Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila. - Wikidata - wikimedia - TriplyDB

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

http://www.wikidata.org/entity/Q34037299

about

PI3K signaling and Stat92E converge to modulate glial responsiveness to axonal injury JAK/STAT pathway dysregulation in tumors: a Drosophila perspective Differential regulation of protein tyrosine kinase signaling by Dock and the PTP61F variants.Pvr expression regulators in equilibrium signal control and maintenance of Drosophila blood progenitors Optomotor-blind negatively regulates Drosophila eye development by blocking Jak/STAT signaling Discovery of transcription factors and regulatory regions driving in vivo tumor development by ATAC-seq and FAIRE-seq open chromatin profiling.JAK/STAT and Hox Dynamic Interactions in an Organogenetic Gene Cascade.Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment.Activated STAT regulates growth and induces competitive interactions independently of Myc, Yorkie, Wingless and ribosome biogenesis.Drosophila Myc integrates multiple signaling pathways to regulate intestinal stem cell proliferation during midgut regeneration.Essential roles for stat92E in expanding and patterning the proximodistal axis of the Drosophila wing imaginal disc.Drosophila as a model to study the role of blood cells in inflammation, innate immunity and cancer.Drosophila: a model for studying genetic and molecular aspects of haematopoiesis and associated leukaemias Regulation of proliferation, cell competition, and cellular growth by the Drosophila JAK-STAT pathway.The Drosophila JAK-STAT pathway in blood cell formation and immunity.A Genetic Screen Reveals an Unexpected Role for Yorkie Signaling in JAK/STAT-Dependent Hematopoietic Malignancies in Drosophila melanogaster.JAK/STAT signaling is required for hinge growth and patterning in the Drosophila wing disc.Expression of lamina proteins Lamin and Kugelkern suppresses stem cell proliferation.

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P2860

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

http://www.wikidata.org/entity/Q34037299

description

2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@ast

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@en

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@nl

type

label

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@ast

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@en

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@nl

prefLabel

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@ast

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@en

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

@nl

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J.YDBIO.2010.05.497

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Developmental Biology

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Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila

@en

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Elizabeth A McMillan

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Foster C Gonsalves

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

Laura A Ekas

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

Maria Sol Flaherty

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Timothy J Cardozo

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P2860

Structural bases of unphosphorylated STAT1 association and receptor binding

Crystal structure of a tyrosine phosphorylated STAT-1 dimer bound to DNA

Interacting regions in Stat3 and c-Jun that participate in cooperative transcriptional activation

Two Drosophila suppressors of cytokine signaling (SOCS) differentially regulate JAK and EGFR pathway activities

Structure of the amino-terminal protein interaction domain of STAT-4

Three-dimensional structure of the Stat3beta homodimer bound to DNA

A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasms

Targeted gene expression as a means of altering cell fates and generating dominant phenotypes

STAT4 requires the N-terminal domain for efficient phosphorylation

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

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