FOXA3 Antibodies

Hepatocyte nuclear factor 3-gamma (FOXA3)

Transcription factor that is thought to serve as a'pioneer' factor opening the compacted chromatin for different proteins through interactions with nucleosomal core histones and thereby replacing linker histones at target enhancer and/or promoter sites (By similarity). Originally described as a transcription activator for a number of liver enzymes such as AFP, albumin, tyrosine aminotransferase, PEPCK, etc.

Interacts with the cis-acting regulatory regions of these genes.

Gene Information

Human
Gene Name:	FOXA3
Uniprot:	P55318
Entrez:	3171

Family

Belongs to:
No superfamily

Alternative Names

FKHH3; Fork head-related protein FKH H3; forkhead box A3; Forkhead box protein A3; hepatocyte nuclear factor 3, gamma; hepatocyte nuclear factor 3-gamma; HNF-3G; HNF-3-gamma; HNF3GTCF-3G; MGC10179; TCF3G; Transcription factor 3G

Molecular Weight

Mass (kDA):
37.14 kDA

Genomic Context

Human
Location:	19q13.32
Sequence:	19; NC_000019.10 (45864326..45873797)

Tissue Specificity

Expressed in erythroleukemia and hepatoma cell lines and in liver and pancreas. Not expressed in any other cell lines or tissues examined.

Subcellular Localizations

Nucleus.

Diseases

• Liver Carcinoma
• Malignant Neoplasms
• Neoplasms
• Diabetes Mellitus
• Liver Neoplasms, Experimental
• Hepatitis B
• Hepatitis
• Metaplasia
• Inflammation
• Liver Neoplasms
• Liver Diseases
• Injury To Liver
• Hypoglycemia

• Diabetes Mellitus, Non-insulin-dependent
• Nervousness
• Pituitary Diseases
• Atrophy
• Hypertrophy
• Inflammatory Response
• Polycystic Ovary Syndrome

Pathways

• Glucose Homeostasis
• Secretion
• Cell Differentiation
• Regulation Of Gene Expression
• Cell Activation
• Cell Proliferation
• Pathogenesis
• Liver Development
• Sensitization
• Gastrulation
• Insulin Secretion
• Hepatocyte Differentiation
• T Cell Activation

• Gluconeogenesis
• Ossification
• Endochondral Ossification
• Regeneration
• Aging
• Immune Response
• Inflammatory Response

PTMs

• Phosphorylation
• Carboxylation
• Reduction
• Deamination

• Glycosylation
• Deacetylation
• Methylation
• Oxidation

Research Areas

• Chromatin Research

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/FOXA3

Best Uses Of The FOXA3 Marker

What is the FOXA3 gene? What is the most effective way to use this gene? This article will give you the best use of this gene, and how to get the best results from it. Read on to learn more. You can also submit your results for a special sample, species, or application to receive credits for your work. This article is relevant for any scientist worldwide.

FoxA3 is a transcription factor

The FoxA3 gene is a member of the family of genes that regulate transcriptional activity in various tissues. This gene is expressed in a variety of tissues and organs, and the Boster Bio antibody is a highly specific antigen that reacts with the FOXA3 protein. There are many uses of the FOXA3 marker in biology. The Boster antibodies are highly specific and have been validated for ELISA, Western Blotting, and Immunohistochemistry.

The FoxA3 protein belongs to the family of genes called the Fox proteins. This family consists of 17 subfamilies and exhibits a winged helix structure in the DNA-binding region. FOXA2 is also involved in hepatocyte differentiation, pulmonary morphogenesis, and osteogenesis. In one study, knockdown of FOXA2 resulted in increased osteoblast differentiation. It also increased alkaline phosphatase activity and bone mineralization. The study also revealed an increase in glucose metabolism in osteoblasts, which influences the differentiation potency of MSCs.

It is a transcription factor

The FOXA3 marker is a DNA binding transcription factor that functions in the endoderm. It acts to open compacted chromatin and promote transcription. It binds to specific cis-acting regulatory regions and cooperates with CEBPA. In addition to its role in glucose homeostasis, the transcription factor also plays a role in neuronal-specific transcription. Further, it has been implicated in spermatogenesis.

The role of FOXA3 in EC is still unclear. It is unknown how it regulates EMT. However, it has a role in EMT. Despite its apparent overlapping functions, it is not known how it compensates for the functions of other members of the FOXA family. Therefore, research is ongoing. This transcription factor is a key player in the process of epithelial-mesenchymal transition, but there is still no consensus on the exact function it plays.

The FOXA3 gene is regulated by the Forkhead DNA-binding motif and two distinct transcriptional activation domains. Both of these regions are important for adipocyte differentiation and expansion. It has been shown that FOXA3 influences fat metabolism in mice, but there are no studies in humans linking it to metabolic outcomes. The gene was sequenced in 392 individuals who were lean, obese, and overweight. The association between FOXA3 SNPs and metabolic parameters was determined by the analysis of common SNPs.

The primer sequences for FOXA3 and GFP were used in real-time PCR. The primers for FOXA3 were 5'-GGTGTCCCGGCATA-3' and GFP was 5'-CGTGTTCATGCCATCATT-3' and FOXA3-2 and FOXA3-4 were each amplification-ready gene marker. When the primers were used in real-time PCR, the transcripts were amplified and analyzed using the 2-DDCq method.

A study on mice revealed that FOXA3 could play an important role in tumorigenesis and progression of EC. EC tumors with increased expression of FOXA3 had improved survival, compared to nontumor tissues. This suggested that the protein is involved in regulating the ability of EC cells to invade and metastasize. The FOXA3 gene may regulate EC cell metabolism and tumor progression.

In a mouse model of hepatocellular development, deletion of FOXA3 relieved excessive lipid accumulation caused by TM. Conversely, FOXA3 deficiency reduced the chronic ER stress of diet-induced db/b mice. Further, ChIP-Seq analysis demonstrated that FOXA3 regulates Period1 transcription and promotes expression of lipogenic genes.

The expression of FOXA3 has implications for cell function. HB cells that lack FOXA3 were not cloned or viable. Knockdown of FOXA3 decreased AFP expression and cellular viability. In addition, FOXA3 downregulation decreased the expression of HNF1A/MYC and ZFHX3.