M
Michael C. Appel
Researcher at University of Massachusetts Medical School
Publications - 39
Citations - 3445
Michael C. Appel is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Islet & Insulitis. The author has an hindex of 25, co-authored 39 publications receiving 3366 citations. Previous affiliations of Michael C. Appel include National Institutes of Health & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses.
Francis Ka-Ming Chan,Francis Ka-Ming Chan,Joanna L. Shisler,Jacqueline G. Bixby,Martin Felices,Lixin Zheng,Michael C. Appel,Jan M. Orenstein,Bernard Moss,Michael J. Lenardo +9 more
TL;DR: TNF-induced programmed necrosis is facilitated by TNFR-2 signaling and caspase inhibition and may play a role in controlling viral infection.
Journal ArticleDOI
Survival of mouse pancreatic islet allografts in recipients treated with allogeneic small lymphocytes and antibody to CD40 ligand
David C. Parker,Dale L. Greiner,Nancy E. Phillips,Michael C. Appel,Alan W. Steele,Fiona H. Durie,Randolph J. Noelle,John P. Mordes,Aldo A. Rossini +8 more
TL;DR: This data indicates that small lymphocytes expressing donor antigens in the absence of appropriate costimulatory signals are tolerogenic for alloreactive host cells and anti-CD40L antibody may prevent host T cells from inducing costimulations in donor lymphocytes or islet grafts.
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Studies of streptozotocin-induced insulitis and diabetes.
TL;DR: It is suggested that multiple injections of streptozotocin induce, in susceptible hosts, the triad of direct beta cell cytotoxicity, virus induction within beta cells, and cell-mediated autoimmune reaction, which appears to induce a destructive insulitis and severe diabetes.
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Requirement of the JIP1 scaffold protein for stress-induced JNK activation
Alan J. Whitmarsh,Chia-Yi Kuan,Norman J. Kennedy,Nyaya Kelkar,Tarik F. Haydar,John P. Mordes,Michael C. Appel,Aldo A. Rossini,Stephen N. Jones,Richard A. Flavell,Pasko Rakic,Roger J. Davis +11 more
TL;DR: Disruption of the Jip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro.
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Spontaneous diabetes mellitus: reversal and prevention in the BB/W rat with antiserum to rat lymphocytes.
TL;DR: Injections of rabbit antiserum to rat lymphocytes reversed hyperglycemia in 36 percent of spontaneously diabetic rats and prevented diabetes in susceptible nondiabetic controls, strengthening the hypothesis that cell-mediated autoimmunity plays a role in the pathogenesis of diabetes in this animal model.