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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
Authors' reply.
Bensussan et al., Paris, France. In Am J Pathol, 30 Apr 2015
This Correspondence is a Reply to Lack of Evidence that HACE1 Is Not a Tumor Suppressor Gene in Natural Killer/T-Cell Lymphoma by Küçük et al.
Lack of Evidence that HACE1 Is Not a Tumor Suppressor Gene in NKTCL: To the Editor-in-Chief.
Chan et al., Duarte, United States. In Am J Pathol, 30 Apr 2015
This Correspondence relates to the article by Sako et al (HACE1, a Potential Tumor Suppressor Gene on 6q21, Is Not Involved in Extranodal Natural Killer/T-Cell Lymphoma Pathophysiology.
Loss of Leucine Zipper Putative Tumor Suppressor 1 (LZTS1) Expression Contributes to Lymph Node Metastasis of Breast Invasive Micropapillary Carcinoma.
Fu et al., Beijing, China. In Pathol Oncol Res, 27 Apr 2015
Expression of leucine zipper putative tumor suppressor 1 (LZTS1) was frequently lost or reduced in breast cancer tissues.
Emerging therapeutic targets in bladder cancer.
Giles et al., United States. In Cancer Treat Rev, 28 Feb 2015
mTOR inhibitors for patients with TSC1 mutations and concomitant targeting of PI3K and MEK represent strategies to block PI3K/AKT/mTOR pathway.
Hepatocyte Nuclear Factor 1A (HNF1A) as a Possible Tumor Suppressor in Pancreatic Cancer.
Li et al., Houston, United States. In Plos One, Dec 2014
CONCLUSION: These observations provide experimental evidence supporting a possible tumor suppressor role of HNF1A in pancreatic cancer.
A Genome-Wide siRNA Screen in Mammalian Cells for Regulators of S6 Phosphorylation.
Avruch et al., Cambridge, United States. In Plos One, Dec 2014
We next examined the effect of RNAi pools directed at 534 of these gene products on S6-P in TSC1 null mouse embryo fibroblasts.
IGF-Binding Protein 2 - Oncogene or Tumor Suppressor?
McCance et al., Belfast, United Kingdom. In Front Endocrinol (lausanne), Dec 2014
However, there are a number of conflicting reports in vitro and in vivo where IGFBP2 acts in a tumor suppressor manner.
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.
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.
mTORC1: turning off is just as important as turning on.
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.
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.
Cumulative haploinsufficiency and triplosensitivity drive aneuploidy patterns and shape the cancer genome.
Elledge et al., Boston, United States. In Cell, 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.
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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