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 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
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Genetics

Foxh1 mouse mutant embryos die by embryonic day (E) 9.5. At E8.5, Foxh1 deficient embryos show a range of phenotypes that fall into three general classes: (1) embryos showing greatly reduced anterior structures, secondary heart field and loss of dorsal midline structures, such as notochord and node, (2) embryos entirely lacking both head and midline structures, and (3) embryos failing to orient the anterior-posterior (A-P) axis correctly, resulting in the lack of structures derived from the embryo proper. A-P patterning defects, but not midline defects, can be rescued by restoration of Foxh1 expression in the visceral endoderm. Foxh1-/- cells fail to populate the definitive endoderm. Furthermore, marker analysis has demonstrated that Foxh1 mutant embryos fail to specify foregut endoderm. Rare embryos surviving to E10.5 exhibit holoprosencephaly and laterality defects [1][2]. Conditional knockout of Foxh1 in the lateral plate mesoderm results in death within a few days after birth. Mutant embryos fail to express Nodal, lefty2 and Pitx2 on the left side during embryogenesis, thus exhibit right isomerism affecting the heart, lungs, and stomach. In humans, sequence variants of FOXH1 have been linked to holoprosencephaly, laterality defects and congenital heart defects. The FOXH1 sequence variants, in combination with variants in other components of the Nodal pathway, likely as a result in reduced Nodal signalling [3]. The Foxh1 gene lies on chromosome 15 in mice and chromosome 8 in humans. The gene has 3 exons with the 3’ UTR overlapping with the 3’ UTR of the neighboring KIFC2 gene.

References
  1. Hoodless PA et al. FoxH1 (Fast) functions to specify the anterior primitive streak in the mouse. Genes Dev., 15(10):1257-71. (PMID 11358869)
  2. Yamamoto M et al. The transcription factor FoxH1 (FAST) mediates Nodal signaling during anterior-posterior patterning and node formation in the mouse. Genes Dev., 15(10):1242-56. (PMID 11358868)
  1. Roessler E et al. Reduced NODAL signaling strength via mutation of several pathway members including FOXH1 is linked to human heart defects and holoprosencephaly. Am. J. Hum. Genet., 83(1):18-29. (PMID 18538293)
MeSH cloud (automatically populated)
About this section
The MeSH cloud below displays MeSH terms that are associated with this transcription factor. The physical size of the terms reflect the significance of their association with the transcription factor as determined by the Fisher's Exact Test. It should be noted that these associations do not necessarily imply a positive correlation between the described MeSH term and this transcription factor. For instance, if the MeSH term "apoptosis" occurs, it may indicate that this transcription factor can induce apoptosis (positive correlation), or prevent apoptosis (negative correlation). Methods: The transcription factor is mapped to a set of Pubmed publications through the gene-to-pubmed association as provided by NCBI. Then, a collection of MeSH terms associated with the papers are compiled, along with the frequency of each MeSH term. The Fisher's Exact Test is conducted on the frequency of each term in the collection, versus its average frequency, to determine its significance in the collection. More information on MeSH can be found on the MeSH homepage.
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MGI mammalian phenotype terms (automatically populated)