The University of Tokyo · 생화학·유전·분자생물학
Yukiko Gotoh 교수의 연구실은 세포 신호전달 경로, 특히 맵키나제(MAPK) 신호 경로의 활성화 메커니즘과 그 기능을 중심으로 연구를 진행하고 있습니다. 산화 스트레스, 세포사멸, 스트레스 반응 등 다양한 세포 신호에 의해 활성화되는 ASK1과 같은 MAPKKK 및 MAPK의 역할을 규명하고 있으며, 특히 TNF-알파, 산화물질, 삼투압 변화 등에 의한 세포 반응에서의 신호 전달 경로의 기여를 분석하고 있습니다. 이들의 연구는 세포 생존과 사멸의 분자 기전을 이해하는 데 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Reactive oxygen species (ROS) have been implicated in the induction of apoptosis by tumor necrosis factor-alpha (TNFalpha) and other cytotoxic insults, although the molecule(s) regulated by ROS in TNFalpha signaling have not been identified. Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase (MAPKKK) superfamily that has been shown to be activated during TNFalpha-induced apoptosis. ASK1 increases apoptosis when overexpressed, but the mec
We have isolated a gene, pmk1+, a third mitogen-activated protein kinase (MAPK) gene homolog from the fission yeast Schizosaccharomyces pombe. The predicted amino acid sequence shows the most homology (63 to 65% identity) to those of budding yeast Saccharomyces Mpk1 and Candida Mkc1. The Pmk1 protein contains phosphorylated tyrosines, and the level of tyrosine phosphorylation was increased in the dsp1 mutant which lacks an attenuating phosphatase for Pmk1. The level of tyrosine phosphorylation a
Mitogen-activated protein kinase (MAPK) and MAPK kinase (MAPKK) are activated during Xenopus oocyte maturation concomitant with the activation of maturation promoting factor (MPF). We reported previously that an anti-MAPKK neutralizing antibody inhibited progesterone- or Mos- induced initiation of oocyte maturation. Here, we show that the injection of CL100 (also called MAPK phosphatase-1) into immature oocytes inhibited progesterone-induced oocyte maturation as well as MAPK activation and that
Osmotic shock induces a variety of biochemical and physiological responses in vertebrate cells. By analyzing extracts obtained from rat 3Y1 fibroblastic cells exposed to hyper-osmolar media, we have found that mitogen-activated protein kinases (MAPKs) and stress-activated protein kinases (SAPKs, also known as JNKs) are both activated in response to osmotic shock. MAPKK1 (MEK1) was also activated markedly. Furthermore, Raf-1 and MEKK were activated strikingly by the osmotic shock. Activation of R
