S
Shane T. Grey
Researcher at Garvan Institute of Medical Research
Publications - 129
Citations - 8260
Shane T. Grey is an academic researcher from Garvan Institute of Medical Research. The author has contributed to research in topics: Transplantation & Islet. The author has an hindex of 48, co-authored 114 publications receiving 7537 citations. Previous affiliations of Shane T. Grey include Alfred Hospital & Beth Israel Deaconess Hospital.
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Journal ArticleDOI
Expression of heme oxygenase-1 can determine cardiac xenograft survival
Miguel P. Soares,Yuan Lin,Josef Anrather,Eva Csizmadia,Ko Takigami,Koichiro Sato,Shane T. Grey,Robert B. Colvin,Augustine M.K. Choi,Kenneth D. Poss,Fritz H. Bach +10 more
TL;DR: It is shown that the expression of the HO-1 gene is functionally associated with xenograft survival, and that rapid expression ofHO-1 in cardiac xenografteds can be essential to ensure long-term xenogRAFT survival.
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In vivo expansion of T reg cells with IL-2–mAb complexes: induction of resistance to EAE and long-term acceptance of islet allografts without immunosuppression
Kylie E. Webster,Stacey N. Walters,Rachel E. Kohler,Tomas Mrkvan,Onur Boyman,Charles D. Surh,Shane T. Grey,Jonathan Sprent +7 more
TL;DR: An in vivo approach for inducing rapid expansion of T reg cells by injecting mice with interleukin (IL)-2 mixed with a particular IL-2 monoclonal antibody (mAb) complexes, which has clinical potential for treating autoimmune disease and promoting organ transplantation.
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Superoxide-mediated activation of uncoupling protein 2 causes pancreatic β cell dysfunction
Stefan Krauss,Chen-Yu Zhang,Luca Scorrano,Louise Torp Dalgaard,Julie St-Pierre,Shane T. Grey,Bradford B. Lowell +6 more
TL;DR: It is demonstrated that endogenously produced mitochondrial superoxide activates UCP2-mediated proton leak, thus lowering ATP levels and impairing glucose-stimulated insulin secretion, and superoxide levels are increased further in the absence of U CP2, demonstrating that the adverse effects of superoxide on beta cell glucose sensing are caused by activation of UCP1.
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BAFF and MyD88 signals promote a lupuslike disease independent of T cells
Joanna R Groom,Carrie A. Fletcher,Stacey N. Walters,Shane T. Grey,Sally V. Watt,Mathew J. Sweet,Mark J. Smyth,Charles R. Mackay,Fabienne Mackay +8 more
TL;DR: Autoimmunity in BAFF Tg mice results from altered B cell tolerance, but requires TLR signaling and is independent of T cell help, and it is possible that SLE patients with elevated levels of BAFF show a similar basis for disease.
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Role for Activating Transcription Factor 3 in Stress-Induced β-Cell Apoptosis
Matthew G. Hartman,Dan Lu,Mi Lyang Kim,Gary J. Kociba,Tala Shukri,Jean Buteau,Xiaozhong Wang,Xiaozhong Wang,Wendy L. Frankel,Denis C. Guttridge,Marc Prentki,Shane T. Grey,David Ron,Tsonwin Hai +13 more
TL;DR: Several lines of evidence supporting a role of ATF3 in stress-induced β-cell apoptosis are described, and results suggest ATF3 to be a novel regulator of stress- induced β- cell apoptosis.