Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Michelle Tait"'
Autor:
Marylene Leboeuf, Miriam Merad, Guillaume Darrasse-Jèze, Andrew J. Murphy, Camille Lobry, Hugo Mouquet, Julie Kalter, Gavin Thurston, Amanda DaNave, George D. Yancopoulos, Ralph M. Steinman, Iannis Aifantis, Wen Zhang, Fabienne Billiard, Dimitris Skokos, Michelle Tait, Xia Liu, Jacquelynn Burton, Apostolos Klinakis, Janelle C. Waite, Juliana Idoyaga, Christos A. Kyratsous
Publikováno v:
The Journal of Experimental Medicine
Blocking Dll4–Notch signaling can reverse established diabetes via Flt3-independent induction of immature thymic DCs that enhance Treg cell generation in mice.
Delta-like ligand 4 (Dll4)–Notch signaling is essential for T cell development an
Delta-like ligand 4 (Dll4)–Notch signaling is essential for T cell development an
Autor:
Andrew J. Murphy, Janelle C. Waite, Guoying Chen, Gavin Thurston, Sandra Coetzee, Fabienne Billiard, Kara Olson, Jessica R. Kirshner, Donna Hylton, Amanda DaNave, Dimitris Skokos, Michelle Tait, Sean Taheri, George D. Yancopoulos, Wen Zhang
Publikováno v:
European Journal of Immunology. 41:2207-2216
The essential role of the Delta-like ligand 4 (Dll4)-Notch signaling pathway in T-lymphocyte development is well established. It has been shown that specific inactivation of Dll4 on thymic stromal cells during early post-natal development leads to a
Autor:
Roland G. Roberts, Tom C. Freeman, Alistair K. Dixon, Elizabeth A. Campbell, Martin Bobrow, Tere-Michelle Tait
Publikováno v:
Journal of Molecular Biology. 270:551-558
We have recently characterised a new member of the dystrophin gene family, DRP2, and its murine counterpart, Drp2, which encode dystrophin-related protein 2 (DRP2). DRP2 is predicted to resemble certain short C-terminal isoforms of dystrophin and dys
Autor:
Tere-Michelle Tait, Alistair K Dixon, Amanda Smith, Elizabeth A. Campbell, Michael R. Stratton, Alan Ashworth, Richard Wooster, Tom C. Freeman, Frances Connor
Publikováno v:
Human molecular genetics. 6(2)
A proportion of human breast cancers result from an inherited predisposition to the disease. Mutations in the BRCA2 gene confer a high risk of breast cancer and are responsible for almost half of these cases. The recent cloning of the human BRCA2 gen