Talk:Embryology History - Shinya Yamanaka
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Cite this page: Hill, M.A. (2026, October 5) Embryology Embryology History - Shinya Yamanaka. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Embryology_History_-_Shinya_Yamanaka |
2008
Pluripotency and nuclear reprogramming
Philos Trans R Soc Lond B Biol Sci. 2008 Jun 27;363(1500):2079-87.
Yamanaka S. Source Center for iPS Cell Research & Application, Kyoto University, Kyoto 606-8507, Japan. yamanaka@frontier.kyoto-u.ac.jp
Abstract
Embryonic stem cells are promising donor cell sources for cell transplantation therapy, which may in the future be used to treat various diseases and injuries. However, as is the case for organ transplantation, immune rejection after transplantation is a potential problem with this type of therapy. Moreover, the use of human embryos presents serious ethical difficulties. These issues may be overcome if pluripotent stem cells are generated from patients' somatic cells. Here, we review the molecular mechanisms underlying pluripotency and the currently known methods of inducing pluripotency in somatic cells.
PMID 18375377
B-MYB is essential for normal cell cycle progression and chromosomal stability of embryonic stem cells
PLoS One. 2008 Jun 25;3(6):e2478.
Tarasov KV, Tarasova YS, Tam WL, Riordon DR, Elliott ST, Kania G, Li J, Yamanaka S, Crider DG, Testa G, Li RA, Lim B, Stewart CL, Liu Y, Van Eyk JE, Wersto RP, Wobus AM, Boheler KR. Source Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Abstract
BACKGROUND: The transcription factor B-Myb is present in all proliferating cells, and in mice engineered to remove this gene, embryos die in utero just after implantation due to inner cell mass defects. This lethal phenotype has generally been attributed to a proliferation defect in the cell cycle phase of G1. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, we show that the major cell cycle defect in murine embryonic stem (mES) cells occurs in G2/M. Specifically, knockdown of B-Myb by short-hairpin RNAs results in delayed transit through G2/M, severe mitotic spindle and centrosome defects, and in polyploidy. Moreover, many euploid mES cells that are transiently deficient in B-Myb become aneuploid and can no longer be considered viable. Knockdown of B-Myb in mES cells also decreases Oct4 RNA and protein abundance, while over-expression of B-MYB modestly up-regulates pou5f1 gene expression. The coordinated changes in B-Myb and Oct4 expression are due, at least partly, to the ability of B-Myb to directly modulate pou5f1 gene promoter activity in vitro. Ultimately, the loss of B-Myb and associated loss of Oct4 lead to an increase in early markers of differentiation prior to the activation of caspase-mediated programmed cell death. CONCLUSIONS/SIGNIFICANCE: Appropriate B-Myb expression is critical to the maintenance of chromosomally stable and pluripotent ES cells, but its absence promotes chromosomal instability that results in either aneuploidy or differentiation-associated cell death.
PMID 18575582
Generation of pluripotent stem cells from adult mouse liver and stomach cells
Science. 2008 Aug 1;321(5889):699-702. Epub 2008 Feb 14.
Aoi T, Yae K, Nakagawa M, Ichisaka T, Okita K, Takahashi K, Chiba T, Yamanaka S. Source Department of Stem Cell Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. Erratum in Science.2008 Aug 1;321(5889): 641.
Abstract
Induced pluripotent stem (iPS) cells have been generated from mouse and human fibroblasts by the retroviral transduction of four transcription factors. However, the cell origins and molecular mechanisms of iPS cell induction remain elusive. This report describes the generation of iPS cells from adult mouse hepatocytes and gastric epithelial cells. These iPS cell clones appear to be equivalent to embryonic stem cells in gene expression and are competent to generate germline chimeras. Genetic lineage tracings show that liver-derived iPS cells are derived from albumin-expressing cells. No common retroviral integration sites are found among multiple clones. These data suggest that iPS cells are generated by direct reprogramming of lineage-committed somatic cells and that retroviral integration into specific sites is not required.
PMID 18276851
