FM19G11: A new modulator of HIF that links mTOR activation with the DNA damage checkpoint pathways. - Test2 - elhamkhani - TriplyDB

FM19G11: A new modulator of HIF that links mTOR activation with the DNA damage checkpoint pathways.

FM19G11: A new modulator of HIF that links mTOR activation with the DNA damage checkpoint pathways.

http://www.wikidata.org/entity/Q39672963

about

Atypical centrioles during sexual reproduction Advances in targeting signal transduction pathways Rapamycin induces pluripotent genes associated with avoidance of replicative senescence Excess centrosomes disrupt endothelial cell migration via centrosome scattering.Causes and consequences of centrosome abnormalities in cancer.Centrosome dynamics as a source of chromosomal instability FM19G11 reverses endothelial dysfunction in rat and human arteries through stimulation of the PI3K/Akt/eNOS pathway, independently of mTOR/HIF-1α activation.Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.The centrosome and bipolar spindle assembly: does one have anything to do with the other?Centrin depletion causes cyst formation and other ciliopathy-related phenotypes in zebrafish.Molecular damage in cancer: an argument for mTOR-driven aging Loss of KLF14 triggers centrosome amplification and tumorigenesis.Kizuna is a novel mitotic substrate for CDC25B phosphatase Inducible, reversible system for the rapid and complete degradation of proteins in mammalian cells The autoregulated instability of Polo-like kinase 4 limits centrosome duplication to once per cell cycle.Mutations and deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades which alter therapy response.HIF2α contributes to antiestrogen resistance via positive bilateral crosstalk with EGFR in breast cancer cells.Polo-like kinase 4 autodestructs by generating its Slimb-binding phosphodegron.Progeria, rapamycin and normal aging: recent breakthrough.Aneuploidy in Cancer and Aging.The expanding relevance of nuclear mTOR in carcinogenesis.PLK4: a link between centriole biogenesis and cancer.FM19G11 and Ependymal Progenitor/Stem Cell Combinatory Treatment Enhances Neuronal Preservation and Oligodendrogenesis after Severe Spinal Cord Injury.Centriole Overduplication is the Predominant Mechanism Leading to Centrosome Amplification in Melanoma.FM19G11 inhibits O6 -methylguanine DNA-methyltransferase expression under both hypoxic and normoxic conditions.ESPL1 is a candidate oncogene of luminal B breast cancers.Centrosome aberrations and chromosome instability contribute to tumorigenesis and intra-tumor heterogeneity

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FM19G11: A new modulator of HIF that links mTOR activation with the DNA damage checkpoint pathways.

http://www.wikidata.org/entity/Q39672963

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

2010年论文

@zh

2010年论文

@zh-cn

name

FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

@en

FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

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type

label

FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

@en

FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

@nl

prefLabel

FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

@en

FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

@nl

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FM19G11: A new modulator of HI ...... NA damage checkpoint pathways.

@en

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Francisco Javier Rodríguez-Jiménez

http://www.w3.org/2001/XMLSchema#string

Inmaculada Royo

http://www.w3.org/2001/XMLSchema#string

Jose María Sánchez-Puelles

http://www.w3.org/2001/XMLSchema#string

José Ramón Murguia

http://www.w3.org/2001/XMLSchema#string

Pablo Mateos-Gregorio

http://www.w3.org/2001/XMLSchema#string

Slaven Erceg

http://www.w3.org/2001/XMLSchema#string

Victoria Moreno-Manzano

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P2860

The Polo kinase Plk4 functions in centriole duplication

Plk4-induced centriole biogenesis in human cells

Centrosome amplification drives chromosomal instability in breast tumor development.

Regulated HsSAS-6 levels ensure formation of a single procentriole per centriole during the centrosome duplication cycle

Deregulated proteolysis by the F-box proteins SKP2 and beta-TrCP: tipping the scales of cancer

Ab ovo or de novo? Mechanisms of centriole duplication

Multipolar spindle pole coalescence is a major source of kinetochore mis-attachment and chromosome mis-segregation in cancer cells

The spindle-assembly checkpoint in space and time

Genetic instabilities in human cancers

Control of meiotic and mitotic progression by the F box protein beta-Trcp1 in vivo

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scholarly article

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10.4161/CC.9.14.12184

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14

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