Prof. Norio Nakatsuji
Assist. Prof. Shinichiro Chuma
This laboratory analyzes molecular and cellular mechanisms to control function of stem cells and
differentiation of mammalian germ cells by using various mouse strains. Particular attention is paid to
the development of germ cells and spermatogenic cells in testes, as well as pluripotent embryonic stem
cells.
Prof. Shinya Yamanaka
Assist. Prof. Masato Nakagawa
The ultimate goal of our laboratory is to generate ES-like pluripotent stem cells directly from somatic
cells by nuclear reprogramming. To this end, we are trying to understand molecular mechanisms
underlying pluripotency and rapid proliferation of ES cells and to identify factors that induce reprogramming.
We have shown that pluripotent stem cells can be induced from mouse embryonic and adult
fibroblast cultures by retrovirus-mediated introduction of four transcription factors (Oct3/4, Sox2, Klf4,
c-Myc). We designated these cells iPS cells for induced pluripotent stem cells. We are now trying to
generate human iPS cells and overcome safety issues.
Prof. Atsuko Sehara
Assist. Prof. Tomohiro Kurisaki
Assist. Prof. Shuji Wakatsuki
Development and regeneration require various kinds of intercellular signaling and adhesion molecules. Our research
has been focused on regulatory mechanisms of such cell-cell interactions. Numerous intercellular signaling molecules
are generated as membrane-anchored proteins, and they are subjected to proteolytic processing to liberate their
extracellular domains (ectodomain shedding). Molecular bases that regulate the ectodomain shedding events are coming
into focus. Evidence suggests that ADAM family proteases are involved in the ecotodmain shedding of various membrane
proteins. We are currently studying roles of ADAM proteases in development and diseases, which will clarify
physiological significance of ecdodomain shedding mediated by ADAM proteases.
Assoc. Prof. Tatsuo Kina
Assist. Prof. Shinji Fujimoto
Our current research activities cover two areas. The first is the molecular mechanism of inflammatory
diseases in BALB/c.CD45.1 mice. These mice spontaneously develop atopic dermatitis and allergic
tympanitis/conjuncitivitis in eyes and ears. We are investigating the cause of these diseases at the molecular
level, and our current hypothesis of regulation of CD45 function is illustrated in Fig.1. The
second research activity is focused on TCR? chain gene rearrangement and the mechanism of
lymphomagenesis during recovery of atrophied thymus.after irradiation or ENU treatment. In connection
with this, we are investigating the role of transcription factor Id2 in the differentiation of T and NK
cells from thymic T/NK common progenitors.
Human Embryonic Stem Cell Project
