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tuberous sclerosis/glutation
A hivatkozás a vágólapra kerül
14 eredmények
Tuberous sclerosis complex neuropathology requires glutamate-cysteine ligase.
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Belépés Regisztrálás
BACKGROUND
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).
p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis.
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Belépés Regisztrálás
p62/sequestosome-1 (SQSTM1) is a multifunctional adaptor protein and autophagic substrate that accumulates in cells with hyperactive mTORC1, such as kidney cells with mutations in the tumor suppressor genes tuberous sclerosis complex (TSC)1 or TSC2. Here we report that p62 is a critical mediator of
Tumors with TSC mutations are sensitive to CDK7 inhibition through NRF2 and glutathione depletion.
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Belépés Regisztrálás
Tuberous sclerosis complex (TSC) is characterized by tumor development in the brain, heart, kidney, and lungs. In TSC tumors, loss of the TSC1/TSC2 protein complex leads to activation of mTORC1 with downstream effects on anabolism and cell growth. Because mTORC1 activation enhances mRNA
Synthetic lethality of combined glutaminase and Hsp90 inhibition in mTORC1-driven tumor cells.
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Belépés Regisztrálás
The mammalian target of rapamycin complex 1 (mTORC1) integrates multiple signals from growth factors, nutrients, and cellular energy status to control a wide range of metabolic processes, including mRNA biogenesis; protein, nucleotide, and lipid synthesis; and autophagy. Deregulation of the mTORC1
Antioxidants in peripheral nerve.
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Oxidative stress and antioxidants have been related in a wide variety of ways with nervous tissue. This review attempts to gather the most relevant information related to a) the antioxidant status in non pathologic nervous tissue; b) the hypothesis and evidence for oxidative stress (considered as
TSC2 Deficiency Unmasks a Novel Necrosis Pathway That Is Suppressed by the RIP1/RIP3/MLKL Signaling Cascade.
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Belépés Regisztrálás
Tuberous sclerosis complex (TSC) is a genetic multiorgan disorder characterized by the development of neoplastic lesions in kidney, lung, brain, heart, and skin. It is caused by an inactivating mutation in tumor suppressor genes coding the TSC1/TSC2 complex, resulting in the hyperactivation of mTOR-
High-throughput drug screen identifies chelerythrine as a selective inducer of death in a TSC2-null setting.
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Belépés Regisztrálás
Tuberous sclerosis complex (TSC) is an autosomal dominant syndrome associated with tumors of the brain, heart, kidney, and lung. The TSC protein complex inhibits the mammalian or mechanistic target of rapamycin complex 1 (mTORC1). Inhibitors of mTORC1, including rapamycin, induce a cytostatic
14-3-3 interacts with the tumor suppressor tuberin at Akt phosphorylation site(s).
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Tuberin, the product of the tuberous sclerosis complex 2 tumor suppressor gene, is a phosphoprotein that negatively regulates phosphatidylinositol 3'-kinase signaling downstream of Akt. Several high stringency 14-3-3 binding sites that overlapped with Akt phosphorylation sites were identified in
mTORC1-Driven Tumor Cells Are Highly Sensitive to Therapeutic Targeting by Antagonists of Oxidative Stress.
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mTORC1 is a central signaling node in controlling cell growth, proliferation, and metabolism that is aberrantly activated in cancers and certain cancer-associated genetic disorders, such as tuberous sclerosis complex (TSC) and sporadic lymphangioleiomyomatosis. However, while mTORC1-inhibitory
Changes in gene expression during chemical-induced nephrocarcinogenicity in the Eker rat.
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Hydroquinone (HQ) is a rodent carcinogen and a potential human carcinogen. Glutathione conjugation of HQ enhances its biological reactivity, and 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ) is a potent nephrotoxicant and nephrocarcinogen in the Eker rat. Moreover, a single exposure of primary
Lithium promotes the production of reactive oxygen species via GSK-3β/TSC2/TOR signaling in the gill of zebrafish (Danio rerio).
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In this study, the mechanism that lithium (Li) promotes the production of reactive oxygen species (ROS) via the glycogen synthase kinase-3β (GSK-3β)/tuberous sclerosis complex 2 (TSC2)/target of rapamycin (TOR) signaling was investigated in the gill of zebrafish (Danio rerio). After the zebrafish
Impairment of gamma-glutamyl transferase 1 activity in the metabolic pathogenesis of chromophobe renal cell carcinoma.
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Chromophobe renal cell carcinoma (ChRCC) accounts for 5% of all sporadic renal cancers and can also occur in genetic syndromes including Birt-Hogg-Dube (BHD) and tuberous sclerosis complex (TSC). ChRCC has a distinct accumulation of abnormal mitochondria, accompanied by characteristic chromosomal
Frenolicin B Targets Peroxiredoxin 1 and Glutaredoxin 3 to Trigger ROS/4E-BP1-Mediated Antitumor Effects.
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Belépés Regisztrálás
Peroxiredoxin 1 (Prx1) and glutaredoxin 3 (Grx3) are two major antioxidant proteins that play a critical role in maintaining redox homeostasis for tumor progression. Here, we identify the prototypical pyranonaphthoquinone natural product frenolicin B (FB) as a selective inhibitor of Prx1 and Grx3
AMP-activated protein kinase signalling pathways are down regulated and skeletal muscle development impaired in fetuses of obese, over-nourished sheep.
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Belépés Regisztrálás
Maternal obesity and over-nutrition give rise to both obstetric problems and neonatal morbidity. The objective of this study was to evaluate effects of maternal obesity and over-nutrition on signalling of the AMP-activated protein kinase (AMPK) pathway in fetal skeletal muscle in an obese pregnant
A legteljesebb gyógynövény-adatbázis, amelyet a tudomány támogat
- Működik 55 nyelven
- A tudomány által támogatott gyógynövényes kúrák
- Gyógynövények felismerése kép alapján
- Interaktív GPS térkép - jelölje meg a gyógynövényeket a helyszínen (hamarosan)
- Olvassa el a keresésével kapcsolatos tudományos publikációkat
- Keresse meg a gyógynövényeket hatásuk szerint
- Szervezze meg érdeklődését, és naprakész legyen a hírkutatással, a klinikai vizsgálatokkal és a szabadalmakkal
Írjon be egy tünetet vagy betegséget, és olvassa el azokat a gyógynövényeket, amelyek segíthetnek, beírhat egy gyógynövényt, és megtekintheti azokat a betegségeket és tüneteket, amelyek ellen használják.
* Minden információ publikált tudományos kutatáson alapul
