Recently visited
Please sign in to see a list of articles you recently visited.
Recently updated
 SOX9
Homo sapiens
 HIF1A
Homo sapiens
 Pax6
Mus musculus
 PAX6
Homo sapiens
 Snai2
Mus musculus
 PPARA
Homo sapiens
 Ppara
Mus musculus
 Thrb
Mus musculus
 SNAI2
Homo sapiens
 Tbr1
Mus musculus
Transcription Factor Encyclopedia  BETA
Comments (post)
There are no comments posted here... Yet.
Overview

Nfia was the first NFI gene disrupted in the mouse and loss of Nfia causes agenesis of the corpus callosum, perinatal lethality and major neuroanatomical defects. Several recent studies show that Nfia is essential for normal brain development and likely plays a role in the "gliogenic switch", the process by which multi-potential neural progenitor cells switch from making neuronal progenitor cell to making glial progenitor cell. Loss of Nfia appears to delay brain maturation as seen by expression profiling and causes defects in cerebellar granule cell differentiation related to changes in cell adhesion molecule expression. Studies of humans with deletions in NFIA led to the discovery of renal defects in Nfia-deficient mice.

See NFIA for general information about the NFI gene family

Figures
FIGURE 1 Fig. 1. Absence of corpus callosum in Nfia-/- mice
Cresyl violet-stained coronal sections thorough the brains of 18 d.p.c. C57BL/6 fetuses. (A and B) Wide field pictures of the brains of -/- and +/+ litter mates with the region surrounding the corpus callosum boxed. (C and D) Expansion of panels A and B showing the corpus callosum in the +/+ animal (labeled cc in panel D) and the absence of the corpus callosum in the -/- animal. Serial sections throughout this region showed a complete absence of callosal development in -/- animals. The bars at the bottom right of panels B and D equal 2 and 1 mm, respectively. Copyright ©1999 by the National Academy of Sciences PNAS Vol. 96, No. 21, p.11946-11951, 1999
This figure was created by the authors of this article. The authors of this article have provided the assurance that this figure constitutes their original work.