High impact information on FOXD1

• Thus, Foxd1 modulates inflammatory reactions and prevents autoimmunity by directly regulating anti-inflammatory regulators of the NF-AT pathway, and by coordinating the suppression of the NF-kappaB pathway via Foxj1 [1].
• Furthermore, we demonstrate that overexpression of Ets-1 in the human embryonic kidney cell line 293 is sufficient to increase freac-4 mRNA levels [2].
• In cotransfection experiments using an Ets-1 expression vector, the induction of freac-4 reporter gene activity is attenuated approximately 6-fold when the three Ets-1 binding sites are mutated [2].
• Through transfection experiments three Ets-1 cis-elements are identified within the first 152 nucleotides upstream of the transcription start in the freac-4 promoter [2].
• There are no similarities in regions outside of the DNA binding domains of FREAC-9 and FREAC-4 and since freac-4 maps to a different chromosome (5q12-q13) it is likely that an evolutionary selection has acted to maintain identical DNA binding domains between these two kidney expressed transcription factors [3].

Biological context of FOXD1

• The amino acid sequence of the DNA binding forkhead motif of FREAC-9 is identical to that of another forkhead protein, FREAC-4, whereas 12 substitutions are present at the nucleotide level [3].

Analytical, diagnostic and therapeutic context of FOXD1

• We describe the cloning and sequence analysis of a nearly full-length cDNA as well as a corresponding 5.2-kilobase pair genomic fragment encoding FREAC-4, a member of the forkhead family of transcription factors [4].

References