FoxP1 Rabbit Polyclonal Antibody (ER1901-25)

UNIPROT #

Q9H334

PROTEIN NAME

FoxP1

SYNONYMS

12CC4 antibody;FLJ23741 antibody;Fork head related protein like B antibody;Forkhead box P1 antibody;Forkhead box protein P1 antibody;FOX P1 antibody;FOXP 1 antibody;foxp1 antibody;FOXP1_HUMAN antibody;Glutamine rich factor 1 antibody;hFKH1B antibody;HSPC215 antibody;MGC12942 antibody;MGC88572 antibody;MGC99551 antibody;QRF 1 antibody;QRF1 antibody

TISSUE SPECIFICITY

Isoform 8 is specifically expressed in embryonic stem cells.

SUBCELLULAR LOCATION

Nucleus.

FUNCTION

Forkhead box protein P1 is a protein that in humans is encoded by the FOXP1 gene. FOXP1 is necessary for the proper development of the brain, heart, and lung in mammals. It is a member of the large FOX family of transcription factors. This gene belongs to subfamily P of the forkhead box (FOX) transcription factor family. Forkhead box transcription factors play important roles in the regulation of tissue- and cell type-specific gene transcription during both development and adulthood. Forkhead box P1 protein contains both DNA-binding- and protein-protein binding-domains. This gene may act as a tumor suppressor as it is lost in several tumor types and maps to a chromosomal region (3p14.1) reported to contain a tumor suppressor gene(s). Foxp1 is a transcription factor; specifically it is a transcriptional repressor. Fox genes are part of a forkhead DNA-binding domain family. This domain binds to sequences in promoters and enhancers of many genes. Foxp1 regulates a variety of important aspects of development including tissue development of: the lungs, brain, thymus and heart. In the heart Foxp1 has 3 vital roles, these include the regulation of cardiac myocyte maturation and proliferation, outflow tract separation of the pulmonary artery and aorta, and expression of Sox4 in cushions and myocardium. Foxp1 is also an important gene in muscle development of the esophagus and esophageal epithelium. Foxp1 is also an important regulator of lung airway morphogenesis. Foxp1 knockout embryos display severe defects in cardiac morphogenesis. A few of these defects include myocyte maturation and proliferation defects that cause a thin ventricular myocardial compact zone, non-separation of the pulmonary artery and aorta, and cardiomyocyte proliferation increase and defective differentiation. These defects, caused by Foxp1 inactivation, lead to fetal death. Disruptions of FoxP1 have been identified in very rare human patients and – similarly to FoxP2 - lead to cognitive dysfunction, including intellectual disability and autism spectrum disorder, together with language impairment.