Chemical inhibition of NAT10 corrects defects of laminopathic cells. - Wikidata - wikimedia - TriplyDB

Chemical inhibition of NAT10 corrects defects of laminopathic cells.

Chemical inhibition of NAT10 corrects defects of laminopathic cells.

http://www.wikidata.org/entity/Q30602438

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Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cells Anchoring a Leviathan: How the Nuclear Membrane Tethers the Genome The nuclear envelope: an intriguing focal point for neurogenetic disease In silico synchronization reveals regulators of nuclear ruptures in lamin A/C deficient model cells.Recent advances in understanding the role of lamins in health and disease Defining the orphan functions of lysine acetyltransferases Human NAT10 is an ATP-dependent RNA acetyltransferase responsible for N4-acetylcytidine formation in 18 S ribosomal RNA (rRNA)Yeast Kre33 and human NAT10 are conserved 18S rRNA cytosine acetyltransferases that modify tRNAs assisted by the adaptor Tan1/THUMPD1 Chromatin Regulates Genome Targeting with Cisplatin.Chemoproteomic profiling of lysine acetyltransferases highlights an expanded landscape of catalytic acetylation Alterations in the nuclear proteome of HIV-1 infected T-cells.Unravelling the genomic targets of small molecules using high-throughput sequencing.RNA cytidine acetyltransferase of small-subunit ribosomal RNA: identification of acetylation sites and the responsible acetyltransferase in fission yeast, Schizosaccharomyces pombe The Power of Sophisticated Phenotypic Screening and Modern Mechanism-of-Action Methods.A Novel Lamin A Mutant Responsible for Congenital Muscular Dystrophy Causes Distinct Abnormalities of the Cell Nucleus.High expression of N-acetyltransferase 10: a novel independent prognostic marker of worse outcome in patients with hepatocellular carcinoma.NAT10 regulates p53 activation through acetylating p53 at K120 and ubiquitinating Mdm2.Permanent farnesylation of lamin A mutants linked to progeria impairs its phosphorylation at serine 22 during interphase Nesprin-2G, a Component of the Nuclear LINC Complex, Is Subject to Myosin-Dependent Tension.The Aging Epigenome A High Throughput Phenotypic Screening reveals compounds that counteract premature osteogenic differentiation of HGPS iPS-derived mesenchymal stem cells.Nuclear lamina remodelling and its implications for human disease.Shaping of interphase chromosomes by the microtubule network.CRISPR-Cas9(D10A) nickase-based genotypic and phenotypic screening to enhance genome editing.The nuclear lamina in health and disease.Synthesis of marmycin A and investigation into its cellular activity.Next-generation phenotypic screening.Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations.Causes and consequences of nuclear envelope alterations in tumour progression.Current insights into LMNA cardiomyopathies: Existing models and missing LINCs Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition.Light up Live Cell Nuclear Envelope in Real-Time Using a Two-Photon Absorption and AIE Chromophore.Nuclear envelopathies: a complex LINC between nuclear envelope and pathology.NAT10 is upregulated in hepatocellular carcinoma and enhances mutant p53 activity.The structure of lamin filaments in somatic cells as revealed by cryo-electron tomography.Inhibition of NAT10 Suppresses Melanogenesis and Melanoma Growth by Attenuating Microphthalmia-Associated Transcription Factor (MITF) Expression Prelamin A impairs 53BP1 nuclear entry by mislocalizing NUP153 and disrupting the Ran gradient A single acetylation of 18 S rRNA is essential for biogenesis of the small ribosomal subunit in Saccharomyces cerevisiae.Moving Cell Boundaries Drive Nuclear Shaping during Cell Spreading.Parallel genome-wide screens identify synthetic viable interactions between the BLM helicase complex and Fanconi anemia.

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P2860

Chemical inhibition of NAT10 corrects defects of laminopathic cells.

http://www.wikidata.org/entity/Q30602438

description

2014 nî lūn-bûn

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2014 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2014 թվականի մայիսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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name

Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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type

label

Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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SCIENCE.1252651

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Chemical inhibition of NAT10 corrects defects of laminopathic cells.

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Delphine Larrieu

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

Mukerrem Demir

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Sébastien Britton

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

P2860

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome

Lamin A-dependent nuclear defects in human aging

RNA helicase module in an acetyltransferase that modifies a specific tRNA anticodon

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

Nucleophosmin/B23 inhibits Eg5-mediated microtubule depolymerization by inactivating its ATPase activity.

Protein farnesylation inhibitors cause donut-shaped cell nuclei attributable to a centrosome separation defect

Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes

Lamin a truncation in Hutchinson-Gilford progeria.

"Laminopathies": a wide spectrum of human diseases.

Histone acetyltransferase hALP and nuclear membrane protein hsSUN1 function in de-condensation of mitotic chromosomes.

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Stephen P Jackson

Raphaël Rodriguez

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