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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.

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, Akt, mTORC1
Papers on Tumor Suppressor
RASSF tumor suppressor gene family: biological functions and regulation.
Review
New
Baksh et al., Edmonton, Canada. In Febs Lett, 19 Sep 2014
Genetic changes through allelic loss and nucleic acid or protein modifications are the main contributors to loss of function of tumor suppressor proteins.
Oxygen sufficiency controls TOP mRNA translation via the TSC-Rheb-mTOR pathway in a 4E-BP-independent manner.
New
Meyuhas et al., Jerusalem, Israel. In J Mol Cell Biol, Jun 2014
This mode of regulation involves TSC and Rheb, as knockout of TSC1 or TSC2 or overexpression of Rheb rescued TOP mRNA translation in oxygen-deprived cells.
Dysregulation of the IGF-I/PI3K/AKT/mTOR signaling pathway in autism spectrum disorders.
Review
New
Li et al., Shanghai, China. In Int J Dev Neurosci, Jun 2014
Tuberous sclerosis complex 1 (TSC1) and TSC2 are upstream regulators of mammalian target of rapamycin (mTOR) and downstream effectors of the PI3K/AKT signaling pathway.
Targeting inhibitors of the tumor suppressor PP2A for the treatment of pancreatic cancer.
New
Sears et al., Durham, United States. In Mol Cancer Res, Jun 2014
Several pathways that have shown to contribute to pancreatic cancer progression are negatively regulated by the tumor suppressor protein phosphatase 2A (PP2A).
BRD7, a tumor suppressor, interacts with p85α and regulates PI3K activity.
New
Cantley et al., Boston, United States. In Mol Cell, May 2014
The unbound p110 protein is unstable, leading to the attenuation of PI3K activity, which suggests how BRD7 could function as a tumor suppressor.
Seeing the forest for the trees: kidney oncogenomes in relation to therapeutic outcomes.
New
Rathmell et al., Chapel Hill, United States. In Clin Cancer Res, May 2014
Oncogenomic analysis of five outliers, who achieved a sustained response with rapalogs, implicates alterations of the TSC1 and mTOR genes and reveals insights into the conserved evolution of tumors.
Mechanism-based treatment in tuberous sclerosis complex.
Review
New
Sahin et al., Boston, United States. In Pediatr Neurol, Apr 2014
BACKGROUND: Tuberous sclerosis complex (TSC) is a genetic multisystem disorder that affects the brain in almost every patient.
Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome.
New
Impact
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.
mTORC1: turning off is just as important as turning on.
New
Impact
Hall et al., Basel, Switzerland. In Cell, Mar 2014
show that mTORC1 deactivation on the lysosome is determined by recruitment of its negative regulator, the tumor suppressor complex TSC1-TSC2.
Monoallelic germline TSC1 mutations are permissive for T lymphocyte development and homeostasis in tuberous sclerosis complex individuals.
New
Mondino et al., Milano, Italy. In Plos One, Dec 2013
We report that, the distribution of peripheral CD4 and CD8 T cell subsets, their cytokine-secretion profile, and responsiveness to in vitro stimulation were largely preserved in TSC subjects with monoallelic TSC1 germline mutations when compared to healthy controls.
Selective anti-cancer agents as anti-aging drugs.
Review
New
Blagosklonny, Buffalo, United States. In Cancer Biol Ther, Dec 2013
Recent groundbreaking discoveries have revealed that IGF-1, Ras, MEK, AMPK, TSC1/2, FOXO, PI3K, mTOR, S6K, and NFκB are involved in the aging process.
Mechanisms regulating neuronal excitability and seizure development following mTOR pathway hyperactivation.
Review
New
Danzer et al., Cincinnati, United States. In Front Mol Neurosci, Dec 2013
Indeed, several causal mutations have been identified in patients with epilepsy, the most prominent of these being mutations in PTEN and tuberous sclerosis complexes 1 and 2 (TSC1, TSC2).
Cumulative haploinsufficiency and triplosensitivity drive aneuploidy patterns and shape the cancer genome.
New
Impact
Elledge et al., Boston, United States. In Cell, Dec 2013
Here, we develop Tumor Suppressor and Oncogene (TUSON) Explorer, a computational method that analyzes the patterns of mutational signatures in tumors and predicts the likelihood that any individual gene functions as a tumor suppressor (TSG) or oncogene (OG).
A tuberous sclerosis complex signalling node at the peroxisome regulates mTORC1 and autophagy in response to ROS.
New
Impact
Walker et al., Houston, United States. In Nat Cell Biol, Oct 2013
We report that the tuberous sclerosis complex (TSC) signalling node, TSC1, TSC2 and Rheb, localizes to peroxisomes, where it regulates mTORC1 in response to reactive oxygen species (ROS).
Prognostic significance of MTOR pathway component expression in neuroendocrine tumors.
New
Impact
Kulke et al., Boston, United States. In J Clin Oncol, Oct 2013
We failed to identify clinical correlations associated with expression of the upstream regulators TSC1, TSC2, AKT, p-AKT, PDPK1, PTEN, PIK3R1, or PIK3CA.
Genome sequencing identifies a basis for everolimus sensitivity.
Impact
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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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