| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2014: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2012: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
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| Outline of Final Research Achievements |
BMPs are key serum-derived factors that act to sustain self-renewal and pluripotency of mouse ES cells. In contrast, human ES cells share defining features with mouse epiblast stem cells (mEpiSC). BMP-4 induces differentiation of mEpiSCs into extraembryonic lineage or mesendoderm. We found that the BMP-Smad pathway is dispensable for maintaining naive pluripotency, and that the transcriptional factor KLF4 plays a key role in the suppression of Smad1 activity. We also found that the MEK5-ERK5 pathway mediates BMP-4-induced self-renewal of mESCs by inducing KLF2.
We have investigated the roles of BMPs in regulation of glioma-initiating cells (GICs). In the orthotopic transplantation model, BMP signaling repressed the tumorigenic activity through loss of stemness properties of GICs. We further performed DNA microarray and RNA-seq analyses to identify novel target genes of BMP signaling in GICs, and found that PRRX1 plays an important role in regulation of the differentiation of GICs.
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