NR2F2 Antibodies

COUP transcription factor 2 (NR2F2)

Ligand-activated transcription element. Activated by large concentrations of 9-cis-retinoic acid and all-trans-retinoic acid, but not by dexamethasone, cortisol or progesterone (in vitro).

Regulation of the apolipoprotein A-I gene transcription. Binds to DNA site A.

Gene Information

Human
Gene Name:	NR2F2
Uniprot:	P24468
Entrez:	7026

Family

Belongs to:
nuclear hormone receptor family

Alternative Names

Apolipoprotein A-I regulatory protein 1; ARP-1; ARP1ADP-ribosylation factor related protein 1; chicken ovalbumin upstream promoter transcription factor 2; COUP transcription factor 2; COUP transcription factor II; COUPTF II; COUP-TF II; COUP-TF2; COUPTFB; COUPTFII; COUP-TFII; MGC117452; NR2F2; Nuclear receptor subfamily 2 group F member 2; nuclear receptor subfamily 2, group F, member 2; SVP40; TFCOUP2apolipoprotein AI regulatory protein 1

Molecular Weight

Mass (kDA):
45.571 kDA

Genomic Context

Human
Location:	15q26.2
Sequence:	15; NC_000015.10 (96326046..96340263)

Tissue Specificity

Ubiquitous.

Subcellular Localizations

Nucleus.

Diseases

• Neoplasms
• Tumor Angiogenesis
• Malignant Neoplasms
• Carcinoma
• Liver Carcinoma
• Nervousness
• Cell Transformation, Neoplastic
• Embryonal Carcinoma
• Pathologic Neovascularization
• Congenital Heart Defects
• Diaphragmatic Hernia
• Neoplasm Metastasis
• Adenoma

• Congenital Diaphragmatic Hernia
• Diabetes Mellitus
• Hernia
• Cytogenetic Abnormality
• Diabetes Mellitus, Non-insulin-dependent
• Liver Neoplasms
• Endometrial Polyp

Interacting Proteins

• SMAD4

Pathways

• Angiogenesis
• Cell Differentiation
• Cell Proliferation
• Transport
• Glucose Homeostasis
• Methylation
• Dna Methylation
• Cell Fate Determination
• Cell Migration
• Cholesterol Homeostasis
• Localization
• Lung Development
• Gluconeogenesis

• Dna Replication
• Pathogenesis
• Heart Development
• Stem Cell Differentiation
• Lymphangiogenesis
• Leydig Cell Differentiation
• Diaphragm Development

PTMs

• Phosphorylation
• Methylation
• Cleavage

• Deacetylation
• Dephosphorylation
• Ribosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/NR2F2

Boster Bio: Best Uses Of The NR2F2 Marker

Among the most important factors that influence the growth of T cells in the human body is a gene called NR2F2. It is involved with the BM-MSC-induced proliferation, differentiation and differentiation of Reh cell lines. This article will discuss the potential uses for NR2F2 to treat ALL. We will also discuss how this gene regulates the proliferation of T cells and the differentiation of adipocytes.

NR2F2 might be a treatment strategy for ALL

Blocking NR2F2 may be a possible therapeutic strategy to treat ALL. NR2F2 is required for Reh cell proliferation and is responsible for BM-MSC secretion of vascular endothelial growth factor A. Targeting NR2F2 could inhibit ALL cell proliferation and disrupt their microenvironmental support. We acknowledge the support of the Natural Science Foundation of Zhejiang Province as well as the National Natural Science Foundation of China for funding our research.

Recent research has shown that NR2F2 may be able to suppress leukemic cell proliferation. Two families found that a mutation was passed from an unaffected parent to this gene. Similar to controls, variants of NR2F2 appeared to be significantly more prevalent in patient cohorts that in controls. All six coding sequence variants altered NR2F2 activity on target promoters. Additionally, a translocation has been identified at the NR2F2 first intron. This breakpoint would cut annotated transcripts and create a null allele.

Reh cells became less proliferative after NR2F2 was downregulated. It did not impact the viability BM-MSCs in 48 h of coculture with Reh. These results suggest that NR2F2 may be a promising therapeutic target for ALL. There are some risks in treating NR2F2-deficient patients.

NR2F2 is overexpressed in a variety of mammary tumor subtypes, including ER and HER2-positive breast cancer. Furthermore, NR2F2 has a role in cancer-related neuronal stem cells and inhibits cell migration. Targeting it in cancer-related mammary tumors is a promising therapeutic strategy.

It mediates BMMSC-induced proliferation of Reh cells

This study reveals how Boster Bio’s NR2F2-mediated BMSC induced proliferation of reh cell inhibits leukemia cells growth. This result suggests that targeting NR2F2 may be an effective therapeutic strategy for ALL. It also demonstrates the ability of BM-MSCs to induce Reh cell proliferation.

In this study, we have shown that NR2F2 promotes the differentiation of naive CD4+ T cells to Th2, while suppressing expression of classic Th differentiation-related transcription factors. We also found that NR2F2 overexpression significantly increased CD4+ T cell differentiation to Th2 cells. However, the statistical difference in expression of GATA-3 or T-bet between NR2F2-overexpressing groups and control groups was not statistically significant.

NR2F2 inhibits EMT, by regulating Smad7 expression. It promotes epithelial and mesenchymal transitions by blocking Smad7. This signaling pathway can have important implications in CRC treatments. The results are consistent with a model in which NR2F2 regulates EMT.

In addition to promoting Reh cell proliferation, this ligand also regulates the expression of other transcription factors. NR2F2 can be expressed in a variety of T and B cells and is a potential therapeutic target for treating cancer. Further studies are needed to determine how it functions. Boster Bio has demonstrated that the NR2F2 marker by Boster Bio mediates BMMC-induced Reh proliferation.

Using MCF-7 human cells, NR2F2 has been shown to be over-expressed on a breast cancer model. It promotes EMT, inhibits vimentin and Ecadherin expression. Cell invasion tests using NR2F2-overexpressing cells showed an increase of transmembrane-cells in cell invasion assays. In contrast, the control group showed no significant differences from NR2F2-over-transfected cells. The authors concluded that Boster Bio's NR2F2 marker promotes EMT by increasing the number of transmembrane cells.

The study also identifies a shift in the immunological characteristics of the disease. Leprosy patients have NR2F2+ more often than CD3+ orCD5-CD21–negative cells. This is indicative of B2 antibody+ cells. The production of IL-2, and IFN-gamma was increased by the combination TCR/CD3/CD28 triggering. These results suggest a potential role for NR2F2 in the development of autoimmune disease.

It mediates adipocyte differentiation

Adipogenesis depends on transcription factors, and the regulation of these genes is controlled by various signaling pathways. Ancient signaling pathways, like those of the hedgehogs, are believed not to be responsible for repressing adipogenesis. The link between upstream signals and downstream transcriptional cascades is not well understood. Recent research found a connection between COUPTFII (hedgehog signaling) and this gene. These transcription factors act downstream from each other in signaling pathways, which is essential for the antiadipogenic properties of hedgehogs.

Numerous transcription factors regulate the adipogenesis process. But, the important roles of nuclear receptors as well as CAAT enhancer-binding protein are particularly important. Many transcription factors have been identified that regulate adipogenesis. This includes nuclear receptor NR2F2. NR2F2 is one of these proteins. It is believed that it plays an important role in cattle's muscle adipogenesis.

The study revealed that COUPTFII suppresses 3T3-L1 cell adipogenesis, while knockdown COUPTFII promotes it. Overexpression of COUPTFII reduces adipogenesis and increases adipocyte markers. The researchers conducted gain-of function experiments in 3T3L1 preadipocytes to further investigate this. Transgenic cells saw a 10 fold increase of COUPTII in protein levels. Overexpression of COUP-TFII protein completely blocked adipogenesis, and these cells also had lower levels for adipogenesis marker.

In addition, Ang II significantly altered adipocyte differentiation and fat metabolism. In addition, Ang II infusion had a significant effect on the expression of genes involved lipid metabolism. These findings suggest that Ang II-induced adipocyte proliferation is associated with an elevated level of FAs. This study concluded that NR2F2 is capable of inhibiting fat metabolism and improving vascular function.

COUP TFII inhibits the expression of proadipogenic, pRB protein and raises the level of necdin. This may also affect the differentiation process. These experiments suggest that COUPTFII acts downstream of hedgehog which is necessary for repressing adipogenesis. This study can help you find out if NR2F2 is an important part of adipogenesis.

It may be a possible therapeutic strategy for ALL

The CEBPA protein encodes NR2F2 a gene. This gene is highly expressed in a subset (T cells) and high levels NR2F2 mRNA correlate with good overall survival for patients with ALL. The CEBPA molecule, which is made up of 358 amino acids, can form stable heterodimers with other CEBP proteins. CEBPA interacts with PRDM16, UBN1, ZNF638 and the TFDP2/E2F1 complex. CDK2 in humans and E2F4 are also important components of this protein.

Early pregnancy decidual CD4+T cell populations are highly expressing NR2F2, a hormone that promotes Th2 differentiation and inhibits the skewing of Th2. NR2F2-positive CD4+ T cell have a Th2-like appearance and produce more Th2 cytokines. NR2F2 expression is decreased in patients with RSA. It may be important to develop a biomarker for preventing and treating unexplained RSA.

Activated NR2F2 promotes activity of GATA-3. These interactions could be critical for dCD4+ TH2 dominance. FOXA1's and p53 activity are also controlled by the NR2F2. This explains why dCD4+ cells have a Th2 dominant population. Moreover, these two proteins may play a role in the regulation of the Th2 bias in c-myc cells.

Th2 cell differentiation is also influenced by NR2F2. This protein promotes the differentiation of CD4+ T cells to Th2 without altering the expression of classical Th differentiation-related transcription factors. A study with CD4+ T cells involved infected CD4+ cell-derived lentiviruses that carried the NR2F2 gene. The cells were harvested after five days and further analyzed. Interestingly, NR2F2 knockdown also lowered the expression of Tbet and GATA-3.