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Article . 2014 . Peer-reviewed
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Article . 2014
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Btk29A Promotes Wnt4 Signaling in the Niche to Terminate Germ Cell Proliferation in Drosophila

Authors: Daisuke Yamamoto; Beston F. Nore; Beston F. Nore; Noriko Hamada-Kawaguchi; C. I. Edvard Smith; Yusuke Kuwada;

Btk29A Promotes Wnt4 Signaling in the Niche to Terminate Germ Cell Proliferation in Drosophila

Abstract

Wnt–β-Catenin in Germ Cells The Wnt–β-catenin pathway contributes to many signaling mechanisms during organismal development and carcinogenesis by regulating both transcription and cell adhesion. Hamada-Kawaguchi et al. (p. 294 ) demonstrate that this pathway must be activated in ovarian somatic cells to stop proliferation of germ cells in Drosophila. Phosphorylation of a tyrosine residue on β-catenin by the tyrosine kinase Btk turns on signaling in the niche cells by promoting transcriptional activity of β-catenin. Failure in this process resulted in ovarian tumors in the flies.

Keywords

Transcription, Genetic, Protein-Tyrosine Kinases, Genomic Instability, Up-Regulation, Wnt Proteins, Drosophila melanogaster, Germ Cells, Gene Knockdown Techniques, Argonaute Proteins, Animals, Drosophila Proteins, Tyrosine, DNA Breaks, Double-Stranded, Phosphorylation, RNA, Small Interfering, beta Catenin, Cell Proliferation, Glycoproteins, Signal Transduction

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
45
Top 10%
Top 10%
Top 10%
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