Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent - Wikidata - awgldk - TriplyDB

Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent

Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent

http://www.wikidata.org/entity/Q24545984

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A novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemia Oncogenic kinase fusions: an evolving arena with innovative clinical opportunities Structural and functional properties of platelet-derived growth factor and stem cell factor receptors Role of platelet-derived growth factors in physiology and medicine PDGFR-A is a therapeutic target in alveolar rhabdomyosarcoma.Response to imatinib mesylate in patients with hypereosinophilic syndrome.FIP1L1-PDGFRA molecular analysis in the differential diagnosis of eosinophilia Targeting the PDGF signaling pathway in tumor treatment FIP1L1 presence in FIP1L1-RARA or FIP1L1-PDGFRA differentially contributes to the pathogenesis of distinct types of leukemia.Eosinophils: changing perspectives in health and disease.R-loop-mediated genome instability in mRNA cleavage and polyadenylation mutants Current concepts on the pathogenesis of the hypereosinophilic syndrome/chronic eosinophilic leukemia.Chronic myeloproliferative disorders: the role of tyrosine kinases in pathogenesis, diagnosis and therapy.Imatinib mesylate in the treatment of hematologic malignancies.Aberrant cytokine signaling in leukemia.Fibroblast growth factor receptor and platelet-derived growth factor receptor abnormalities in eosinophilic myeloproliferative disorders.Molecular drug targets in myeloproliferative neoplasms: mutant ABL1, JAK2, MPL, KIT, PDGFRA, PDGFRB and FGFR1.Recent breakthroughs in the understanding and management of chronic eosinophilic leukemia.Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.Autocrine PDGF stimulation in malignancies.Review of current classification, molecular alterations, and tyrosine kinase inhibitor therapies in myeloproliferative disorders with hypereosinophilia.The platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) are major players in oncogenesis, drug resistance, and attractive oncologic targets in cancer.The tyrosine phosphatase SHP2 is required for cell transformation by the receptor tyrosine kinase mutants FIP1L1-PDGFRα and PDGFRα D842V.Development of a siRNA and shRNA screening system based on a kinase fusion protein.ETV6-PDGFRB and FIP1L1-PDGFRA stimulate human hematopoietic progenitor cell proliferation and differentiation into eosinophils: the role of nuclear factor-κB.Centrosomal targeting of tyrosine kinase activity does not enhance oncogenicity in chronic myeloproliferative disorders.Systematic screen for tyrosine kinase rearrangements identifies a novel C6orf204-PDGFRB fusion in a patient with recurrent T-ALL and an associated myeloproliferative neoplasm.Quantification of PDGFRA alternative transcripts improves the screening for X-PDGFRA fusions by reverse transcriptase-polymerase chain reaction.Critical role of the platelet-derived growth factor receptor (PDGFR) beta transmembrane domain in the TEL-PDGFRbeta cytosolic oncoprotein.The fusion proteins TEL-PDGFRbeta and FIP1L1-PDGFRalpha escape ubiquitination and degradation The lymphoma-associated fusion tyrosine kinase ITK-SYK requires pleckstrin homology domain-mediated membrane localization for activation and cellular transformation.Refractory myeloid sarcoma with a FIP1L1-PDGFRA rearrangement detected by clinical high throughput somatic sequencing Leukemogenic kinase FIP1L1-PDGFRA and a small ubiquitin-like modifier E3 ligase, PIAS1, form a positive cross-talk through their enzymatic activities Platelet-derived growth factors and their receptors in normal and malignant hematopoiesis Generation of the Fip1l1-Pdgfra fusion gene using CRISPR/Cas genome editing.Multiple MYO18A-PDGFRB fusion transcripts in a myeloproliferative neoplasm patient with t(5;17)(q32;q11).A novel t(3;13)(q13;q12) translocation fusing FLT3 with GOLGB1: toward myeloid/lymphoid neoplasms with eosinophilia and rearrangement of FLT3?Lyn mediates FIP1L1-PDGFRA signal pathway facilitating IL-5RA intracellular signal through FIP1L1-PDGFRA/JAK2/Lyn/Akt network complex in CEL.The oncogenic FIP1L1-PDGFRα fusion protein displays skewed signaling properties compared to its wild-type PDGFRα counterpart.F604S exchange in FIP1L1-PDGFRA enhances FIP1L1-PDGFRA protein stability via SHP-2 and SRC: a novel mode of kinase inhibitor resistance.

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Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent

http://www.wikidata.org/entity/Q24545984

description

2006 nî lūn-bûn

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2006 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2006 թվականի մայիսին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

@ast

Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

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Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

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type

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Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

@ast

Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

@en

Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

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prefLabel

Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

@ast

Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

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Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

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Proceedings of the National Academy of Sciences of the United States of America

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Activation of FIP1L1-PDGFRalph ...... lpha and is FIP1L1-independent

@en

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Benjamin H Lee

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

Cedric Folens

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D Gary Gilliland

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Elizabeth H Stover

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Jing Chen

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Nicole Mentens

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Peter Marynen

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P2860

Role of the nucleophosmin (NPM) portion of the non-Hodgkin's lymphoma-associated NPM-anaplastic lymphoma kinase fusion protein in oncogenesis

Human Fip1 is a subunit of CPSF that binds to U-rich RNA elements and stimulates poly(A) polymerase.

Discovery of a fusion kinase in EOL-1 cells and idiopathic hypereosinophilic syndrome

The structural basis for autoinhibition of FLT3 by the juxtamembrane domain

A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.

Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors

CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy

ZNF198-FGFR1 transforming activity depends on a novel proline-rich ZNF198 oligomerization domain

PDGFRA activating mutations in gastrointestinal stromal tumors.

Gastrointestinal stromal tumors in a mouse model by targeted mutation of the Kit receptor tyrosine kinase.

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8078-8083

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10.1073/PNAS.0601192103

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21

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103

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2006-05-11T00:00:00Z

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7090137

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16690743

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1472432

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