Depletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors. - Wikidata - awgldk - TriplyDB

Depletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors.

Depletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors.

http://www.wikidata.org/entity/Q33804459

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Translational progress on tumor biomarkers Cancer cells with irons in the fire Drugging the addict: non-oncogene addiction as a target for cancer therapy Prediction of Genetic Interactions Using Machine Learning and Network Properties The function of phosphatidylinositol 5-phosphate 4-kinase γ (PI5P4Kγ) explored using a specific inhibitor that targets the PI5P-binding site A Gene Gravity Model for the Evolution of Cancer Genomes: A Study of 3,000 Cancer Genomes across 9 Cancer Types Method for Assaying the Lipid Kinase Phosphatidylinositol-5-phosphate 4-kinase α in Quantitative High-Throughput Screening (qHTS) Bioluminescent Format The Lipid Kinase PI5P4Kβ Is an Intracellular GTP Sensor for Metabolism and Tumorigenesis.Copy number analysis of whole-genome data using BIC-seq2 and its application to detection of cancer susceptibility variants.The role of PI3K/AKT-related PIP5K1α and the discovery of its selective inhibitor for treatment of advanced prostate cancer.Association Between PIP4K2A Polymorphisms and Acute Lymphoblastic Leukemia Susceptibility.Exploring phosphatidylinositol 5-phosphate 4-kinase function.Polyphosphoinositide binding domains: Key to inositol lipid biology.Genome-wide detection of DNase I hypersensitive sites in single cells and FFPE tissue samples.PIP4kγ is a substrate for mTORC1 that maintains basal mTORC1 signaling during starvation Chemoproteomics Reveals Novel Protein and Lipid Kinase Targets of Clinical CDK4/6 Inhibitors in Lung Cancer.Somatic Copy Number Alterations at Oncogenic Loci Show Diverse Correlations with Gene Expression.Deletion of the gene Pip4k2c, a novel phosphatidylinositol kinase, results in hyperactivation of the immune system Prevention of Proliferative Vitreoretinopathy by Suppression of Phosphatidylinositol 5-Phosphate 4-Kinases.Mechanism of substrate specificity of phosphatidylinositol phosphate kinases.In B cells, phosphatidylinositol 5-phosphate 4-kinase-α synthesizes PI(4,5)P2 to impact mTORC2 and Akt signaling The Hidden Conundrum of Phosphoinositide Signaling in Cancer Antitumor mechanisms when pRb and p53 are genetically inactivated.The basal transcription complex component TAF3 transduces changes in nuclear phosphoinositides into transcriptional output.Nuclear Phosphatidylinositol Signaling: Focus on Phosphatidylinositol Phosphate Kinases and Phospholipases C.Type I γ Phosphatidylinositol Phosphate 5-Kinase i5 Controls the Ubiquitination and Degradation of the Tumor Suppressor Mitogen-inducible Gene 6 The activation loop of PIP5K functions as a membrane sensor essential for lipid substrate processing.Structural reverse genetics study of the PI5P4Kβ-nucleotide complexes reveals the presence of the GTP bioenergetic system in mammalian cells A targeted knockdown screen of genes coding for phosphoinositide modulators identifies PIP4K2A as required for acute myeloid leukemia cell proliferation and survival.Molecularly targeted therapies for p53-mutant cancers.MANF regulates hypothalamic control of food intake and body weight.The p53 tetramer shows an induced-fit interaction of the C-terminal domain with the DNA-binding domain.Amplification of Chromosome 1q Genes Encoding the Phosphoinositide Signalling Enzymes PI4KB, AKT3, PIP5K1A and PI3KC2B in Breast Cancer.Signalling: a new target for p53-null tumours.Dual blockade of the lipid kinase PIP4Ks and mitotic pathways leads to cancer-selective lethality.Putting p53 in Context.2013: Signaling breakthroughs of the year.Phosphoinositide 3-kinase pathways and autophagy require phosphatidylinositol phosphate kinases.Phosphatidylinositol-5-Phosphate 4-Kinases Regulate Cellular Lipid Metabolism By Facilitating Autophagy.Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers

P2860

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P2860

Depletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors.

http://www.wikidata.org/entity/Q33804459

description

2013 nî lūn-bûn

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2013 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2013 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Depletion of a putatively drug ...... its growth of p53-null tumors.

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Andrea Bullock

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Atsuo T Sasaki

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Eric L Bell

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John M Asara

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Jonathan B Hurov

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Characterization of MTMR3. an inositol lipid 3-phosphatase with novel substrate specificity

Phosphatidylinositol-5-phosphate activation and conserved substrate specificity of the myotubularin phosphatidylinositol 3-phosphatases

The cDNA cloning and characterization of inositol polyphosphate 4-phosphatase type II. Evidence for conserved alternative splicing in the 4-phosphatase family

The isolation and characterization of cDNA encoding human and rat brain inositol polyphosphate 4-phosphatase

Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2.

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A new pathway for synthesis of phosphatidylinositol-4,5-bisphosphate

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