The University of Osaka · 의학
이 교수의 연구실은 전사 인자인 MITF와 관련된 면역세포, 특히 마스터세포의 분화 및 기능 조절 메커니즘을 중심으로 연구를 진행하고 있습니다. 특히 마스터세포 특이성 단백질 분해효소(MMCP-5, MMCP-6)의 발현 조절을 통해 면역 반응과 관련된 유전자 조절 네트워크를 규명하고 있으며, 암세포의 생존 및 전이 메커니즘을 규명하기 위한 CDCP1과 ALDH1 등의 마커 단백질 연구도 함께 수행하고 있습니다. 이는 암의 발병 기전과 치료 저항성에 대한 기초적 이해를 심화하는 데 기여합니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The mi locus of mice encodes a member of the basic-helix-loop-helix-leucine zipper (bHLH-Zip) protein family of transcription factors (hereafter called MITF). Because the expression of the mouse mast cell protease 6 (MMCP-6) gene is remarkably reduced in mast cells of mi/mi mutant mice, we investigated the effect of MITF on the transcription of the MMCP-6 gene. First, we introduced the normal (+) MITF cDNA into mi/mi cultured mast cells using the retroviral vector. Overexpression of +-MITF but n
CUB domain containing protein (CDCP1), a transmembrane protein with intracellular tyrosine residues which are phosphorylated upon activation, is supposed to be engaged in proliferative activities and resistance to apoptosis of cancer cells. Expression level of CDCP1 was examined in lung adenocarcinoma, and its clinical implications were evaluated. CDCP1 expression was immunohistochemically examined in lung adenocarcinoma from 200 patients. Staining intensity of cancer cells was categorized as lo
Mast cells contain a lot of mast cell-specific proteases. We have reported that the expression of mouse mast cell protease 6 (MMCP-6) is remarkably reduced in both cultured mast cells (CMCs) and skin mast cells of mi/mi mutant mice. In the present study, we found that the expression of MMCP-5 was reduced in CMCs but not in skin mast cells of mi/mi mice, and we compared the regulation mechanisms of MMCP-5 with those of MMCP-6. The mi locus encodes a member of the basic-helix-loop-helix-leucine zi
Aldehyde dehydrogenase 1 (ALDH1) is expressed in stem/progenitor cells, including cancer-initiating cells (CIC) of various organs. In the present study, ALDH1 expression was immunohistochemically examined in uterine endometrioid adenocarcinoma. The ALDH1 was expressed in a small portion of tumor cells, and these ALDH1-expressing cells were less mature than ALDH1-non-expressing cells. The ALDH1-expressing (ALDH1-hi) cells were more tumorigenic, resistant to anti-cancer agents and more invasive th