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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 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
Fastest Time to Cancer by Loss of Tumor Suppressor Genes.
New
Wan et al., Irvine, United States. In Bull Math Biol, 23 Nov 2014
With the loss of tumor suppressor gene function known to be responsible for a high percentage of breast and colorectal cancer (and a good fraction of lung cancer and other types as well), it is important to understand how genetic instability can be orchestrated toward carcinogenesis.
The Paracrine Hormone for the GUCY2C Tumor Suppressor, Guanylin, Is Universally Lost in Colorectal Cancer.
New
Waldman et al., Philadelphia, United States. In Cancer Epidemiol Biomarkers Prev, 10 Nov 2014
GUCY2C has emerged as an intestine-specific tumor suppressor controlling epithelial homeostasis through circuits canonically disrupted in cancer.
MiR-23a Functions as a Tumor Suppressor in Osteosarcoma.
New
Yang et al., Wuhan, China. In Cell Physiol Biochem, 08 Nov 2014
Conclusion: We identified miR-23a as a tumor suppressor in osteosarcoma.
DEAR1, a Novel Tumor Suppressor That Regulates Cell Polarity and Epithelial Plasticity.
Review
New
Killary et al., Houston, United States. In Cancer Res, 26 Oct 2014
This review will highlight the role of the novel TRIM protein DEAR1 (annotated as TRIM62) in the regulation of apical-basal polarity and acinar morphogenesis as well as its function as a chromosome 1p35 tumor suppressor and negative regulator of TGFβ-driven epithelial-mesenchymal transition (EMT).
Coordinated regulation of protein synthesis and degradation by mTORC1.
New
Impact
Manning et al., Boston, United States. In Nature, 18 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.
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.
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.
Tumor Suppression and Promotion by Autophagy.
Review
New
Quest et al., Santiago, Chile. In Biomed Res Int, Dec 2013
Specifically, tumor suppressor genes that negatively regulate mTOR, such as PTEN, AMPK, LKB1, and TSC1/2 stimulate autophagy while, conversely, oncogenes that activate mTOR, such as class I PI3K, Ras, Rheb, and AKT, inhibit autophagy, suggesting that autophagy is a tumor suppressor mechanism.
Reassessment of the Role of TSC, mTORC1 and MicroRNAs in Amino Acids-Meditated Translational Control of TOP mRNAs.
New
Meyuhas et al., Jerusalem, Israel. In Plos One, Dec 2013
This mode of regulation involves TSC as knockout of TSC1 or TSC2 rescued TOP mRNAs translation in amino acid-starved cells.
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).
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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