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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 11 Dec 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
LPTS: A Novel Tumor Suppressor Gene and a Promising Drug Target for Cancer Intervention.
New
Liu et al., Chongqing, China. In Recent Pat Anticancer Drug Discov, 04 Jan 2015
UNLABELLED: Liver-related putative tumor suppressor(lpts) is a liver-related tumor suppressor candidate gene initially isolated by positional candidate cloning method.
Surfactant Dysfunction and Lung Inflammation in the Female Mouse Model of Lymphangioleiomyomatosis (LAM).
New
Krymskaya et al., Philadelphia, United States. In Am J Respir Cell Mol Biol, 04 Jan 2015
UNLABELLED: Pulmonary lymphangioleiomyomatosis (LAM) is a rare lung disease caused by mutations of the tumor suppressor genes Tuberous Sclerosis Complex (TSC1 or TSC2).
Inhibition of Pluripotency Networks by the Rb Tumor Suppressor Restricts Reprogramming and Tumorigenesis.
New
Impact
Wernig et al., Stanford, United States. In Cell Stem Cell, 13 Dec 2014
UNLABELLED: Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human cancer.
Comparison of Akt/mTOR/4E-BP1 pathway signal activation and mutations of PIK3CA in Merkel cell polyomavirus-positive and Merkel cell polyomavirus-negative carcinomas.
New
Hayashi et al., Tottori, Japan. In Hum Pathol, 23 Nov 2014
Expression of mTOR, TSC1, and TSC2 messenger RNA was significantly higher in MCPyV-negative MCCs, and Akt (T308) phosphorylation also was significantly higher (92% vs 66%; P = .019),
Coordinated regulation of protein synthesis and degradation by mTORC1.
New
Impact
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.
New
Impact
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.
Targeting the genetic alterations of the PI3K-AKT-mTOR pathway: Its potential use in the treatment of bladder cancers.
Review
New
Pourquier et al., Nîmes, France. In Pharmacol Ther, Jul 2014
Despite the recent pivotal study evidencing specific mutations of TSC1 in bladder cancer patients responding to everolimus and the encouraging results obtained with other derivatives than rapalogs, few clinical trials are ongoing in bladder cancers.
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.
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.
MiR-32 Functions as a Tumor Suppressor and Directly Targets EZH2 in Human Oral Squamous Cell Carcinoma.
New
Xiao et al., Wenzhou, China. In Med Sci Monit, Dec 2013
Conclusions These findings indicate that miR-32 may act as a tumor suppressor in OSCC and could serve as a novel therapeutic agent for miR-based therapy.
RTP801/REDD1: a stress coping regulator that turns into a troublemaker in neurodegenerative disorders.
Review
New
Malagelada et al., Barcelona, Spain. In Front Cell Neurosci, Dec 2013
Although the mechanism is not completely understood, RTP801 inactivates mTOR and Akt via the tuberous sclerosis complex (TSC1/TSC2) in many cellular contexts.
Genetic Modeling of PIM Proteins in Cancer: Proviral Tagging and Cooperation with Oncogenes, Tumor Suppressor Genes, and Carcinogens.
Review
New
Blanco-Aparicio et al., Madrid, Spain. In Front Oncol, Dec 2013
The PIM proteins, which were initially discovered as proviral insertion sites in Moloney-murine leukemia virus infection, are a family of highly homologous serine/threonine kinases that have been reported to be overexpressed in hematological malignancies and solid tumors.
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).
Connection between Tumor Suppressor BRCA1 and PTEN in Damaged DNA Repair.
Review
New
Matsuda et al., Nara, Japan. In Front Oncol, Dec 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.
[Subependymal Giant Cell Astrocytoma Associated with Tuberous Sclerosis Complex -  Pharmacological Treatment using mTOR Inhibitors.]
New
Zitterbart, In Klin Onkol, Dec 2013
UNLABELLED: Tuberous sclerosis complex is a neurocutaneous syndrome that results from a germline mutation in TSC1 or TSC2 genes.
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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