BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms. - Wikidata - awgldk - TriplyDB

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

http://www.wikidata.org/entity/Q39113216

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Drug Delivery Using Nanoparticles for Cancer Stem-Like Cell Targeting Evolving Therapeutic Strategies for the Classic Philadelphia-Negative Myeloproliferative Neoplasms Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia Epigenetic regulators as promising therapeutic targets in acute myeloid leukemia The bromodomain: from epigenome reader to druggable target Acetyl-lysine Binding Site of Bromodomain-Containing Protein 4 (BRD4) Interacts with Diverse Kinase Inhibitors Inhibition of BET bromodomains as a therapeutic strategy for cancer drug discovery Registered report: Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukemia BET protein inhibitor JQ1 attenuates Myc-amplified MCC tumor growth in vivo.Inhibition of LSD1 reduces herpesvirus infection, shedding, and recurrence by promoting epigenetic suppression of viral genomes The BET-Bromodomain Inhibitor JQ1 Reduces Inflammation and Tau Phosphorylation at Ser396 in the Brain of the 3xTg Model of Alzheimer's Disease Pharmacological targeting of BET proteins inhibits renal fibroblast activation and alleviates renal fibrosis Investigational epigenetically targeted drugs in early phase trials for the treatment of haematological malignancies.Epigenetic pathway targets for the treatment of disease: accelerating progress in the development of pharmacological tools: IUPHAR Review 11.Epigenetic Therapy in Acute Myeloid Leukemia: Current and Future Directions.Inhibition of bromodomain and extra-terminal proteins (BET) as a potential therapeutic approach in haematological malignancies: emerging preclinical and clinical evidence.BET inhibitors in cancer therapeutics: a patent review.Bromodomain inhibitors and cancer therapy: From structures to applications.Recurrent mutations, including NPM1c, activate a BRD4-dependent core transcriptional program in acute myeloid leukemia Non-kinase targets of protein kinase inhibitors.A Novel Epi-drug Therapy Based on the Suppression of BET Family Epigenetic Readers.Novel BET protein proteolysis-targeting chimera exerts superior lethal activity than bromodomain inhibitor (BETi) against post-myeloproliferative neoplasm secondary (s) AML cells.First Barcelona Conference on Epigenetics and Cancer.Potent Dual BET Bromodomain-Kinase Inhibitors as Value-Added Multitargeted Chemical Probes and Cancer Therapeutics.Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms.Promoter-bound METTL3 maintains myeloid leukaemia by m6A-dependent translation control.

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BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

http://www.wikidata.org/entity/Q39113216

description

2013 nî lūn-bûn

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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

@zh-hk

2013年論文

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2013年論文

@zh-tw

2013年论文

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2013年论文

@zh

2013年论文

@zh-cn

name

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

@en

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

@nl

type

label

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

@en

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

@nl

prefLabel

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

@en

BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

@nl

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BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.

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A Godfrey

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A R Green

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B Huntly

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B S Wyspiańska

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E Cannizzaro

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F J Calero-Nieto

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I Barbieri

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I Rioja

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J Li

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J Nangalia

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P2860

JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin

Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

BET bromodomain inhibition as a therapeutic strategy to target c-Myc

Recruitment of P-TEFb for stimulation of transcriptional elongation by the bromodomain protein Brd4

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis

Targeting MYC dependence in cancer by inhibiting BET bromodomains

RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia

A gain-of-function mutation of JAK2 in myeloproliferative disorders

Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis.

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1

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