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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 01 Sep 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, mTORC1, CAN, Akt
Papers on Tumor Suppressor
Regulation of mTORC1 by PI3K signaling.
Review
New
Cantley et al., Boston, United States. In Trends Cell Biol, 30 Sep 2015
We focus on how PI3K-dependent activation of Akt and spatial regulation of the tuberous sclerosis complex (TSC) complex (TSC complex) [composed of TSC1, TSC2, and Tre2-Bub2-Cdc16-1 domain family member 7 (TBC1D7)] switches on Rheb at the lysosome, where mTORC1 is activated.
mTORC1 and mTORC2 have largely distinct functions in Purkinje cells.
New
Rüegg et al., Basel, Switzerland. In Eur J Neurosci, 22 Sep 2015
Comparison of mTORC1-deficient Purkinje cells with those deficient for the mTORC1 inhibitor TSC1 revealed a striking overlap in Purkinje cell degeneration and death, which included neurofilamentopathy and reactive gliosis.
The PTEN Tumor Suppressor Forms Homodimers in Solution.
New
Lösche et al., Pittsburgh, United States. In Structure, 19 Sep 2015
UNASSIGNED: As the phosphoinositol-3-kinase antagonist in the PI3K pathway, the PTEN tumor suppressor exerts phosphatase activity on diacylphosphatidylinositol triphosphate in the plasma membrane.
Mammalian target of rapamycin and tuberous sclerosis complex.
Review
New
Wataya-Kaneda, Ōsaka, Japan. In J Dermatol Sci, 31 Aug 2015
TSC is a multiple hamartomas syndrome with epilepsy, autism, mental retardation and hypopigmented macules that are caused by the constitutive activation of mTORC1 resulting from genetic mutation of TSC1 or TSC2.
Transcriptional Regulation of the p16 Tumor Suppressor Gene.
Review
New
Okamoto et al., Fukuoka, Japan. In Anticancer Res, 31 Aug 2015
The p16 tumor suppressor gene encodes a specific inhibitor of cyclin-dependent kinase (CDK) 4 and 6 and is found altered in a wide range of human cancers.
Akt3 promotes prostate cancer proliferation cells through regulation of Akt, B-Raf, & TSC1/TSC2.
New
Chuu et al., Taiwan. In Oncotarget, 10 Aug 2015
Overexpression of AKT3 increased the protein expression of total AKT, phospho-AKT S473, phospho-AKT T308, B-Raf, c-Myc, Skp2, cyclin E, GSK3β, phospho-GSK3β S9, phospho-mTOR S2448, and phospho-p70S6K T421/S424, but decreased TSC1 (tuberous sclerosis 1) and TSC2 (tuberous Sclerosis Complex 2) proteins in PC-3 PCa cells.
Neurological and neuropsychiatric aspects of tuberous sclerosis complex.
New
Impact
de Vries et al., Roma, Italy. In Lancet Neurol, Jul 2015
Mutations in the TSC1 or TSC2 genes lead to disruption of the TSC1-TSC2 intracellular protein complex, causing overactivation of the mammalian target of rapamycin (mTOR) protein complex.
Long-Term Everolimus Treatment in Individuals With Tuberous Sclerosis Complex: A Review of the Current Literature.
Review
New
Zupanc et al., Orange, United States. In Pediatr Neurol, Jul 2015
BACKGROUND: Tuberous sclerosis complex is a genetic disease usually caused by mutations to either TSC1 or TSC2, where its gene products are involved in the inhibition of the mammalian target of rapamycin pathway.
Tuberous sclerosis complex.
Review
New
Ebrahimi-Fakhari et al., Hartford, United States. In Pediatr Clin North Am, Jun 2015
The genetic cause is mutations in the TSC1 gene, found on chromosome 9q34, and TSC2 gene, found on chromosome 16p13.
Chromosome Condensation 1-Like (Chc1L) Is a Novel Tumor Suppressor Involved in Development of Histiocyte-Rich Neoplasms.
New
Wen et al., Toronto, Canada. In Plos One, Dec 2014
Human chromosomal region 13q14 is a deletion hotspot in prostate cancer, multiple myeloma, and chronic lymphocytic leukemia.
Tumor Suppressor WWOX Contributes to the Elimination of Tumorigenic Cells in Drosophila melanogaster.
New
Richards et al., Adelaide, Australia. In Plos One, Dec 2014
Together these results provide a molecular basis for the tumor suppressor functions of WWOX and the better prognosis observed in cancer patients with higher levels of WWOX activity.
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.
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.
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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