Kyoto University · 생화학·유전·분자생물학
이 교수의 연구실은 Drosophila를 모델로 삼아 세포 경쟁, 세포 사멸 조절 메커니즘, 그리고 종양 미세환경이 조직 내 세포 간 상호작용을 통해 종양 진행에 기여하는 메커니즘을 연구하고 있습니다. 특히 Bcl-2 가족 단백질과 IAP 단백질이 세포 사멸을 어떻게 조절하는지, 그리고 내재적 스트레스 반응(예: 내막망 스트레스)이 세포 경쟁을 유도하는지에 초점을 맞추고 있습니다. 또한, 유전자 변이가 있는 세포가 주변 세포의 성장과 전이에 영향을 주는 '온코지닉 니치 세포'(ONCs)의 형성 메커니즘을 규명하며 비자기적 종양 진행 메커니즘을 밝혀내고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The Bcl-2/CED-9 family of proteins, which includes both antiapoptotic and proapoptotic members, plays key regulating roles in programmed cell death. We report here the identification and characterization of Drob-1, the first Drosophila member of the Bcl-2/CED-9 family to be isolated. Drob-1 contains four conserved Bcl-2 homology domains (BH1, BH2, BH3, and BH4) and a C-terminal hydrophobic domain. Ectopic expression of Drob-1 in the developing Drosophila eye resulted in a rough-eye phenotype. Fu
Members of the inhibitor of apoptosis protein (IAP) family can inhibit caspases and cell death in a variety of insect and vertebrate systems. Drosophila IAP1 (DIAP1) inhibits cell death to facilitate normal embryonic development. Here, using RNA interference, we showed that down-regulation of DIAP1 is sufficient to induce cell death in Drosophila S2 cells. Although this cell death process was accompanied by elevated caspase activity, this activation was not essential for cell death. We found tha
Cell competition is a context-dependent cell elimination through short-range cell-cell interaction, in which cells with higher fitness eliminate neighboring less-fit or oncogenic cells within the growing tissue. Cell competition can be triggered by many different factors such as heterozygous mutations in the ribosomal protein genes (which are called "Minute" mutations), elevated Myc, Yorkie/YAP, Wg/Wnt, JAK-STAT, Ras, or Src activity, and loss of Mahjong/VprBP, endocytic pathway components, or a
Cell competition is a context-dependent cell elimination via cell-cell interaction whereby unfit cells ('losers') are eliminated from the tissue when confronted with fitter cells ('winners'). Despite extensive studies, the mechanism that drives loser's death and its physiological triggers remained elusive. Here, through a genetic screen in Drosophila, we find that endoplasmic reticulum (ER) stress causes cell competition. Mechanistically, ER stress upregulates the bZIP transcription factor Xrp1,
