PMC:2944667 / 12034-13169 JSONTXT

{"project":"TEST0","denotations":[{"id":"20877431-230-238-637133","span":{"begin":356,"end":360},"obj":"[\"8439411\"]"},{"id":"20877431-217-225-637134","span":{"begin":580,"end":584},"obj":"[\"10195217\"]"},{"id":"20877431-177-185-637135","span":{"begin":764,"end":768},"obj":"[\"10864959\"]"},{"id":"20877431-198-206-637136","span":{"begin":785,"end":789},"obj":"[\"11826116\"]"},{"id":"20877431-212-220-637137","span":{"begin":1004,"end":1008},"obj":"[\"10864959\"]"}],"text":"Fibroblast growth factor signaling is important for the regulation of neurogenesis in the developing cortex. Studies in vitro originally suggested that the ability of a cortical NSC to stop self-renewing and begin the differentiation process was somehow delayed by increased FGF signaling, resulting in an expanded stem cell pool (Kilpatrick and Bartlett, 1993). The first in vivo demonstration was provided by injection of an FGF ligand, FGF2, in rat embryonic brain ventricles, which resulted in an expanded cortex with increased excitatory neuron production (Vaccarino et al., 1999). Conversely, the deletion of the fgf2 gene resulted in a cortex with reduced numbers of glutamatergic excitatory neurons, particularly in the anterior neocortex (Raballo et al., 2000; Korada et al., 2002). This was not due to a change in the cell cycle or by alterations in cell survival, suggesting that FGF signaling might affect the early amplification of stem cells or their immediate descendants (Raballo et al., 2000). This was confirmed by later work performed on FGF receptor knockout mice (see FGFs and the Developing Dorsal Telencephalon)."}

{"project":"0_colil","denotations":[{"id":"20877431-8439411-637133","span":{"begin":356,"end":360},"obj":"8439411"},{"id":"20877431-10195217-637134","span":{"begin":580,"end":584},"obj":"10195217"},{"id":"20877431-10864959-637135","span":{"begin":764,"end":768},"obj":"10864959"},{"id":"20877431-11826116-637136","span":{"begin":785,"end":789},"obj":"11826116"},{"id":"20877431-10864959-637137","span":{"begin":1004,"end":1008},"obj":"10864959"}],"text":"Fibroblast growth factor signaling is important for the regulation of neurogenesis in the developing cortex. Studies in vitro originally suggested that the ability of a cortical NSC to stop self-renewing and begin the differentiation process was somehow delayed by increased FGF signaling, resulting in an expanded stem cell pool (Kilpatrick and Bartlett, 1993). The first in vivo demonstration was provided by injection of an FGF ligand, FGF2, in rat embryonic brain ventricles, which resulted in an expanded cortex with increased excitatory neuron production (Vaccarino et al., 1999). Conversely, the deletion of the fgf2 gene resulted in a cortex with reduced numbers of glutamatergic excitatory neurons, particularly in the anterior neocortex (Raballo et al., 2000; Korada et al., 2002). This was not due to a change in the cell cycle or by alterations in cell survival, suggesting that FGF signaling might affect the early amplification of stem cells or their immediate descendants (Raballo et al., 2000). This was confirmed by later work performed on FGF receptor knockout mice (see FGFs and the Developing Dorsal Telencephalon)."}

{"project":"2_test","denotations":[{"id":"20877431-8439411-38520410","span":{"begin":356,"end":360},"obj":"8439411"},{"id":"20877431-10195217-38520411","span":{"begin":580,"end":584},"obj":"10195217"},{"id":"20877431-10864959-38520412","span":{"begin":764,"end":768},"obj":"10864959"},{"id":"20877431-11826116-38520413","span":{"begin":785,"end":789},"obj":"11826116"},{"id":"20877431-10864959-38520414","span":{"begin":1004,"end":1008},"obj":"10864959"}],"text":"Fibroblast growth factor signaling is important for the regulation of neurogenesis in the developing cortex. Studies in vitro originally suggested that the ability of a cortical NSC to stop self-renewing and begin the differentiation process was somehow delayed by increased FGF signaling, resulting in an expanded stem cell pool (Kilpatrick and Bartlett, 1993). The first in vivo demonstration was provided by injection of an FGF ligand, FGF2, in rat embryonic brain ventricles, which resulted in an expanded cortex with increased excitatory neuron production (Vaccarino et al., 1999). Conversely, the deletion of the fgf2 gene resulted in a cortex with reduced numbers of glutamatergic excitatory neurons, particularly in the anterior neocortex (Raballo et al., 2000; Korada et al., 2002). This was not due to a change in the cell cycle or by alterations in cell survival, suggesting that FGF signaling might affect the early amplification of stem cells or their immediate descendants (Raballo et al., 2000). This was confirmed by later work performed on FGF receptor knockout mice (see FGFs and the Developing Dorsal Telencephalon)."}