Disease relevance of Foxg1

• Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular disease (CVD) with myocardial infarction [1].
• Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular disease with myocardial infarction (CVD) [2].
• Platelet-associated IgG (PAIgG) on the platelet surface mediates platelet destruction by the reticuloendothelial system in the autoimmune thrombocytopenic purpura (ATP) of W/BF1 mice [3].
• An average of 250 colonies of metastasis in the lungs was counted in mice (BF10 mice) at 14 days after the inoculation of 2 x 10(5) B16F10 cells/mouse, while <20 colonies were detected in mice (BF1 mice) inoculated with the same number of B16F1 cells [4].
• Also, an increase in the number of pulmonary melanoma was demonstrated in BF1 mice treated with 10 microg/kg murine rIL-4 [4].

High impact information on Foxg1

• These results suggest that BF-1 controls the morphogenesis of the telencephalon by regulating the rate of neuroepithelial cell proliferation and the timing of neuronal differentiation [5].
• Telencephalic neuroepithelial cells are specified in the BF-1 mutant, but their proliferation is reduced [5].
• These results suggest that BF-1 plays an important role in the establishment of the regional subdivision of the developing brain and in the development of the telencephalon [6].
• Animals carrying a floxed Rb allele were interbred with mice in which cre was knocked into the Foxg1 locus [7].
• Moreover, coexpression of Grg6 and BF-1 in cortical progenitor cells leads to a decrease in the number of proliferating cells and increased neuronal differentiation [8].

Chemical compound and disease context of Foxg1

• Autoimmune-prone (NZW x BXSB)F1 (W/BF1) mice escape severe thrombocytopenia after treatment with deoxyspergualin, an immunosuppressant [9].
• In this study, we found that dapsone increased the number of platelets and decreased the number of red blood cells in male (NZWxBXSB)F1 (W/BF1) mice, an animal model of idiopathic thrombocytopenic purpura [10].

Biological context of Foxg1

• As much of the increased ipsilateral projection in Foxg1-/- embryos arises from temporal RGCs that are unlikely to have an autonomous requirement for Foxg1, we propose that the phenotype reflects at least in part a requirement for Foxg1 outwith the RGCs themselves, most likely at the optic chiasm [11].
• Analysis of Foxg1 expression using lacZ reporter transgenes shows that Foxg1 is normally expressed in most, if not all, nasal RGCs but not in most temporal RGCs, neither at the time they project nor earlier in their lineage [11].
• We provide evidence that the hypoplasia results from decreased Foxg1 expression, reduced cell proliferation and increased cell death [12].
• This technique is used to demonstrate that the cell cycle is prematurely lengthened in the Foxg1-null telencephalon [13].
• Foxg1 is required for specification of ventral telencephalon and region-specific regulation of dorsal telencephalic precursor proliferation and apoptosis [13].

Anatomical context of Foxg1

• Foxg1 is also expressed at the optic chiasm [11].
• The winged helix transcription factor Foxg1 facilitates retinal ganglion cell axon crossing of the ventral midline in the mouse [11].
• Molecular analyses indicated that expression of Shh, Nkx2.1 and BF-1 was increased and their expression domains expanded dorsally in the ventral telencephalon in embryos of diabetic mice at embryonic day 11 [14].
• Foxg1 is required for morphogenesis and histogenesis of the mammalian inner ear [15].
• Foxg1, encoding for one of these factors, previously was reported to be necessary for basal ganglia morphogenesis, proper tuning of cortical neuronal differentiation rates, and the switching of cortical neuroblasts from early generation of primordial plexiform layer to late production of cortical plate [16].

Associations of Foxg1 with chemical compounds

• This cyclic adenosine-3',5'-monophosphate regulatory element (CRE)-like sequence, named H-2 binding factor 1 (H-2 BF1) binding motif, is highly conserved among species [17].

Physical interactions of Foxg1

• We show that BF-2 is a sequence-specific DNA binding protein with a binding specificity distinct from BF-1 [18].

Regulatory relationships of Foxg1

• We observed occasional cells with diencephalic character in the Foxg1 (forkhead box)-expressing Gli3(Xt/Xt) telencephalon at embryonic day 10.5, a day after the anatomical subdivision of the forebrain vesicle [19].
• We found that ectopic expression of BF-1 in vitro inhibits TGF-beta mediated growth inhibition and transcriptional activation [20].
• Therefore, we investigated whether BF-1 can inhibit Smad-dependent transcriptional responses by interacting with Smads or Smad binding partners [20].

Other interactions of Foxg1

• Disruption of early events in thalamocortical tract formation in mice lacking the transcription factors Pax6 or Foxg1 [21].
• Bmp co-expression overlaps that of Msx1 and Hfh4, and is complementary to that of Bf1 [22].
• Several Fox genes (Foxi1, Foxg1) are expressed in the developing otocyst of both zebrafish and mammals [15].
• We also investigated the proper patterning of structures adjacent to the prechordal plate by performing in situ hybridization of HNF-3beta, Six-3 and BF-1, genes whose expression domains remained unchanged [23].
• Remarkably, in the absence of Foxg1, additional inactivation of the medial fates promoter Emx2, although not suppressing cortical specification, conversely rescues overproduction of Reelin(on) neurons [16].

Analytical, diagnostic and therapeutic context of Foxg1

• Reciprocal haploidentical marrow transplantations between W/BF1 and autoimmune-resistent B6C3F1 mice were made [24].
• The (NZW x BXSB)F1 (W/BF1) mouse is known to be an animal model of systemic lupus erythematosus (SLE) and immune thrombocytopenic purpura (ITP) [25].
• Immunohistochemistry of heart and kidney tissue revealed significant amelioration of degenerative CVD and glomerulonephritis in the majority of W/BF1 recipients of marrow transplants from B6C3/F1 donors [26].

References