Results 71 to 80 of about 257,231 (311)

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

open access: yesMolecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni   +11 more
wiley   +1 more source

Safety Profile of Rapamycin Perfluorocarbon Nanoparticles for Preventing Cisplatin-Induced Kidney Injury

open access: yesNanomaterials, 2022
Cancer treatment-induced toxicities may restrict maximal effective dosing for treatment and cancer survivors’ quality of life. It is critical to develop novel strategies that mitigate treatment-induced toxicity without affecting the efficacy of anti ...
Qingyu Zhou   +10 more
doaj   +1 more source

Macrophage autophagy in atherosclerosis [PDF]

open access: yes, 2013
Macrophages play crucial roles in atherosclerotic immune responses. Recent investigation into macrophage autophagy (AP) in atherosclerosis has demonstrated a novel pathway through which these cells contribute to vascular inflammation.
Carnuccio, R.   +5 more
core   +2 more sources

Total Synthesis of Rapamycin

open access: yesAngewandte Chemie International Edition, 2007
AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.
Maddess, M   +7 more
openaire   +3 more sources

Rapamycin decelerates cellular senescence [PDF]

open access: yesCell Cycle, 2009
When the cell cycle is arrested but cellular growth is not, then cells senesce, permanently losing proliferative potential. Here we demonstrated that the duration of cell cycle arrest determines a progressive loss of proliferative capacity. In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative ...
Zoya N, Demidenko   +5 more
openaire   +2 more sources

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov   +3 more
wiley   +1 more source

Liuwei Dihuang Pills Inhibit Podocyte Injury and Alleviate IgA Nephropathy by Directly Altering Mesangial Cell-Derived Exosome Function and Secretion

open access: yesFrontiers in Pharmacology, 2022
Background: Immunoglobulin A nephropathy (IgAN) is the most common glomerular disease worldwide. Its pathological features include IgA immune complex deposition, accompanied by mesangial cell proliferation and mesangial matrix expansion.
Xiaodong Zhu   +6 more
doaj   +1 more source

Ornithine Decarboxylase mRNA is Stabilized in an mTORC1-dependent Manner in Ras-transformed Cells [PDF]

open access: yes, 2012
Upon Ras activation, ODC (ornithine decarboxylase) is markedly induced, and numerous studies suggest that ODC expression is controlled by Ras effector pathways. ODC is therefore a potential target in the treatment and prevention of Ras-driven tumours. In
Albig   +51 more
core   +2 more sources

Rapamycin and rapalogs

open access: yes, 2021
Inhibition of mTORC1 (mechanistic Target Of Rapamycin Complex 1) signaling promotes health and longevity in diverse model organisms. Over the past decade, excitement has built over the possibility that treatment with the mTORC1 inhibitor rapamycin can be utilized to treat or prevent age-related disease in humans. However, concerns over the side effects
openaire   +2 more sources

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

open access: yesMolecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak   +10 more
wiley   +1 more source

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