Results 41 to 50 of about 23,999 (238)

Hypomyelination following deletion of Tsc2 in oligodendrocyte precursors [PDF]

open access: yesAnnals of Clinical and Translational Neurology, 2015
AbstractObjectiveWhile abnormalities in myelin in tuberous sclerosis complex (TSC) have been known for some time, recent imaging‐based data suggest myelin abnormalities may be independent of the pathognomonic cortical lesions (“tubers”). Multiple mouse models of TSC exhibit myelination deficits, though the cell types responsible and the mechanisms ...
Carson, Robert P.   +9 more
openaire   +2 more sources

Hypoxia-inducible factor-1α polymorphisms and TSC1/2 mutations are complementary in head and neck cancers

open access: yesMolecular Cancer, 2006
Background Polymorphisms or mutations in hypoxia inducible factor-1 alpha (HIF-1alpha) that increases its activity and stability under normoxia have recently been identified.
Nikitakis Nikolaos G   +5 more
doaj   +1 more source

Exosomes originating from neural stem cells undergoing necroptosis participate in cellular communication by inducing TSC2 upregulation of recipient cells following spinal cord injury

open access: yesNeural Regeneration Research
We previously demonstrated that inhibiting neural stem cells necroptosis enhances functional recovery after spinal cord injury. While exosomes are recognized as playing a pivotal role in neural stem cells exocrine function, their precise function in ...
Shiming Li   +7 more
doaj   +1 more source

Exome sequencing of Saudi Arabian patients with ADPKD

open access: yesRenal Failure, 2019
Purpose: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive development of kidney cysts and enlargement and dysfunction of the kidneys. The Consortium of Radiologic Imaging Studies of the Polycystic Kidney Disease (CRISP)
Fahad A. Al-Muhanna   +19 more
doaj   +1 more source

Upregulation of acid ceramidase contributes to tumor progression in tuberous sclerosis complex

open access: yesJCI Insight, 2023
Tuberous sclerosis complex (TSC) is characterized by multisystem, low-grade neoplasia involving the lung, kidneys, brain, and heart. Lymphangioleiomyomatosis (LAM) is a progressive pulmonary disease affecting almost exclusively women.
Aristotelis Astrinidis   +23 more
doaj   +1 more source

Hepatoma‐Derived Growth Factor Coordinates STAT3 Pathway and Exosome‐Mediated Intrahepatic Crosstalk to Control Hepatic Steatosis and MASLD

open access: yesAdvanced Science, EarlyView.
Hepatic HDGF as a key mediator in coordinating hepatic steatosis and intrahepatic crosstalk in MASLD. Activation of HDGF facilitates its interaction with both STAT3 and S6K1, driving the S6K1‐dependent STAT3 phosphorylation and subsequently enhancing hepatic lipogenesis.
Jian Wen   +28 more
wiley   +1 more source

TSC2 N-terminal lysine acetylation status affects to its stability modulating mTORC1 signaling and autophagy

open access: yes, 2016
There is a growing evidence of the role of protein acetylation in different processes controlling metabolism. Sirtuins (histone deacetylases nicotinamide adenine dinucleotide-dependent) activate autophagy playing a protective role in cell homeostasis ...
Bartolome, A   +9 more
core   +2 more sources

Rapamycin-insensitive up-regulation of adipocyte phospholipase A2 in tuberous sclerosis and lymphangioleiomyomatosis. [PDF]

open access: yesPLoS ONE, 2014
Tuberous sclerosis syndrome (TSC) is an autosomal dominant tumor suppressor gene syndrome affecting multiple organs, including renal angiomyolipomas and pulmonary lymphangioleiomyomatosis (LAM).
Chenggang Li   +10 more
doaj   +1 more source

Renal organoid modeling of tuberous sclerosis complex reveals lesion features arise from diverse developmental processes

open access: yesCell Reports, 2022
Summary: Tuberous sclerosis complex (TSC) is a multisystem tumor-forming disorder caused by loss of TSC1 or TSC2. Renal manifestations predominately include cysts and angiomyolipomas. Despite a well-described monogenic etiology, the cellular pathogenesis
Adam Pietrobon   +3 more
doaj   +1 more source

mTORC2 Phosphorylation of GSDME‐N Drives Cullin4B‐Mediated Proteasomal Degradation to Suppress Pyroptosis and Confer Radioresistance in Small Cell Lung Cancer

open access: yesAdvanced Science, EarlyView.
Radioresistance severely limits the efficacy of therapies for small cell lung cancer (SCLC). This study reveals a novel mechanism of resistance driven by the active suppression of pyroptosis. Specifically, the mTORC2 complex directly phosphorylates GSDME‐N and promotes its CUL4B‐mediated ubiquitination and proteasomal degradation.
Qing‐qing Xu   +11 more
wiley   +1 more source

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