ophthalmology, 2012
TSC2 mutations are more frequent in patients with retinal findings than in those without retinal findings.
Identification of TSC1 and TSC2 mutations in Korean patients with tuberous sclerosis complex.
Ki et al., Seoul, South Korea. In Pediatr Neurol, 2012
This study presented that the mutation rate of the TSC1 and TSC2 genes in Korean patients with tuberous sclerosis complex was 100%.
Functional assessment of TSC1 missense variants identified in individuals with tuberous sclerosis complex.
Nellist et al., Rotterdam, Netherlands. In Hum Mutat, 2012
New data confirm finding that the N-terminal region of TSC1 is essential for TSC1 function.
Regulable neural progenitor-specific Tsc1 loss yields giant cells with organellar dysfunction in a model of tuberous sclerosis complex.
Kwiatkowski et al., Boston, United States. In Proc Natl Acad Sci U S A, 2011
TSC brain model provides insights into the pathogenesis and organelle dysfunction of giant cells, as well as epilepsy control in patients with TSC
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