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- W2085287554 abstract "In the testis, a subset of spermatogonia retains stem cell potential, while others differentiate to eventually become spermatozoa. This delicate balance must be maintained, as defects can result in testicular cancer or infertility. Currently, little is known about the gene products and signaling pathways directing these critical cell fate decisions. Retinoic acid (RA) is a requisite driver of spermatogonial differentiation and entry into meiosis, yet the mechanisms activated downstream are undefined. Here, we determined a requirement for RA in the expression of KIT, a receptor tyrosine kinase essential for spermatogonial differentiation. We found that RA signaling utilized the PI3K/AKT/mTOR signaling pathway to induce the efficient translation of mRNAs for Kit, which are present but not translated in undifferentiated spermatogonia. Our findings provide an important molecular link between a morphogen (RA) and the expression of KIT protein, which together direct the differentiation of spermatogonia throughout the male reproductive lifespan." @default.
- W2085287554 created "2016-06-24" @default.
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- W2085287554 date "2015-01-01" @default.
- W2085287554 modified "2023-09-29" @default.
- W2085287554 title "Retinoic acid regulates Kit translation during spermatogonial differentiation in the mouse" @default.
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- W2085287554 doi "https://doi.org/10.1016/j.ydbio.2014.10.020" @default.
- W2085287554 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4268412" @default.
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