SCOTT OAKESSummaryAffiliation: University of California Country: USA Publications
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Publications
The control of endoplasmic reticulum-initiated apoptosis by the BCL-2 family of proteinsScott A Oakes
Department of Pathology, University of California, San Francisco, 94143, USA
Curr Mol Med 6:99-109. 2006..Recent work has shown that the BCL-2 family of proteins plays a central role in regulating this form of cell death, both locally at the ER and from a distance at the mitochondrial membrane...
Mitochondria control calcium entry at the immunological synapseScott A Oakes
Department of Pathology, University of California, San Francisco, CA 94143-0511, USA
Proc Natl Acad Sci U S A 104:15171-2. 2007- Caspase-2 cleavage of BID is a critical apoptotic signal downstream of endoplasmic reticulum stressJohn Paul Upton
Department of Pathology, Medicine, University of California, San Francisco, California 94143, USA
Mol Cell Biol 28:3943-51. 2008..Our work defines a novel signaling pathway that couples the ER and mitochondria and establishes a principal apoptotic effector downstream of ER stress... - IRE1alpha kinase activation modes control alternate endoribonuclease outputs to determine divergent cell fatesDan Han
Department of Medicine, University of California, San Francisco, San Francisco, CA 94143 2520, USA
Cell 138:562-75. 2009..We propose that divergent cell fates during ER stress hinge on a balance between IRE1alpha RNase outputs that can be tilted with kinase inhibitors to favor survival... - A kinase inhibitor activates the IRE1alpha RNase to confer cytoprotection against ER stressDan Han
Department of Medicine, University of California, San Francisco, San Francisco, CA 94143 2520, USA
Biochem Biophys Res Commun 365:777-83. 2008..Thus kinase inhibitors of IRE1alpha are useful for altering the apoptotic outcome to ER stress, and could possibly be developed into drugs to treat ER stress-related diseases... - Blocking the mitochondrial apoptotic pathway preserves motor neuron viability and function in a mouse model of amyotrophic lateral sclerosisNichole A Reyes
Department of Pathology, University of California, San Francisco, San Francisco, California 94143 0511, USA
J Clin Invest 120:3673-9. 2010..Hence, inhibiting apoptosis upstream of mitochondrial permeabilization represents a possible therapeutic strategy for preserving functional motor neurons in ALS and other MNDs... - Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulumScott A Oakes
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:105-10. 2005..These findings support a model in which BCL-2 family members regulate IP3R-1 phosphorylation to control the rate of ER Ca(2+) leak from intracellular stores... - Untangling the web: mitochondrial fission and apoptosisScott A Oakes
Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Dev Cell 7:460-2. 2004..A new study by Szabadkai et al. in the October 8th issue of Molecular Cell shows that dynamin-related protein 1 (Drp1)-induced scission hinders the ability of mitochondria to transport calcium across the cell and mediate apoptosis... - Phosphorylation of BCL-2 regulates ER Ca2+ homeostasis and apoptosisMichael C Bassik
Department of Pathology and Medicine, Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
EMBO J 23:1207-16. 2004..Unexpectedly, the regulation of ER Ca(2+) dynamics is a principal avenue whereby BCL-2 phosphorylation alters susceptibility to apoptosis... - Regulation of endoplasmic reticulum Ca2+ dynamics by proapoptotic BCL-2 family membersScott A Oakes
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Boston, USA
Biochem Pharmacol 66:1335-40. 2003..Thus, BAX and BAK control apoptosis not only at the mitochondria, but also at the ER, an obligate checkpoint for Ca(2+)-dependent apoptotic stimuli... - BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosisLuca Scorrano
Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Department of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
Science 300:135-9. 2003..Thus, BAX and BAK operate in both the ER and mitochondria as an essential gateway for selected apoptotic signals... - A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosisLuca Scorrano
Howard Hughes Medical Institute, Department of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, 02115, Boston, MA, USA
Dev Cell 2:55-67. 2002..This reorganization does not require tBID's BH3 domain and is independent of BAK, but is inhibited by CsA. During this process, individual cristae become fused and the junctions between the cristae and the intermembrane space are opened...
Research Grants
- BAX/BAK control ER-mitochondria apoptotic crosstalkSCOTT OAKES; Fiscal Year: 2007..Dr. Scott Oakes, the Principal Investigator, is an M.D...
- Signaling Cell Death from the Endoplasmic ReticulumSCOTT OAKES; Fiscal Year: 2009..This projects sets out to define how cellular stress normally leads to apoptosis and what goes wrong with this process in cancer-in the hopes of finding new therapeutic targets through which to kill tumor cells. ..
- Signaling Cell Death from the Endoplasmic ReticulumScott A Oakes; Fiscal Year: 2010..This projects sets out to define how cellular stress normally leads to apoptosis and what goes wrong with this process in cancer-in the hopes of finding new therapeutic targets through which to kill tumor cells. ..