Gina E. Elsen
Seattle Children's Research Institute
19 Papers
122 Citations
Gina E. Elsen is an academic researcher from Seattle Children's Research Institute. The author has contributed to research in topics: Hindbrain & Cellular differentiation. The author has an hindex of 13, co-authored 19 publications. Previous affiliations of Gina E. Elsen include Boston Children's Hospital & University of Chicago.
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Papers
Tbr1 regulates regional and laminar identity of postmitotic neurons in developing neocortex
Francesco Bedogni,Rebecca D. Hodge,Gina E. Elsen,Branden R. Nelson,Ray A. M. Daza,Richard P. Beyer,Theo K. Bammler,John L.R. Rubenstein,Robert F. Hevner +8 more
TL;DR: Tbr1 coordinately regulates regional and laminar identity of postmitotic cortical neurons, and exhibits ectopic axon projections to the hypothalamus and cerebral peduncle.
335
Zebrafish Hoxb1a regulates multiple downstream genes including prickle1b
TL;DR: It is demonstrated that the Hoxb1a target Prickle1b functions cell-autonomously to control facial neuron migration, a single aspect of r4 identity.
111
Zic1 and Zic4 regulate zebrafish roof plate specification and hindbrain ventricle morphogenesis.
TL;DR: It is concluded that Zic1 and Zic4 control zebrafish 4th ventricle morphogenesis by regulating multiple mechanisms including cell proliferation and fate specification in the dorsal hindbrain.
72
Neurog2 Simultaneously Activates and Represses Alternative Gene Expression Programs in the Developing Neocortex
Christopher P. Kovach,Rajiv Dixit,Saiqun Li,Pierre Mattar,Grey Wilkinson,Gina E. Elsen,Deborah M. Kurrasch,Robert F. Hevner,Carol Schuurmans +8 more
TL;DR: This work demonstrates that Neurog2 functions as an activator to both extinguish Pax6 expression in radial glial cells and initiate Tbr2 expression in intermediate neuronal progenitors, and activates several genetic off-switches, each with distinct transcriptional targets, revealing an unappreciated level of specificity for how neurog2 prevents inappropriate gene expression during neocortical development.
β-Noradrenergic receptor activation specifically modulates the generation of sighs in vivo and in vitro.
TL;DR: The results suggest that the selective β-NR action of sighs may result from the modulation of INap pacemaker activity and that disturbances in noradrenergic system may contribute to abnormal arousal response.