Motonari Kondo
Stanford University
18 Papers
384 Citations
Motonari Kondo is an academic researcher from Stanford University. The author has contributed to research in topics: Lymphopoiesis & Haematopoiesis. The author has an hindex of 15, co-authored 17 publications. Previous affiliations of Motonari Kondo include Tohoku University.
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Papers
Identification of Clonogenic Common Lymphoid Progenitors in Mouse Bone Marrow
TL;DR: The Lin(-)IL-7R(+)Thy-1(-)Sca-1loc-Kit(lo) population from adult mouse bone marrow possessed a rapid lymphoid-restricted (T, B, and NK) reconstitution capacity in vivo but completely lacked myeloid differentiation potential either in vivo or in vitro.
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Bcl-2 Rescues T Lymphopoiesis in Interleukin-7 Receptor–Deficient Mice
TL;DR: It is shown that enforced expression of the bcl-2 gene in T-lymphoid cells (by crossing in the Emu-bcl- 2 transgene) in IL-7R alpha-deficient mice results in a significant restoration of thymic positive selection and T cell numbers and function.
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The interleukin-2 receptor gamma chain: its role in the multiple cytokine receptor complexes and T cell development in XSCID.
Kazuo Sugamura,Hironobu Asao,Motonari Kondo,Nobuyuki Tanaka,Naoto Ishii,Kazuyuki Ohbo,Masataka Nakamura,Toshikazu Takeshita +7 more
TL;DR: The molecular identification of the gamma chain brought a grasp of the structures and functions of the cytokine receptor and an in-depth understanding of the cause of human XSCID.
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Cell-fate conversion of lymphoid-committed progenitors by instructive actions of cytokines
Motonari Kondo,David C. Scherer,Toshihiro Miyamoto,Angela G. King,Koichi Akashi,Kazuo Sugamura,Irving L. Weissman +6 more
TL;DR: It is concluded that cytokine signalling can regulate cell-fate decisions and proposed that a critical step in lymphoid commitment is downregulation of cytokine receptors that drive myeloid cell development.
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Bcl-2 Rescues T Lymphopoiesis, but Not B or NK Cell Development, in Common γ Chain–Deficient Mice
TL;DR: The forced expression of Bcl-2 restored all stages of T lymphopoiesis, but not B or NK cell development, indicating that a primary function of gamma(c)-mediated signals in the T lineage might be to maintain cell survival.
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