• Publications
  • Influence
FGF23 induces left ventricular hypertrophy.
Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascularExpand
  • 1,292
  • 98
  • PDF
An essential role for Rac in Ras transformation
THE GTPase Racl is a key component in the reorganization of the actin cytoskeleton that is induced by growth factors or oncogenic Ras1. Here we investigate the role of Racl in cell transformation andExpand
  • 891
  • 45
Induction of Caspase-3-Like Protease May Mediate Delayed Neuronal Death in the Hippocampus after Transient Cerebral Ischemia
Delayed neuronal death after transient cerebral ischemia may be mediated, in part, by the induction of apoptosis-regulatory gene products. Caspase-3 is a newly characterized mammalian cysteineExpand
  • 697
  • 39
Stress Proteins and Tolerance to Focal Cerebral Ischemia
Stress proteins are induced after a variety of neuronal injuries. The inducible 72-kDa heat shock protein (hsp70) is a stress protein that protects neurons from glutamate toxicity in vitro. Hsp70 hasExpand
  • 307
  • 20
Early Detection of DNA Strand Breaks in the Brain After Transient Focal Ischemia: Implications for the Role of DNA Damage in Apoptosis and Neuronal Cell Death
Abstract: Using in situ DNA polymerase I‐mediated biotin‐dATP nick‐translation (PANT) and terminal deoxynucleotidyl‐transferase‐mediated dUTP nick end‐labeling (TUNEL), we investigated the evolutionExpand
  • 302
  • 15
Mobilization of hematopoietic stem cells during homeostasis and after cytokine exposure.
We created parabiotic mice, joining ROSA26 and PeP3b animals, to study the trafficking of hematopoietic stem cells (HSCs) from marrow to blood and their return to marrow. The transfer of HSCs wasExpand
  • 241
  • 10
  • PDF
Ischemic tolerance in the brain
Brief episodes of brain ischemia define a patient population at increased risk for stroke. These brief events (TIAs) warrant urgent evaluation and treatment. It is therefore counterintuitive thatExpand
  • 219
  • 9
Optimal B-cell proliferation requires phosphoinositide 3-kinase-dependent inactivation of FOXO transcription factors.
Transcription factors of the Forkhead Box, class O (FOXO) family promote cell-cycle arrest and/or apoptosis in a variety of cell types. Mitogenic stimuli inactivate FOXO function by way of anExpand
  • 142
  • 9
  • PDF
Th1/Th2 Functional Imbalance After Acute Myocardial Infarction: Coronary Arterial Inflammation or Myocardial Inflammation
Objectives: The study clarified whether the T-helper (Th)1/Th2 imbalance existed only in coronary arterial inflammation or in both coronary arterial inflammation and myocardial inflammation andExpand
  • 75
  • 8
Expression of the Apoptosis‐Effector Gene, Bax, Is Up‐Regulated in Vulnerable Hippocampal CA1 Neurons Following Global Ischemia
Abstract: The observation that delayed death of CA1 neurons after global ischemia is inhibited by protein synthesis inhibitors suggests that the delayed death of these neurons is an active processExpand
  • 237
  • 7