نتایج جستجو برای: tuberous sclerosis complex tsc

تعداد نتایج: 845362  

2015
Maria M. Alves Gwenny M. Fuhler Karla C.S. Queiroz Jetse Scholma Susan Goorden Jasper Anink C. Arnold Spek Marianne Hoogeveen-Westerveld Marco J. Bruno Mark Nellist Ype Elgersma Eleonora Aronica Maikel P. Peppelenbosch

Tuberous sclerosis complex (TSC) is caused by inactivating mutations in either TSC1 or TSC2 and is characterized by uncontrolled mTORC1 activation. Drugs that reduce mTOR activity are only partially successful in the treatment of TSC, suggesting that mTOR-independent pathways play a role in disease development. Here, kinome profiles of wild-type and Tsc2(-/-) mouse embryonic fibroblasts (MEFs) ...

Journal: :Clinical genetics 2012
M E Black S S Hedgire S Camposano E Paul M Harisinghani E A Thiele

Hepatic manifestations of tuberous sclerosis complex: a genotypic and phenotypic analysis. A retrospective review of the clinical records and radiological images of 205 patients with tuberous sclerosis complex (TSC) was performed to evaluate the prevalence and progression of hepatic lesions; examine the association of hepatic phenotype with genotype, age, and gender; and investigate the relatio...

2017
Tanjala T Gipson Michael V Johnston

Tuberous sclerosis complex (TSC) is a multi-system disorder resulting from mutations in either the TSC1 or TSC2 genes leading to hyperactivation of mechanistic target of rapamycin (mTOR) signaling. TSC is commonly associated with autism (61%), intellectual disability (45%), and behavioral, psychiatric, intellectual, academic, neuropsychological, and psychosocial difficulties that are collective...

2015
Anna R. Malik Ewa Liszewska Agnieszka Skalecka Malgorzata Urbanska Anand M. Iyer Lukasz J. Swiech Malgorzata Perycz Kamil Parobczak Patrycja Pietruszka Malgorzata M. Zarebska Matylda Macias Katarzyna Kotulska Julita Borkowska Wieslawa Grajkowska Magdalena E. Tyburczy Sergiusz Jozwiak David J. Kwiatkowski Eleonora Aronica Jacek Jaworski

INTRODUCTION Tuberous sclerosis complex (TSC) is a genetic disease resulting from mutation in TSC1 or TSC2 and subsequent hyperactivation of mammalian Target of Rapamycin (mTOR). Common TSC features include brain lesions, such as cortical tubers and subependymal giant cell astrocytomas (SEGAs). However, the current treatment with mTOR inhibitors has critical limitations. We aimed to identify ne...

Journal: :Nature communications 2011
Shaowei Li Rajesh L Thangapazham Ji-An Wang Sangeetha Rajesh Tzu-Cheg Kao Leonard Sperling Joel Moss Thomas N Darling

Hamartomas are composed of cells native to an organ but abnormal in number, arrangement or maturity. In the tuberous sclerosis complex (TSC), hamartomas develop in multiple organs because of mutations in TSC1 or TSC2. Here we show that TSC2-null fibroblast-like cells grown from human TSC skin hamartomas induced normal human keratinocytes to form hair follicles and stimulated hamartomatous chang...

Journal: :Diagnostic and interventional radiology 2007
Anjumara Bora Abhijit Soni Nisha Sainani Deepak Patkar

Angiomyolipomas (AMLs) are hamartomatous lesions consisting of abnormal blood vessels, smooth muscle, and adipose tissue. Bilateral AMLs invariably point to a diagnosis of tuberous sclerosis complex (TSC). The risk of hemorrhage in AML is related to tumor size, growth of the tumor, hypervascularization, presence of aneurysms, and association with TSC. We report a case of a young male who presen...

Journal: :Epilepsy currents 2014
Michael Wong

Commentary The mammalian target of rapamycin (mTOR) is a ubiquitous protein kinase that has received extensive attention in recent years as a potential mediator of epilepsy. mTOR, particularly a specific complex of proteins called mTORC1, regulates numerous cellular and physiologic functions, including protein synthesis , cell growth, proliferation, autophagy, and metabolism. Abnormal regulatio...

Journal: :Genes & development 2004
Michael N Corradetti Ken Inoki Nabeel Bardeesy Ronald A DePinho Kun-Liang Guan

Tuberous sclerosis complex (TSC) and Peutz-Jeghers syndrome (PJS) are dominantly inherited benign tumor syndromes that share striking histopathological similarities. Here we show that LKB1, the gene mutated in PJS, acts as a tumor suppressor by activating TSC2, the gene mutated in TSC. Like TSC2, LKB1 inhibits the phosphorylation of the key translational regulators S6K and 4EBP1. Furthermore, w...

2011
Tomihiro Wakamiya Yasuo Sugita Mariko Hashiguchi Tsuyoshi Iwasaka Osamu Tokunaga

Tuberous sclerosis complex (TSC) is associated with benign and malignant tumors, including lymphangioleiomyomatosis (LAM) and angiomyolipoma (AML). We herein describe the TSC case of a 50-year-old woman having a papillary serous carcinoma of the peritoneum (PSCP), LAM, and AML. On microscopic examination, the PSCP cells showed a cuboidal to columnar shape, proliferated into the papillae, and in...

Journal: :Cell reports 2015
Uk Yeol Moon Jun Young Park Raehee Park Jennifer Y Cho Lucinda J Hughes James McKenna Laura Goetzl Seo-Hee Cho Peter B Crino Michael J Gambello Seonhee Kim

Tuberous sclerosis complex (TSC) is associated with neurodevelopmental abnormalities, including defects in neuronal migration. However, the alterations in cell signaling mechanisms critical for migration and final positioning of neurons in TSC remain unclear. Our detailed cellular analyses reveal that reduced Tsc2 in newborn neurons causes abnormalities in leading processes of migrating neurons...

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