The University of Tokyo · 의학
Toshio Kitamura 교수의 연구실은 백혈병 및 골수성 악성질환의 분자 기전을 규명하는 데 초점을 맞추고 있으며, 특히 혈액세포 성장인자와 수용체의 기능, STAT 신호전달 경로, 그리고 ASXL1 유전자 변이가 허혈성 혈액줄기세포의 기능과 분화에 미치는 영향을 중심으로 연구를 진행하고 있습니다. GM-CSF, IL-3, EPO 등의 세포 성장인자와 그 수용체의 상호작용, 그리고 비정상적인 신호전달이 백혈병 발생에 기여하는 메커니즘을 분석하고 있습니다. 또한, 유전자 변이가 허혈성 혈액세포의 분화 및 생존에 미치는 영향을 유전자 조작 모델을 통해 실시간으로 규명하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
We have established a novel cell line, designated as TF-1, from a patient with erythroleukemia, which showed complete growth dependency on granulocyte-macrophage colony-stimulating factor (GM-CSF) or on interleukin-3 (IL-3) and carried a homogeneous chromosomal abnormality (54X). Erythropoietin (EPO) also sustained the short-term growth of TF-1, but did not induce erythroid differentiation. These three hematopoietic growth factors acted on TF-1 synergistically. Transforming growth factor-beta an
STAT (signal transducers and activators of transcription) proteins are transcription factors which are activated by phosphorylation on tyrosine residues upon stimulation by cytokines. Seven members of the STAT family are known, including the closely related STAT5A and STAT5B, which are activated by various cytokines. Except for prolactin-dependent beta-casein production in mammary gland cells, the biological consequences of STAT5 activation in various systems are not clear. We applied PCR-driven
The high-affinity receptor for human granulocyte/macrophage colony-stimulating factor (hGM-CSF) is composed of two subunits, alpha and beta. The alpha subunit binds GM-CSF with low affinity, whereas the beta subunit does not bind GM-CSF by itself. The alpha and beta subunits together form the high-affinity GM-CSF receptor. The beta subunit has extensive sequence homology with the mouse interleukin 3 (IL-3) receptor (AIC2A) and its homologue (AIC2B) that does not bind IL-3 or other cytokines incl
Additional sex combs like 1 (ASXL1) is frequently mutated in myeloid malignancies and clonal hematopoiesis of indeterminate potential (CHIP). Although loss of ASXL1 promotes hematopoietic transformation, there is growing evidence that ASXL1 mutations might confer an alteration of function. In this study, we identify that physiological expression of a C-terminal truncated Asxl1 mutant in vivo using conditional knock-in (KI) results in myeloid skewing, age-dependent anemia, thrombocytosis, and mor
