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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

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
A Phase I Trial of Temsirolimus and Pemetrexed in Patients with Advanced Non-Small Cell Lung Cancer.
Govindan et al., In Chemotherapy, Feb 2016
This combination may be further evaluated in patients with mTOR pathway activation, particularly in those with TSC1 or STK11 mutations.
Lymphangioleiomyomatosis: Current understanding and potential treatments.
Moir, Sydney, Australia. In Pharmacol Ther, Jan 2016
UNASSIGNED: Lymphangioleiomyomatosis (LAM) is a rare neoplastic disease affecting predominantly young women.
A Tumor Suppressor Function for Notch Signaling in Forebrain Tumor Subtypes.
Taylor et al., Basel, Switzerland. In Cancer Cell, Jan 2016
Here, we identify an unexpected tumor suppressor function for Notch in forebrain tumor subtypes.
Discovery of 2-(1H-indol-5-ylamino)-6-(2,4-difluorophenylsulfonyl)-8-methylpyrido[2,3-d]pyrimidin-7(8H)-one (7ao) as a potent selective inhibitor of Polo like kinase 2 (PLK2).
Reddy et al., New York City, United States. In Bioorg Med Chem, Jan 2016
PLK2 (SNK), which is highly homologous to PLK1, has been shown to play a critical role in centriole duplication and is also believed to play a regulatory role in the survival pathway by physically stabilizing the TSC1/2 complex in tumor cells under hypoxic conditions.
Loss of Tumor Suppressor ARID1A Protein Expression Correlates with Poor Prognosis in Patients with Primary Breast Cancer.
Lee et al., Ch'┼Ćnan, South Korea. In J Breast Cancer, Dec 2015
PURPOSE: Somatic mutations of the chromatin remodeling AT-rich interactive domain 1A (SWI-like) gene (ARID1A) have been identified in many human cancers, including breast cancer.
Mammalian Target of Rapamycin Inhibitors and Life-Threatening Conditions in Tuberous Sclerosis Complex.
Curatolo et al., Roma, Italy. In Semin Pediatr Neurol, Dec 2015
In the last decades, there has been a great progress in understanding the pathophysiology of TSC-related manifestations, which are mainly linked to the hyperactivation of the so-called mammalian target of rapamycin (mTOR) pathway, as a consequence of the mutation in 1 of the 2 genes TSC1 or TSC2.
Genotype/Phenotype Correlations in Tuberous Sclerosis Complex.
Graziola et al., Roma, Italy. In Semin Pediatr Neurol, Dec 2015
TSC is caused by the mutation in one of the 2 genes TSC1, at 9q34, and TSC2, at 16p13.3.
Loss of Mitochondrial Tumor Suppressor Genes Expression Is Associated with Unfavorable Clinical Outcome in Head and Neck Squamous Cell Carcinoma: Data from Retrospective Study.
Kayani et al., Islamabad, Pakistan. In Plos One, Dec 2015
A family of orthologues of yeast silent information regulator 3 (SIRT3), 4 (SIRT4) and mitochondrial tumor suppressor 1 (MTUS1) are important mitochondrial tumor suppressor genes which play an important role in the progression of multiple cancers.
Leukemia inhibitory factor (LIF) withdrawal activates mTOR signaling pathway in mouse embryonic stem cells through the MEK/ERK/TSC2 pathway.
Pospelov et al., Saint Petersburg, Russia. In Cell Death Dis, Dec 2015
LIF removal strongly activates ERK activity indicating that ERK can be involved in either direct phosphorylation of mTOR or phosphorylation of an upstream negative regulator of mTOR - TSC1/TSC2 proteins.
hnRNP K Is a Haploinsufficient Tumor Suppressor that Regulates Proliferation and Differentiation Programs in Hematologic Malignancies.
Post et al., Houston, United States. In Cancer Cell, Nov 2015
Together, these data implicate hnRNP K in the development of hematological disorders and suggest hnRNP K acts as a tumor suppressor.
Neurological and neuropsychiatric aspects of tuberous sclerosis complex.
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.
Transducer of ERBB2.1 (TOB1) as a Tumor Suppressor: A Mechanistic Perspective.
Shin et al., Seoul, South Korea. In Int J Mol Sci, 2014
As most of the other tumor suppressor proteins, TOB1 is inactivated in many human cancers.
Studies of Tumor Suppressor Genes via Chromosome Engineering.
Oshimura et al., Yonago, Japan. In Cancers (basel), 2014
The development and progression of malignant tumors likely result from consecutive accumulation of genetic alterations, including dysfunctional tumor suppressor genes.
Coordinated regulation of protein synthesis and degradation by mTORC1.
Manning et al., Boston, United States. In Nature, 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, 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.
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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