Forkhead box P1 (FOXP1) is one of four members of the FOXP subfamily of forkhead transcription factors ^[1][2]. The FOXP subfamily is somewhat atypical because of the C-terminal location of the forkhead domain and the N-terminal zinc finger and leucine zipper, which are required for transcriptional repression and both homo- and hetero-FOXP dimerisation ^[3].

The FOXP1 protein is widely but not ubiquitously expressed in human and murine tissues ^[2]. Studies on human FOXP1 have focused primarily on its role in human malignancy and in cellular differentiation ^[4]. The human FOXP1 gene maps to a candidate tumour suppressor locus at 3p14.1. Loss of FOXP1 has been reported in several types of carcinoma and this confers poor prognosis in breast cancer ^[5]. In contrast the FOXP1 locus is targeted by recurrent chromsome translocations ^[6] and amplifications in large B-cell lymphomas, where high level expression of FOXP1 correlates with a poor prognosis ^[7]. This may reflect expression of oncogenic smaller isoforms of the protein ^[8]. FOXP1 is also an autoantigen in eye disease and recent studies have implicated FOXP1 in human heart failure, mesenchymal stem cell renewal ^[9], osteoclast biology, and monocyte and macrophage differentiation ^[10].

Biochemical and molecular studies of murine Foxp1 have focussed on defining the functional domains of the protein, alternative splice forms, the Foxp1 DNA binding consensus and interacting proteins ^[3][11]. Studies using knockout mice have made a significant contribution by demonstrating that Foxp1 has an essential developmental role, involving cardiac ^[12], B-cell ^[13] and lung development, together with the coordination of neuron development in conjunction with Hox genes ^[14].