EWS/FLI and its downstream target NR0B1 interact directly to modulate transcription and oncogenesis in Ewing's sarcoma. - Wikidata - wikimedia - TriplyDB

EWS/FLI and its downstream target NR0B1 interact directly to modulate transcription and oncogenesis in Ewing's sarcoma.

EWS/FLI and its downstream target NR0B1 interact directly to modulate transcription and oncogenesis in Ewing's sarcoma.

http://www.wikidata.org/entity/Q37461081

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Therapeutic opportunities in Ewing sarcoma: EWS-FLI inhibition via LSD1 targeting Molecular mechanisms of ETS transcription factor-mediated tumorigenesis Understanding the Biology of Bone Sarcoma from Early Initiating Events through Late Events in Metastasis and Disease Progression Children's Oncology Group's 2013 blueprint for research: bone tumors Potential approaches to the treatment of Ewing's sarcoma Clinical and biochemical function of polymorphic NR0B1 GGAA-microsatellites in Ewing sarcoma: a report from the Children's Oncology Group Ewing Sarcoma, an enigmatic malignancy of likely progenitor cell origin, driven by transcription factor oncogenic fusions.Dual targeting of EWS-FLI1 activity and the associated DNA damage response with trabectedin and SN38 synergistically inhibits Ewing sarcoma cell growth Ewing sarcoma EWS protein regulates midzone formation by recruiting Aurora B kinase to the midzone Emergent Properties of EWS/FLI Regulation via GGAA Microsatellites in Ewing's Sarcoma.Cell Cycle Deregulation in Ewing's Sarcoma Pathogenesis Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis.Synthesis and structure-activity relationship studies of small molecule disruptors of EWS-FLI1 interactions in Ewing's sarcoma.Ewing sarcoma ewsa protein regulates chondrogenesis of Meckel's cartilage through modulation of Sox9 in zebrafish.Meningeal Ewing Sarcoma/Peripheral PNET: Clinicopathological, Immunohistochemical and FISH study of four cases.RanBPM expression regulates transcriptional pathways involved in development and tumorigenesis.Recent advances in the molecular pathogenesis of Ewing's sarcoma.Molecular pathogenesis of Ewing sarcoma: new therapeutic and transcriptional targets.Englerin A Inhibits EWS-FLI1 DNA Binding in Ewing Sarcoma Cells Oncogenic partnerships: EWS-FLI1 protein interactions initiate key pathways of Ewing's sarcoma.The dual inhibitory effect of thiostrepton on FoxM1 and EWS/FLI1 provides a novel therapeutic option for Ewing's sarcoma MicroRNA function and dysregulation in bone tumors: the evidence to date Minireview: role of orphan nuclear receptors in cancer and potential as drug targets Gene expression signature based screening identifies ribonucleotide reductase as a candidate therapeutic target in Ewing sarcoma.The orphan nuclear receptors at their 25-year reunion.Blocking the road, stopping the engine or killing the driver? Advances in targeting EWS/FLI-1 fusion in Ewing sarcoma as novel therapy.EWS/FLI1 Target Genes and Therapeutic Opportunities in Ewing Sarcoma.microRNA and Bone Cancer.Suppression of FOXO1 is responsible for a growth regulatory repressive transcriptional sub-signature of EWS-FLI1 in Ewing sarcoma.Factors Affecting EWS-FLI1 Activity in Ewing's Sarcoma.Mechanism and relevance of EWS/FLI-mediated transcriptional repression in Ewing sarcoma.The Ewing's sarcoma fusion protein, EWS-FLI, binds Runx2 and blocks osteoblast differentiation.Dr. Jekyll and Mr. Hyde: The Two Faces of the FUS/EWS/TAF15 Protein Family.Identification of Mithramycin Analogues with Improved Targeting of the EWS-FLI1 Transcription Factor Microsatellites with macro-influence in ewing sarcoma Ewing's Sarcoma: Development of RNA Interference-Based Therapy for Advanced Disease.Lurbinectedin Inactivates the Ewing Sarcoma Oncoprotein EWS-FLI1 by Redistributing It within the Nucleus.Chemical Proteomics Identifies Druggable Vulnerabilities in a Genetically Defined Cancer.Proteasomal Degradation of the EWS-FLI1 Fusion Protein Is Regulated by a Single Lysine Residue.RETRACTED: Pediatric sarcomas.

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EWS/FLI and its downstream target NR0B1 interact directly to modulate transcription and oncogenesis in Ewing's sarcoma.

http://www.wikidata.org/entity/Q37461081

description

2009 nî lūn-bûn

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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2009年學術文章

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2009年學術文章

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name

EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@en

EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@nl

type

label

EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@en

EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@nl

prefLabel

EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@en

EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@nl

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0008-5472.CAN-09-1540

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Cancer Research

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EWS/FLI and its downstream tar ...... ncogenesis in Ewing's sarcoma.

@en

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Anita K Iyer

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Edward R B McCabe

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

Michelle Kinsey

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

Richard Smith

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

Stephen L Lessnick

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P2860

EWS/FLI mediates transcriptional repression via NKX2.2 during oncogenic transformation in Ewing's sarcoma

Molecular mechanisms of DAX1 action

Dosage-sensitive sex reversal adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX1) (NR0B1) and small heterodimer partner (SHP) (NR0B2) form homodimers individually, as well as DAX1-SHP heterodimers

The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1

Histone deacetylase activity is required for full transcriptional repression by mSin3A

Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma

A protein interaction network for pluripotency of embryonic stem cells

An extended transcriptional network for pluripotency of embryonic stem cells

Loss of tumorigenicity of Ewing's sarcoma cells expressing antisense RNA to EWS-fusion transcripts

Chromosomes in Ewing's sarcoma. I. An evaluation of 85 cases of remarkable consistency of t(11;22)(q24;q12)

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