Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program
about
From rapalogs to anti-aging formula.INK4 locus of the tumor-resistant rodent, the naked mole rat, expresses a functional p15/p16 hybrid isoformGrowth hormone action predicts age-related white adipose tissue dysfunction and senescent cell burden in mice.The structural basis for cancer treatment decisions.Hippo pathway mediates resistance to cytotoxic drugs.Senescence of tumor cells induced by oxaliplatin increases the efficiency of a lipid A immunotherapy via the recruitment of neutrophils.Gerosuppression in confluent cells.Tumor promoter-induced cellular senescence: cell cycle arrest followed by geroconversion.Fasting levels of hepatic p-S6 are increased in old miceRegulating the stability and localization of CDK inhibitor p27(Kip1) via CSN6-COP1 axis.LIF-JAK1-STAT3 signaling delays contact inhibition of human corneal endothelial cellsGeroconversion: irreversible step to cellular senescenceComparison of rapamycin schedules in mice on high-fat diet.Stem Cell-Soluble Signals Enhance Multilumen Formation in SMG Cell Clusters.The interplay between TEAD4 and KLF5 promotes breast cancer partially through inhibiting the transcription of p27Kip1.ASC Induces Apoptosis via Activation of Caspase-9 by Enhancing Gap Junction-Mediated Intercellular Communication.Rejuvenating immunity: "anti-aging drug today" eight years later.Comparing individual-based approaches to modelling the self-organization of multicellular tissuesKoschei the immortal and anti-aging drugsA novel autosomal recessive TERT T1129P mutation in a dyskeratosis congenita family leads to cellular senescence and loss of CD34+ hematopoietic stem cells not reversible by mTOR-inhibitionDual mTORC1/C2 inhibitors suppress cellular geroconversion (a senescence program).Role of dual specificity tyrosine-phosphorylation-regulated kinase 1B (Dyrk1B) in S-phase entry of HPV E7 expressing cells from quiescenceEpithelial morphological reversion drives Profilin-1-induced elevation of p27(kip1) in mesenchymal triple-negative human breast cancer cells through AMP-activated protein kinase activation.The B56γ3 regulatory subunit-containing protein phosphatase 2A outcompetes Akt to regulate p27KIP1 subcellular localization by selectively dephosphorylating phospho-Thr157 of p27KIP1.Preclinical validation of a novel compound targeting p70S6 kinase in breast cancer.Rapamycin reverses the senescent phenotype and improves immunoregulation of mesenchymal stem cells from MRL/lpr mice and systemic lupus erythematosus patients through inhibition of the mTOR signaling pathway.SIRT2 inhibits non-small cell lung cancer cell growth through impairing Skp2-mediated p27 degradation.p27(KIP1) loss promotes proliferation and phagocytosis but prevents epithelial-mesenchymal transition in RPE cells after photoreceptor damage.Rapamycin Prolongs the Survival of Corneal Epithelial Cells in Culture.Gerosuppression by pan-mTOR inhibitors.The mTOR and PP2A Pathways Regulate PHD2 Phosphorylation to Fine-Tune HIF1α Levels and Colorectal Cancer Cell Survival under Hypoxia.SIRT1-mediated downregulation of p27Kip1 is essential for overcoming contact inhibition of Kaposi's sarcoma-associated herpesvirus transformed cellsDisabled cell density sensing leads to dysregulated cholesterol synthesis in glioblastoma.Aberrant mTOR activation in senescence and aging: A mitochondrial stress response?Principles of K-Ras effector organization and the role of oncogenic K-Ras in cancer initiation through G1 cell cycle deregulation.The bicellular tensile force sorts the localization of LSRs in bicellular and tricellular junctions.Mechanistic contribution of electroconductive hydroxyapatite-titanium disilicide composite on the alignment and proliferation of cells.STAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence.Irinotecan treatment and senescence failure promote the emergence of more transformed and invasive cells that depend on anti-apoptotic Mcl-1.Dormant cancer cells accumulate high protoporphyrin IX levels and are sensitive to 5-aminolevulinic acid-based photodynamic therapy.
P2860
Q33829205-D1BCD53B-E1E8-44EF-BF7C-5A5C9C1DD2CEQ34042900-C09AB7AD-847C-49D9-9FA9-79AC97D3F545Q34128617-36977E9B-5EA4-4B36-9BB9-F6A2037EE12EQ34365654-8A33AF90-7A2D-4E4C-9D99-CEA35D38FE51Q34555337-FE0F1399-BD73-4C63-8EC4-B0139E9C11EBQ34956634-631E1ADF-AA13-487A-AEA9-9760886355A2Q34982499-5CF0FAFC-872B-48F9-B4A0-36C7C1D0DB1DQ35149607-22867AC4-5CBC-4F6D-9B3B-0075B511A4A2Q36182265-3454ACB5-37CD-4AC6-89AE-2A9A03CAFD1FQ36183877-54876E29-46B0-45D8-B100-F10F7B66F009Q36184750-34E91470-A61B-4D53-B863-CE100892EBE5Q36186369-46ED2AD2-DE3F-4D42-B1DF-FB81AD281D25Q36189078-1B0E9987-10A3-4888-8955-B84F4572D4E4Q36212313-A11DA733-0657-40DD-A6BF-C1E16242A8B1Q36232136-CA8048F3-CD21-4DD1-A0F7-39E4DFACFCF8Q36240325-B407448E-187E-443B-AA41-EE158C3943BAQ36260537-99FCE0EB-D836-4A5F-9FE2-6AB06CB2DF04Q36278407-CF399E75-F626-40F4-AFC4-73B892EC6F9BQ36292001-C2BF8E10-82FA-4492-9384-DD55247F426BQ36411101-20DE76EA-5ED2-4C13-ADBD-2E8CA14C9981Q36414149-12AC02F1-ABCC-41B1-ABCB-96D85EA18CF6Q36544412-FB65FD0A-EBB2-468A-83F0-3CA5F882A932Q36780655-22A54EF4-414E-4F7A-950E-5D1E0A7FDF1DQ36782507-C2E0FA42-EC91-43EE-9AB3-4986A65A7048Q37062488-75832F70-C874-4211-B366-052CB0C69CCEQ37062514-8EC4D232-4610-4818-B8E1-DF12B96B4D51Q37109899-47DA52CF-D48D-4CE2-8A6D-498BA7B0D6C5Q37292705-925F5D78-3C3E-4981-8E96-E53839D63AABQ37561446-E85723E1-1836-4DC8-B0A6-67F17027B84EQ37610218-9D81A216-D319-43F7-84BD-7762C6E86BCFQ37654508-1E20EBC9-1161-4DBC-AA18-0365BBD7C0E2Q37689009-BD040830-0C38-4421-BF02-CC51FA50948FQ37716459-B7344548-8DB8-476F-BA18-E46D2A8246D6Q38275627-7BFB2285-7B18-41B0-B573-57DBD048B940Q38614956-3D8BFC3D-6527-4139-A8D1-02878A81DBA5Q38703949-C8FC7623-E48C-49EC-A4BF-9ADAB67AAA57Q38788723-A2DA02A9-592D-428F-8BFD-F3D95E67A12FQ38790057-AE72234C-1A7B-4463-9F83-CA3ED96D4787Q38922461-706902DB-BCBD-4747-9234-90DAA4B76611Q39179209-984B69AE-F48C-4970-9F77-2C0C48E32BA1
P2860
Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program
description
2014 nî lūn-bûn
@nan
2014 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2014 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
name
Contact inhibition and high ce ...... ressing the senescence program
@ast
Contact inhibition and high ce ...... ressing the senescence program
@en
type
label
Contact inhibition and high ce ...... ressing the senescence program
@ast
Contact inhibition and high ce ...... ressing the senescence program
@en
prefLabel
Contact inhibition and high ce ...... ressing the senescence program
@ast
Contact inhibition and high ce ...... ressing the senescence program
@en
P2093
P2860
P3181
P356
P1476
Contact inhibition and high ce ...... ressing the senescence program
@en
P2093
Blagosklonny MV
Demidenko ZN
Leontieva OV
P2860
P304
P3181
P356
10.1073/PNAS.1405723111
P407
P577
2014-06-02T00:00:00Z