Forkhead box protein F1 Antibodies

Forkhead box protein F1 (FOXF1)

Probable transcription activator for a number of lung- specific genes. .

Gene Information

Human
Gene Name:	FOXF1
Uniprot:	Q12946
Entrez:	2294

Family

Belongs to:
No superfamily

Alternative Names

FKHL5; FKHL5MGC105125; forkhead box F1; forkhead box protein F1; Forkhead, drosophila, homolog-like 5; Forkhead-related activator 1; Forkhead-related protein FKHL5; Forkhead-related transcription factor 1; FoxF1; FREAC-1; FREAC1ACDMPV

Molecular Weight

Mass (kDA):
40.122 kDA

Genomic Context

Human
Location:	16q24.1
Sequence:	16; NC_000016.10 (86510527..86515422)

Tissue Specificity

Expressed in lung and placenta.

Subcellular Localizations

Nucleus.

Diseases

• Neoplasms
• Malignant Neoplasms
• Haploinsufficiency
• Dysplasia
• Carcinoma
• Congenital Abnormality
• Tissue Adhesions
• Malignant Neoplasm Of Breast
• Hyperplasia
• Neoplasm Metastasis
• Carcinogenesis
• Hemorrhage
• Malignant Neoplasm Of Lung

• Pulmonary Hemorrhage
• Cell Transformation, Neoplastic
• Rhabdomyosarcoma
• Basal Cell Carcinoma
• Cell Invasion
• Tracheoesophageal Fistula
• Pathologic Fistula

Pathways

• Lung Development
• Cell Adhesion
• Vasculogenesis
• Lung Morphogenesis
• Cell Growth
• Cell Migration
• Cell Cycle
• Cell Differentiation
• Regeneration
• Pathogenesis
• Cell Fate Determination
• Paracrine Signaling
• Cell Proliferation

• Localization
• Methylation
• Dna Replication
• Tissue Homeostasis
• Transport
• Cell Activation
• Developmental Process

PTMs

• Methylation

• Phosphorylation

• Cleavage

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/FOXF1

Best Uses Of The FOXF1 Marker

Are you interested in the most effective way of treating lung disease? Small molecules that target the FOXF1 gene could be the key to lung protection. Read on to learn more about this transcription factor and its potential use. Here are some small molecules that target FOXF1

FoxF1 transcription factor

Research has shown that the FoxF1 gene is a key factor in the development of acute respiratory distress syndrome. This potentially deadly disease leaves millions of people hospitalized every year. A recent study has identified the FoxF1 gene as a target for treatment. Researchers have created a small chemical that stabilizes FOXF1 molecules to better understand the role of FoxF1 gene in lung disease. The molecule inhibits lung inflammation. It also protects experimental mice from the harmful effects of infections.

It plays an important role in lung protection

The FOXF1 signal is involved not only in lung protection but also in various physiological processes. The purpose of this study was to examine whether FOXF1 plays a crucial role in the regulation eicosanoid synthesis in pulmonary epithelia. Total RNA was extracted from human lung tissue samples in order to determine its level. After being paraffinized using a graded series of ethanol, the samples were incubated for 10 minutes in 3% hydrogen peroxide to inhibit endogenous peroxidase. Tissue sections were then injected with a primary human FOXF1 antigen and left to incubate overnight at 4°C. Quantitation of the ectopic expression was carried out using the Streptavidin-peroxidase method.

SIX1 (and EYA1) are two genes involved in lung protection. This molecule can be found in the alveolar Epithelium and plays a crucial role in lung growth. SIX1 is present at the saccular stage of lung growth in mice. It is a member of the SIX families. It has a DNA binding homeobox and a conserved SIXdomain. SIX1 acts as a transcription factor and collaborates with the Eyes absent family (EYA). It has also been linked to breast cancer.

Recent research has shown that FOXF1 expression in HCC cells inhibits tumorigenesis. Additionally, patients with HCC who have high levels of FOXF1 are more likely to survive. Further studies will examine if FOXF1 hyperexpression is associated with better survival rates in HCC patients. These results suggest that the FOXF1 biomarker may be useful in clinical practice.

Idiopathic lung fibrosis (IPF), which is a progressive debilitating disorder with unknown etiology is a progressive disease. The median survival time for patients with IPF is currently three to five more years. The disease is caused due to an abnormal lung epithelium. The disease is caused by an abnormal lung epithelium. Fibroblasts release excessive amounts of extracellular matrix protein and remodel the lung's architecture.

Recent research showed that FOXF1 gene expression was inducible in lung cells from IPF patients whose periostin levels were low. It was also found that lung-fibroblasts were able to express periostin dependent genes. In addition, periostin inhibited cell proliferation and decreased the expression of cell-cycle-related genes. This study suggests that the FOXF1 mark plays a critical role for lung protection.

It can also be targeted with small molecules

A small molecule known as LINC00022 can target FOXF1 in CRC cancer tissues. This compound may increase FOXF1 expression through competitive binding to miR375-3p. This promotes the development CRC. In a previous study, LINC00022 knockdown increased the level of VEGFA, c-Myc, and cleaved caspase 3 protein. It was shown that miR375-3p could be reduced in LINC00022 suppressed cells while upregulating it would increase FOXF1 levels.

The F-box protein contains a C-terminal Nictaba-like domain and is specifically targeted to poly-N-acetyllactosamine and peptides, which are the primary components of blood cells. The protein targets also motifs related to blood types B, C, and D. Small molecules may be able to target this gene, which regulates production of many proteins.

FOXh2 is crucial for the differentiation of PSMN and human iPSCs. Its expression increased throughout the reprogramming process. Three shRNAs were introduced to cells in OSKM-transduced HDFs. The shRNAs were able to reduce iPSC colonies by 50%, but not the proliferation transduced HDFs.