Emanuel M. DiCicco-Bloom

UMDNJ-Robert Wood Johnson Medical School, Piscataway Township, NJ, United States 
Embryonic neurogenesis, PACAP
"Emanuel DiCicco-Bloom"
Mean distance: 15.47 (cluster 6)
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Prem S, Millonig JH, DiCicco-Bloom E. (2020) Dysregulation of Neurite Outgrowth and Cell Migration in Autism and Other Neurodevelopmental Disorders. Advances in Neurobiology. 25: 109-153
Turkalj L, Mehta M, Matteson P, et al. (2020) Using iPSC-Based Models to Understand the Signaling and Cellular Phenotypes in Idiopathic Autism and 16p11.2 Derived Neurons. Advances in Neurobiology. 25: 79-107
Gupta A, Li X, DiCicco-Bloom E, et al. (2018) Altered salt taste response and increased tongue epithelium Scnna1 expression in adult Engrailed-2 null mice. Physiology & Behavior
Williams M, Prem S, Zhou X, et al. (2018) Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs). Journal of Visualized Experiments : Jove
Connacher RJ, DiCicco-Bloom E, Millonig JH. (2018) Using Human Induced Neural Precursor Cells to Define Early Neurodevelopmental Defects in Syndromic and Idiopathic Autism Current Pharmacology Reports. 4: 422-435
Mony TJ, Lee JW, Dreyfus C, et al. (2016) Valproic Acid Exposure during Early Postnatal Gliogenesis Leads to Autistic-like Behaviors in Rats. Clinical Psychopharmacology and Neuroscience : the Official Scientific Journal of the Korean College of Neuropsychopharmacology. 14: 338-344
Verpeut JL, DiCicco-Bloom E, Bello NT. (2016) Ketogenic diet exposure during the juvenile period increases social behaviors and forebrain neural activation in adult Engrailed 2 null mice. Physiology & Behavior
Lee HJ, Dreyfus C, DiCicco-Bloom E. (2015) Valproic acid stimulates proliferation of glial precursors during cortical gliogenesis in developing rat. Developmental Neurobiology
Dever DP, Adham ZO, Thompson B, et al. (2015) Aryl hydrocarbon receptor deletion in cerebellar granule neuron precursors impairs neurogenesis. Developmental Neurobiology
Genestine M, Lin L, Durens M, et al. (2015) Engrailed-2 (En2) deletion produces multiple neurodevelopmental defects in monoamine systems, forebrain structures and neurogenesis and behavior. Human Molecular Genetics
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