Disease relevance of Foxb1

• A 14-day course of TWH extract treatment at a daily dose of 400 microg kg(-1), which began on the day of the first C II immunization, suppressed the development of arthritis, as well as antibody production and delayed-type hypersensitivity to C II [1].
• The effects of TWH extract on GVHD were assessed by measuring both the degree of splenomegaly and the total serum IgE levels 3 weeks after the cell transfer [2].

Psychiatry related information on Foxb1

• Foxb1 mutant mice showed no deficits in such hippocampal-dependent tasks as contextual fear conditioning and social transmission of food preference [3].

High impact information on Foxb1

• Foxb1 is expressed in a large hypothalamic neuronal group (the mammillary body), which gives origin to a major axonal bundle with branches to thalamus, tectum and tegmentum [4].
• As a model, we have used the role of winged helix transcription factor gene Foxb1 in the emergence of a very specific morphological trait of the diencephalon, the mammillary axonal complex [4].
• Winged helix transcription factor Foxb1 is essential for access of mammillothalamic axons to the thalamus [4].
• Analysis of chimeric brains with wild-type and Foxb1 mutant cells suggests that correct expression of Foxb1 in the thalamic palisade is sufficient to rescue the normal phenotype [4].
• Fkh5-deficient mice show dysgenesis in the caudal midbrain and hypothalamic mammillary body [5].

Biological context of Foxb1

• Finally, morphological defects in the inferior colliculi of the midbrain in Foxb1-/- mice correlate with the inability to lactate, suggesting that the midbrain defect, but not the loss of the mammillothalamic tract, may be responsible for the lactation defect [6].
• The winged helix gene, Foxb1, controls development of mammary glands and regions of the CNS that regulate the milk-ejection reflex [6].
• Since Mf3 is located in a region of Chromosome 9 containing many well-characterized mouse mutations such as short ear (se), ashen (ash), and dilute (d), we have analyzed deletion mutants to determine the location of Mf3 more precisely [7].

Anatomical context of Foxb1

• Mammary glands from C57BL/6 Foxb1-/- mice have incomplete lobuloalveolar development [6].
• Early embryonic Fkh5 expression is restricted to the mammiliary body region of the caudal hypothalamus, midbrain, hindbrain and spinal cord [5].
• The murine winged helix gene Fkh5 is specifically expressed in the developing central nervous system (CNS) [5].
• In the early embryo, transcripts for Mf3 are restricted to the presomitic mesoderm and anterior neurectoderm and mesoderm [8].
• In the superior colliculus, Fkh5/Mf3 is expressed by cells of layers 4a and 4c since early in development [9].

Other interactions of Foxb1

• In the midbrain, Fkh5/Mf3 is expressed in the superior colliculus, in the ventricular layer of the inferior colliculus and in the isthmus [9].

Analytical, diagnostic and therapeutic context of Foxb1

• Treatment with TWH extract, which started on the same day as the booster immunization, also resulted in inhibition of development of arthritis and of immune responses to C II [1].
• These results strongly suggest that TWH extract will be an addition to the cohort of immunosuppressive therapies used in solid organ and bone marrow transplantation [2].

References