In embryonic cells, Nfix has been shown to regulate
intermediate progenitor cell (IPC) generation by promoting the transcription of the protein inscuteable (INSC). INSC regulates spindle orientation to facilitate the division of
radial glia cells into IPC's. Nfix is thought to be necessary for the commitment of glia progeny into the intermediate progenitors. Mutations may cause overproduction of radial glia, impaired and improperly timed IPC development, and underproduction of neurons. [10]
In adult development, the timing of neural differentiation is regulated by Nfix to promote ongoing growth of the
hippocampus and proper memory function. Nfix may suppress
oligodendrocyte expression so cells remain committed to neuron development within the
dentate gyrus. Intermediate progenitor cells can divide to produce
neuroblasts. Neurons produced by Nfix null IPC's do not mature, usually die, and can contribute to cognitive impairments.[11]
Nfix interacts with
myostatin and regulates temporal progression of muscle regeneration through modulation of myostatin expression. Nfix also inhibits the slow-twitch muscle phenotype.[12][13]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Seisenberger C, Winnacker EL, Scherthan H (Aug 1993). "Localisation of the human nuclear factor I/X (NFI/X) gene to chromosome 19p13 and detection of five other related loci at 1p21-22, 1q42-43, 5q15, 11p13 and 20q13 by FISH". Hum Genet. 91 (6): 535–537.
doi:
10.1007/bf00205076.
PMID8340106.
S2CID22365562.
^Qian F, Kruse U, Lichter P, Sippel AE (Dec 1995). "Chromosomal localization of the four genes (NFIA, B, C, and X) for the human transcription factor nuclear factor I by FISH". Genomics. 28 (1): 66–73.
doi:
10.1006/geno.1995.1107.
PMID7590749.
In embryonic cells, Nfix has been shown to regulate
intermediate progenitor cell (IPC) generation by promoting the transcription of the protein inscuteable (INSC). INSC regulates spindle orientation to facilitate the division of
radial glia cells into IPC's. Nfix is thought to be necessary for the commitment of glia progeny into the intermediate progenitors. Mutations may cause overproduction of radial glia, impaired and improperly timed IPC development, and underproduction of neurons. [10]
In adult development, the timing of neural differentiation is regulated by Nfix to promote ongoing growth of the
hippocampus and proper memory function. Nfix may suppress
oligodendrocyte expression so cells remain committed to neuron development within the
dentate gyrus. Intermediate progenitor cells can divide to produce
neuroblasts. Neurons produced by Nfix null IPC's do not mature, usually die, and can contribute to cognitive impairments.[11]
Nfix interacts with
myostatin and regulates temporal progression of muscle regeneration through modulation of myostatin expression. Nfix also inhibits the slow-twitch muscle phenotype.[12][13]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Seisenberger C, Winnacker EL, Scherthan H (Aug 1993). "Localisation of the human nuclear factor I/X (NFI/X) gene to chromosome 19p13 and detection of five other related loci at 1p21-22, 1q42-43, 5q15, 11p13 and 20q13 by FISH". Hum Genet. 91 (6): 535–537.
doi:
10.1007/bf00205076.
PMID8340106.
S2CID22365562.
^Qian F, Kruse U, Lichter P, Sippel AE (Dec 1995). "Chromosomal localization of the four genes (NFIA, B, C, and X) for the human transcription factor nuclear factor I by FISH". Genomics. 28 (1): 66–73.
doi:
10.1006/geno.1995.1107.
PMID7590749.