期刊论文详细信息
BMC Developmental Biology
Progenitor expansion in apc mutants is mediated by Jak/Stat signaling
Richard I Dorsky1  Xu Wang1  Junji Lin1 
[1]Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
关键词: zebrafish;    progenitor;    Stat3;    APC;    Wnt;   
Others  :  1086958
DOI  :  10.1186/1471-213X-11-73
 received in 2011-09-02, accepted in 2011-12-02,  发布年份 2011
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【 摘 要 】

Background

Mutations in APC, a negative regulator of the Wnt/ß-catenin pathway, can cause cancer as well as profound developmental defects. In both cases, affected cells adopt a proliferative progenitor state and fail to differentiate. While the upregulation of some target genes of Wnt/ß-catenin signaling has been shown to mediate these phenotypes in individual tissues, it is unclear whether a common mechanism underlies the defects in APC mutants.

Results

Here we show that stat3, a known oncogene and a target of ß-catenin in multiple tissues, is upregulated in apc mutant zebrafish embryos. We further demonstrate that Jak/Stat signaling is necessary for the increased level of proliferation and neural progenitor gene expression observed in apc mutants.

Conclusions

Together, our data suggest that the regulation of Jak/Stat signaling may represent a conserved mechanism explaining the expansion of undifferentiated cells downstream of APC mutations.

【 授权许可】

   
2011 Lin et al; licensee BioMed Central Ltd.

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