Yuriko Nozaki

Publications (2)31.34 Total impact

• Article: Sirt1, p53, and p38(MAPK) are crucial regulators of detrimental phenotypes of embryonic stem cells with Max expression ablation.

  Tomoaki Hishida, Yuriko Nozaki, Yutaka Nakachi, Yosuke Mizuno, Hiroyoshi Iseki, Miyuki Katano, Masayoshi Kamon, Masataka Hirasaki, Masazumi Nishimoto, Yasushi Okazaki, Akihiko Okuda
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  ABSTRACT: c-Myc participates in diverse cellular processes including cell cycle control, tumorigenic transformation, and reprogramming of somatic cells to induced pluripotent cells. c-Myc is also an important regulator of self-renewal and pluripotency of embryonic stem cells (ESCs). We recently demonstrated that loss of the Max gene, encoding the best characterized partner for all Myc family proteins, causes loss of the pluripotent state and extensive cell death in ESCs strictly in this order. However, the mechanisms and molecules that are responsible for these phenotypes remain largely obscure. Here, we show that Sirt1, p53, and p38(MAPK) are crucially involved in the detrimental phenotype of Max-null ESCs. Moreover, our analyses revealed that these proteins are involved at varying levels to one another in the hierarchy of the pathway leading to cell death in Max-null ESCs.
  Stem Cells 06/2012; 30(8):1634-44. · 7.78 Impact Factor
• Article: Indefinite self-renewal of ESCs through Myc/Max transcriptional complex-independent mechanisms.

  Tomoaki Hishida, Yuriko Nozaki, Yutaka Nakachi, Yosuke Mizuno, Yasushi Okazaki, Masatsugu Ema, Satoru Takahashi, Masazumi Nishimoto, Akihiko Okuda
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  ABSTRACT: Embryonic stem cells (ESCs) can self-renew indefinitely under the governance of ESC-specific transcriptional circuitries in which each transcriptional factor regulates distinct or overlapping sets of genes with other factors. c-Myc is a key player that is crucially involved in maintaining the undifferentiated state and the self-renewal of ESCs. However, the mechanism by which c-Myc helps preserve the ESC status is still poorly understood. Here we addressed this question by performing loss-of-function studies with the Max gene, which encodes the best-characterized partner protein for all Myc family proteins. Although Myc/Max complexes are widely regarded as crucial regulators of the ESC status, our data revealed that ESCs do not absolutely require these complexes in certain contexts and that this requirement is restricted to empirical ESC culture conditions without a MAPK inhibitor.
  Cell stem cell 07/2011; 9(1):37-49. · 23.56 Impact Factor