• Publications
  • Influence
Altered gene expression in neurons during programmed cell death: identification of c-jun as necessary for neuronal apoptosis
We have examined the hypothesis that neuronal programmed cell death requires a genetic program; we used a model wherein rat sympathetic neurons maintained in vitro are deprived of NGF andExpand
  • 851
  • 36
  • PDF
Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: developmental culling and cancer.
Germline NF1, c-RET, SDH, and VHL mutations cause familial pheochromocytoma. Pheochromocytomas derive from sympathetic neuronal precursor cells. Many of these cells undergo c-Jun-dependent apoptosisExpand
  • 482
  • 27
Phosphatidylinositol 3-Kinase and Akt Protein Kinase Are Necessary and Sufficient for the Survival of Nerve Growth Factor-Dependent Sympathetic Neurons
Recent studies have suggested a role for phosphatidylinositol (PI) 3-kinase in cell survival, including the survival of neurons. We used rat sympathetic neurons maintained in vitro to characterizeExpand
  • 584
  • 21
  • PDF
Analysis of cell cycle-related gene expression in postmitotic neurons: Selective induction of cyclin D1 during programmed cell death
Sympathetic neurons undergo RNA and protein synthesis-dependent programmed cell death when deprived of nerve growth factor. To test the hypothesis that neuronal programmed cell death is a consequenceExpand
  • 571
  • 18
Nerve Growth Factor-Dependent Activation of NF-κB Contributes to Survival of Sympathetic Neurons
Neurotrophins activate multiple signaling pathways in neurons. However, the precise roles of these signaling molecules in cell survival are not well understood. In this report, we show that nerveExpand
  • 242
  • 15
  • PDF
JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death
Glaucoma is a neurodegenerative disease characterized by the apoptotic death of retinal ganglion cells (RGCs). The primary insult to RGCs in glaucoma is thought to occur to their axons as they exitExpand
  • 105
  • 9
  • PDF
Oxygen-Regulated β2-Adrenergic Receptor Hydroxylation by EGLN3 and Ubiquitylation by pVHL
Hypoxia reduces proline hydroxylation and ubiquitylation of a G protein–coupled receptor, preventing down-regulation. Oxygen-Regulated GPCR Down-Regulation Adrenergic signaling through β-adrenergicExpand
  • 132
  • 7
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 Region
The anticoagulant factor protein S (PS) protects neurons from hypoxic/ischemic injury. However, molecular mechanisms mediating PS protection in injured neurons remain unknown. Here, we show mouseExpand
  • 46
  • 6
Glycogen Synthase Kinase-3β Activity Is Critical for Neuronal Death Caused by Inhibiting Phosphatidylinositol 3-Kinase or Akt but Not for Death Caused by Nerve Growth Factor Withdrawal*
Numerous studies reveal that phosphatidylinositol (PI) 3-kinase and Akt protein kinase are important mediators of cell survival. However, the survival-promoting mechanisms downstream of these enzymesExpand
  • 192
  • 5
  • PDF
NGF deprivation-induced gene expression: after ten years, where do we stand?
Nerve growth factor (NGF) is required for the survival of developing sympathetic and sensory neurons. In the absence of NGF, these neurons undergo protein synthesis-dependent apoptosis. Ten yearsExpand
  • 85
  • 4
...
1
2
3
4
5
...