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This study showed that three genes were found to be consistently regulated by Brn3a throughout postnatal retina development - Mapk10, Tusc5 and Cdh4.
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Double morphant embryos targeted with morpholino oligonucleotides to both TFs develop significant cardiac defects (looping abnormalities and valve defects) suggesting essential roles for Brn-3a and Brn-3b in developing hearts.
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Study demonstrates a sequential expression order of NEUROD1>ISL1>POU4F1>POU4F2 during the inner ear neurogenesis.
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Pou4f1 and pou4f2 are dispensable for the long-term survival of adult retinal ganglion cells in mice.
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The deficiency of Pou4f1 who perform poorly in motivation-based locomotor behaviors, such as voluntary wheel running and the accelerating rotarod, but show only minor abnormalities in gait and balance and exhibit normal levels of basal locomotion.
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Data indicate that Brn3 transcription factors Brn3b affects Brn3a and Brn3c positive Retinal Ganglion Cells (RGCs) in cell autonomous and non-cell autonomous fashion.
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The results demonstrated a critical role for Brn3a in generating dorsal root ganglia sensory neuron diversity and regulating sensory afferent projections to the central targets.
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neither Brn3a nor Brn3c are expressed in intrinsically photosensitive retinal ganglion cells
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Brn3 gene expression patterns in the retina and inner ear, these experiments suggest a deep functional similarity among primary somatosensory neurons, spiral and vestibular ganglion neurons, and retinal ganglion cells
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Progressive increase in IOP and loss of Brn3a signals in D2 animals were consistent with glaucoma progression starting after 6 months of age.
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An epistatic interaction between Brn3a and Isl1 is key to sensory neuron specification, in their absence almost all known markers of sensory neurons are lost. Data support the hypothesis that Brn3a and Isl1 bind to shared enhancers in target genes.
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Data show a longitudinal domain positive for both Nkx6.1 and Nkx6.2 that is medial to the Pou4f1-positive red nucleus. This domain could correspond to part of the reticular formation, which extends from the diencephalon and the mesencephalon.
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data define AR as a direct Brn-3a interactor and verify a simple interacting protein prediction methodology that is likely to be useful for many other proteins
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Data show that Brn3a acts upstream of the Runx factors, which then repress TrkB expression to allow establishment of the non-overlapping Trk receptor profiles and correct terminally differentiated phenotypes.
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Brn3a regulates the transition from neurogenesis to terminal differentiation and represses non-neural gene expression in the trigeminal ganglion.
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Deficiency of Brn-3a may cause the increase and decrease of Cgrp-immunoreactive expression in small dorsal root ganglion (DRG) neurons projecting to the dorsal column and large DRG neurons projecting to the deep dorsal horn, respectively.
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Nociceptors and low-threshold mechanoreceptors with medium-sized to large cell bodies in the trigeminal ganglion may be sensitive to the loss of Brn-3a.
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Brn3a locus functions as a self-regulating unit to maintain a constant expression level of this key regulator of neural development.Sensory expression of Brn3a is regulated by a specific enhancer, Brn3a binds to conserved sites within this enhancer
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Axon growth is markedly disturbed in Brn3a knockout mice; it is unlikely that Brn3a targets Bcl-2 or mediates the defects in axon guidance and neuronal survival observed in the sensory ganglia of Brn3a knockout mice.
