Research Topics
Species | Robert FreemanSummaryAffiliation: University of Rochester Country: USA Publications
Research Grants
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Detail Information
Publications
Protein S blocks the extrinsic apoptotic cascade in tissue plasminogen activator/N-methyl D-aspartate-treated neurons via Tyro3-Akt-FKHRL1 signaling pathwayHuang Guo
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery and Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA
Mol Neurodegener 6:13. 2011..abstract:..
SM-20, EGL-9, and the EGLN family of hypoxia-inducible factor prolyl hydroxylasesRobert S Freeman
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Mol Cells 16:1-12. 2003..elegans important for normal egg laying...- NGF deprivation-induced gene expression: after ten years, where do we stand?Robert S Freeman
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
Prog Brain Res 146:111-26. 2004..In this chapter, we discuss the evidence that these genes act as regulators of neuronal cell death. We also suggest a hypothesis for how one gene, SM-20, may function to suppress a self-protection mechanism in NGF-deprived neurons... 
Inhibition of NGF deprivation-induced death by low oxygen involves suppression of BIMEL and activation of HIF-1Liang Xie
Department of Pharmacology and Physiology, University of Rochester School of Medicine, Rochester, NY 14642, USA
J Cell Biol 168:911-20. 2005..These data suggest a new model for how O(2) tension can influence apoptotic events that underlie trophic factor deprivation-induced cell death...- Prolyl hydroxylase inhibitors delay neuronal cell death caused by trophic factor deprivationDavid J Lomb
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
J Neurochem 103:1897-906. 2007..Thus, while HIF prolyl hydroxylase inhibitors can delay cell death in NGF-deprived neurons, they do so through distinct mechanisms that, at least in the case of DHB, are partly independent of HIF stabilization... - Induction of SM-20 in PC12 cells leads to increased cytochrome c levels, accumulation of cytochrome c in the cytosol, and caspase-dependent cell deathJennifer A Straub
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
J Neurochem 85:318-28. 2003..These results suggest that SM-20 promotes caspase-dependent cell death through a mechanism involving cytochrome c... - A shortcut to mitochondrial signaling and pathology: a commentary on "Nonenzymatic formation of succinate in mitochondria under oxidative stress"Paul S Brookes
Department of Anesthesiology, University of Rochester Medical Center, Box 604, 601 Elmwood Avenue, Rochester, NY 14642, USA
Free Radic Biol Med 41:41-5. 2006 - EGLN3 prolyl hydroxylase regulates skeletal muscle differentiation and myogenin protein stabilityJian Fu
Cardiovascular Research Institute and Department of Medicine, Univeristy of Rochester Medical Center, Rochester, NY 14642, USA
J Biol Chem 282:12410-8. 2007..In addition, this report provides evidence for a novel pathway that regulates myogenin expression and skeletal muscle differentiation... - Targeting hypoxia-inducible factor (HIF) as a therapeutic strategy for CNS disordersRobert S Freeman
Department of Pharmacology and Physiology, University of Rochester School of Medicine, Rochester, NY 14642, USA. edu
Curr Drug Targets CNS Neurol Disord 4:85-92. 2005.... - Pin1 promotes cell death in NGF-dependent neurons through a mechanism requiring c-Jun activityMaria Cecilia Barone
Department of Pharmacology and Physiology, University of Rochester School of Medicine, Rochester, New York, USA
J Neurochem 106:734-45. 2008..Finally, cell death induced by ectopic Pin1 was largely blocked by expression of dominant negative c-Jun. These results suggest a novel mechanism by which Pin1 promotes cell death involving activation of c-Jun... - Prolyl hydroxylase inhibitors depend on extracellular glucose and hypoxia-inducible factor (HIF)-2alpha to inhibit cell death caused by nerve growth factor (NGF) deprivation: evidence that HIF-2alpha has a role in NGF-promoted survival of sympathetic neurDavid J Lomb
Department of Pharmacology and Physiology, University of Rochester School of Medicine, Rochester, NY 14642, USA
Mol Pharmacol 75:1198-209. 2009..These results implicate HIF-2alpha in the neuroprotective mechanisms of prolyl hydroxylase inhibitors and in an endogenous cell survival pathway activated by NGF in developing neurons... - Protein S protects neurons from excitotoxic injury by activating the TAM receptor Tyro3-phosphatidylinositol 3-kinase-Akt pathway through its sex hormone-binding globulin-like regionZhihui Zhong
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery and Neurology, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurosci 30:15521-34. 2010.... - Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: developmental culling and cancerSungwoo Lee
Department of Medical Oncology, Dana Farber Cancer Institute and Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Cell 8:155-67. 2005..Moreover, EglN3 proapoptotic activity requires SDH activity because EglN3 is feedback inhibited by succinate. These studies suggest that failure of developmental apoptosis plays a role in pheochromocytoma pathogenesis... - Angiotensin II's antiproliferative effects mediated through AT2-receptors depend on down-regulation of SM-20Gunter Wolf
Department of Medicine, Division of Nephrology and Osteology, University of Hamburg, Hamburg, Germany
Lab Invest 82:1305-17. 2002..This gene apparently plays an important role in the regulatory processes determining whether a cell should undergo differentiation, apoptosis, or proliferation... - Apoptosis signaling by the novel compound 3-Cl-AHPC involves increased EGFR proteolysis and accompanying decreased phosphatidylinositol 3-kinase and AKT kinase activitiesLulu Farhana
John D Dingell VA Medical Center, Karmanos Cancer Institute, Department of Internal Medicine, Wayne State University, Detroit, MI 48201, USA
Oncogene 23:1874-84. 2004..Inhibition of AKT activity by this compound results in the inability of AKT to phosphorylate and inactivate the proapoptotic forkhead transcription factor...
Research Grants
- Mechanisms of Neurotrophin dependent SurvivalRobert Freeman; Fiscal Year: 2005..Together these experiments will test the importance of NF-kB for neurotrophinregulated survival and they will uncover important new information concerning the mechanisms by which neurotrophins protect neurons from cell death. ..
- Genes That Regulate Neuronal Cell DeathRobert Freeman; Fiscal Year: 2007..They will also provide new information concerning the function of EGLN-catalyzed proline hydroxylation as a novel mechanism for altering protein function in neurons. ..
- Multidisciplinary Training in Developmental NeuroscienceRobert Freeman; Fiscal Year: 2007..A plan is also in place that will increase the pool of predoctoral applicants from underrepresented racial and ethnic groups. ..
- Prolyl Hydroxylation and Neuronal Cell DeathRobert S Freeman; Fiscal Year: 2010..Information gained from this project will further our understanding of normal development and could help identify new targets for therapies aimed at preventing pathological neuronal cell death. ..
- GENES THAT REGULATE NEURONAL DEATHRobert Freeman; Fiscal Year: 2002..This work should further our long-term goals of elucidating the molecular mechanism of neuronal PCD and of developing the means to manipulate the process pharmacologically. ..
- Prolyl Hydroxylation and Neuronal Cell DeathRobert Freeman; Fiscal Year: 2009..Information gained from this project may help identify new targets for therapies aimed at preventing neuronal loss. ..