• Publications
  • Influence
Retinoic acid selectively regulates Fgf10 expression and maintains cell identity in the prospective lung field of the developing foregut.
Although respiratory tract defects that result from disruption of retinoic acid (RA) signaling have been widely reported, the mechanism by which endogenous RA regulates early lung morphogenesis isExpand
  • 122
  • 8
An evolutionarily conserved mechanism of calcium-dependent neurotoxicity in a zebrafish model of fetal alcohol spectrum disorders.
BACKGROUND Fetal alcohol spectrum disorders (FASD) are a leading cause of neurodevelopmental disability. Nonhuman animal models offer novel insights into its underlying mechanisms. Although theExpand
  • 28
  • 4
CaMKII activation is a novel effector of alcohol’s neurotoxicity in neural crest stem/progenitor cells
J. Neurochem. (2011) 118, 646–657.
  • 38
  • 3
Ethanol triggers neural crest apoptosis through the selective activation of a pertussis toxin-sensitive G protein and a phospholipase Cbeta-dependent Ca2+ transient.
BACKGROUND Alcohol is a potent neurotoxin that triggers the selective apoptosis of neuronal populations in the developing fetus. For neural crest cells, clinically relevant ethanol levels (0.3%)Expand
  • 49
  • 2
Increased Fibronectin Deposition in Embryonic Hearts of Retinol-Binding Protein–Null Mice
Abstract— Precise regulation of retinoid levels is critical for normal heart development. Retinol-binding protein (RBP), an extracellular retinol transporter, is strongly secreted by cardiogenicExpand
  • 38
  • 2
  • PDF
Structural constraints for alcohol-stimulated Ca2+ release in neural crest, and dual agonist/antagonist properties of n-octanol.
BACKGROUND Prenatal ethanol exposure is a leading cause of mental retardation. Alcohol damages susceptible neuronal populations through its alteration of signaling pathways that direct cellularExpand
  • 22
  • 2
Adequacy of Maternal Iron Status Protects against Behavioral, Neuroanatomical, and Growth Deficits in Fetal Alcohol Spectrum Disorders
Fetal alcohol spectrum disorders (FASD) are the leading non-genetic cause of neurodevelopmental disability in children. Although alcohol is clearly teratogenic, environmental factors such asExpand
  • 37
  • 1
  • PDF
Neural crest development in fetal alcohol syndrome.
Fetal alcohol spectrum disorder (FASD) is a leading cause of neurodevelopmental disability. Some affected individuals possess distinctive craniofacial deficits, but many more lack overt facialExpand
  • 57
  • 1
CaMKII represses transcriptionally active β‐catenin to mediate acute ethanol neurodegeneration and can phosphorylate β‐catenin
Prenatal ethanol exposure causes persistent neurodevelopmental deficits by inducing apoptosis within neuronal progenitors including the neural crest. The cellular signaling events underlying thisExpand
  • 40
  • 1
A ryanodine receptor-dependent Cai2+ asymmetry at Hensen's node mediates avian lateral identity
In mouse, the establishment of left-right (LR) asymmetry requires intracellular calcium (Cai2+) enrichment on the left of the node. The use of Cai2+ asymmetry by other vertebrates, and its originsExpand
  • 21
  • 1
  • PDF