C
Christopher D. Ferris
Researcher at Johns Hopkins University School of Medicine
Publications - 53
Citations - 12138
Christopher D. Ferris is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Inositol & Inositol phosphate. The author has an hindex of 37, co-authored 53 publications receiving 11783 citations. Previous affiliations of Christopher D. Ferris include Johns Hopkins University & Vanderbilt University.
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Journal ArticleDOI
Protein S-nitrosylation: a physiological signal for neuronal nitric oxide.
Samie R. Jaffrey,Hediye Erdjument-Bromage,Christopher D. Ferris,Paul Tempst,Solomon H. Snyder +4 more
TL;DR: Protein S-nitrosylation is established as a physiological signalling mechanism for neuronally generated NO in mice harbouring a genomic deletion of neuronal NO synthase (nNOS).
Journal ArticleDOI
d-Serine is an endogenous ligand for the glycine site of the N-methyl-d-aspartate receptor
Jean-Pierre Mothet,Angèle T. Parent,Angèle T. Parent,Herman Wolosker,Roscoe O. Brady,David J. Linden,Christopher D. Ferris,Michael A. Rogawski,Solomon H. Snyder +8 more
TL;DR: D-serine is an endogenous modulator of the glycine site of NMDA receptors and fully occupies this site at some functional synapses and greatly attenuates NMDA receptor-mediated neurotransmission as assessed by using whole-cell patch-clamp recordings or indirectly by using biochemical assays of the sequelae of NMda receptor- mediated calcium flux.
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Biliverdin reductase: a major physiologic cytoprotectant.
TL;DR: It is reported that bilirubin is a major physiologic antioxidant cytoprotectant that can protect cells from a 10,000-fold excess of H2O2 and markedly augments tissue levels of reactive oxygen species and causes apoptotic cell death.
Journal ArticleDOI
S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding
Makoto R. Hara,Nishant Agrawal,Sangwon F. Kim,Matthew B. Cascio,Masahiro Fujimuro,Yuji Ozeki,Masaaki Takahashi,Jaime H. Cheah,Stephanie Tankou,Lynda D. Hester,Christopher D. Ferris,S. Diane Hayward,Solomon H. Snyder,Akira Sawa +13 more
TL;DR: A signalling pathway in which nitric oxide generation that follows apoptotic stimulation elicits S-nitrosylation of GAPDH, which triggers binding to Siah1 (an E3 ubiquitin ligase), nuclear translocation and apoptosis, which is prevented by NO deletion is reported.