MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation - Wikidata - awgldk - TriplyDB

MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation

MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation

http://www.wikidata.org/entity/Q36405926

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ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases "Inflammaging" as a Druggable Target: A Senescence-Associated Secretory Phenotype-Centered View of Type 2 Diabetes Cellular Pathways in Response to Ionizing Radiation and Their Targetability for Tumor Radiosensitization Inflamma-miRs in Aging and Breast Cancer: Are They Reliable Players?Changes in Regenerative Capacity through Lifespan Potential therapeutic effects of the MTOR inhibitors for preventing ageing and progeria-related disorders Better Living through Chemistry: Caloric Restriction (CR) and CR Mimetics Alter Genome Function to Promote Increased Health and Lifespan Redox control of senescence and age-related disease Aging and adipose tissue: potential interventions for diabetes and regenerative medicine CELL BIOLOGY. GATA get a hold on senescence Identification of Salvia haenkei as gerosuppressant agent by using an integrated senescence-screening assay Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism Glucose metabolism-targeted therapy and withaferin A are effective for epidermal growth factor receptor tyrosine kinase inhibitor-induced drug-tolerant persisters.Mitochondria are required for pro-ageing features of the senescent phenotype.Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age.Simvastatin suppresses breast cancer cell proliferation induced by senescent cells 17α-Estradiol Alleviates Age-related Metabolic and Inflammatory Dysfunction in Male Mice Without Inducing Feminization Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse.The Unfolded Protein Response Plays a Predominant Homeostatic Role in Response to Mitochondrial Stress in Pancreatic Stellate Cells.Restricting the induction of NGF in ovarian stroma engenders selective follicular activation through the mTOR signaling pathway.AMPK activation protects from neuronal dysfunction and vulnerability across nematode, cellular and mouse models of Huntington's disease.NKG2D ligands mediate immunosurveillance of senescent cells.Context-dependent effects of cellular senescence in cancer development.From Ancient Pathways to Aging Cells-Connecting Metabolism and Cellular Senescence.Increased IL-6 secretion by aged human mesenchymal stromal cells disrupts hematopoietic stem and progenitor cells' homeostasis.Ageing and the pathogenesis of osteoarthritis.SFRP2 augments WNT16B signaling to promote therapeutic resistance in the damaged tumor microenvironment Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases.Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli A senescence secretory switch mediated by PI3K/AKT/mTOR activation controls chemoprotective endothelial secretory responses.NF-κB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.TGF-β and NF-κB signaling pathway crosstalk potentiates corneal epithelial senescence through an RNA stress response Conditioned medium derived from rat amniotic epithelial cells confers protection against inflammation, cancer, and senescence Interleukin 1α and the inflammatory process.Shining the Light on Senescence Associated LncRNAs.Progressive slowdown/prevention of cellular senescence by CD9-targeted delivery of rapamycin using lactose-wrapped calcium carbonate nanoparticles.Advances in Therapeutic Approaches to Extend Healthspan: a perspective from the 2nd Scripps Symposium on the Biology of Aging.Senescence and cancer: An evolving inflammatory paradox.From inflamm-aging to immune-paralysis: a slippery slope during aging for immune-adaptation.

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MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation

http://www.wikidata.org/entity/Q36405926

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MTOR regulates the pro-tumorig ...... by promoting IL1A translation

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MTOR regulates the pro-tumorig ...... by promoting IL1A translation

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MTOR regulates the pro-tumorig ...... by promoting IL1A translation

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Nature Cell Biology

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MTOR regulates the pro-tumorig ...... by promoting IL1A translation

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Adam Freund

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Albert R Davalos

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Arturo V Orjalo

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Chandani Limbad

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Christopher C Benz

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Christopher K Patil

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Gene B Hubbard

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Judith Campisi

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Kathleen A Wilson-Edell

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Lili Zhou

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P2860

WNT16B is a new marker of cellular senescence that regulates p53 activity and the phosphoinositide 3-kinase/AKT pathway

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

The TOR pathway comes of age

Senescence of activated stellate cells limits liver fibrosis

Next-generation drug-eluting stents in coronary artery disease: focus on everolimus-eluting stent (Xience V)

Rapamycin fed late in life extends lifespan in genetically heterogeneous mice

Targeting the mTOR signaling network for cancer therapy

Targeted polypharmacology: discovery of dual inhibitors of tyrosine and phosphoinositide kinases

Immunity, Inflammation, and Cancer

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10.1038/NCB3195

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8

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26147250

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