TSC1 Stabilizes TSC2 by Inhibiting the Interaction between TSC2 and the HERC1 Ubiquitin Ligase [PDF]
Journal of Biological Chemistry, 2006 Tuberous sclerosis complex (TSC) is an autosomal dominant disease characterized by hamartoma formation in various organs. Two genes responsible for the disease, TSC1 and TSC2, have been identified. The TSC1 and TSC2 proteins, also called hamartin and tuberin, respectively, have been shown to regulate cell growth through inhibition of the mammalian ...
Chong-Kopera, Huira +6 more
openaire +5 more sources
Lymphangioleiomyomatosis and TSC2 -/- Cells [PDF]
Lymphatic Research and Biology, 2010 The cells comprising pulmonary lymphangioleiomyomatosis (LAM) and renal angiomyolipomas (AMLs) are heterogeneous, with variable mixtures of cells exhibiting differentiation towards smooth muscle, fat, and vessels. Cells grown from LAM and AMLs have likewise tended to be heterogeneous.
T. N. Darling +5 more
openaire +3 more sources
Regulation of TSC2 lysosome translocation and mitochondrial turnover by TSC2 acetylation status
Scientific ReportsAbstractSirtuin1 (SIRT1) activity decreases the tuberous sclerosis complex 2 (TSC2) lysine acetylation status, inhibiting the mechanistic target of rapamycin complex 1 (mTORC1) signalling and concomitantly, activating autophagy. This study analyzes the role of TSC2 acetylation levels in its translocation to the lysosome and the mitochondrial turnover ...
Patricia Marqués +8 more
core +7 more sources
The Methylation of the TSC2 Promoter Underlies the Abnormal Growth of TSC2 Angiomyolipoma-Derived Smooth Muscle Cells [PDF]
The American Journal of Pathology, 2009 Tuberous sclerosis complex (TSC) is an autosomal-dominant disease that is caused by mutations in either the TSC1 or TSC2 gene. Smooth muscle-like cells (ASMs) were isolated from an angiomyolipoma of a patient with TSC. These cells lacked tuberin, were labeled by both HMB45 and CD44v6 antibodies, and had constitutive S6 phosphorylation. The cells bear a
E. Lesma +8 more
openaire +5 more sources
TSC2 (tuberous sclerosis 2) [PDF]
Atlas of Genetics and Cytogenetics in Oncology and Haematology, 2011 Review on TSC2 (tuberous sclerosis 2), with data on DNA, on the protein encoded, and where the gene is implicated.
A Astrinidis, Henske E Petri
openaire +2 more sources
Heterozygous inactivation of tsc2 enhances tumorigenesis in p53 mutant zebrafish
Disease Models & Mechanisms, 2013 SUMMARY Tuberous sclerosis complex (TSC) is a multi-organ disorder caused by mutations of the TSC1 or TSC2 genes. A key function of these genes is to inhibit mTORC1 (mechanistic target of rapamycin complex 1) kinase signaling. Cells deficient for TSC1 or
Seok-Hyung Kim +4 more
doaj +2 more sources
Aquaculture ReportsThis study was performed to evaluate the role of TSC2 (tuberous sclerosis complex 2) in the regulation of growth inhibition of fish exposed to chronic ammonia nitrogen.
Xiangyang Yuan +6 more
doaj +2 more sources
Loss of myeloid Tsc2 predisposes to angiotensin II-induced aortic aneurysm formation in mice
Cell Death and Disease, 2022 Rationale Genetic studies have proved the involvement of Tuberous sclerosis complex subunit 2 (Tsc2) in aortic aneurysm. However, the exact role of macrophage Tsc2 in the vascular system remains unclear.
Xue Liu +4 more
doaj +1 more source
p38 regulates the tumor suppressor PDCD4 via the TSC-mTORC1 pathway
Cell Stress, 2021 Programmed cell death protein 4 (PDCD4) exerts critical functions as tumor suppressor and in immune cells to regulate inflammatory pro-cesses. The phosphoinositide 3-kinase (PI3K) promotes degradation of PDCD4 via mammalian target of rapamycin complex 1 (
Clarissa Braun +6 more
doaj +1 more source
Tsc2 shapes olfactory bulb granule cell molecular and morphological characteristics
Frontiers in Molecular Neuroscience, 2022 Tuberous Sclerosis Complex (TSC) is a neurodevelopmental disorder caused by mutations that inactivate TSC1 or TSC2. Hamartin and tuberin are encoded by TSC1 and TSC2 which form a GTPase activating protein heteromer that inhibits the Rheb GTPase from ...
Victoria A. Riley +3 more
doaj +1 more source