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- Table of Contents
Facts about Forkhead box protein L2.
Prevents trans- differentiation of ovary to testis via transcriptional repression of the Sertoli cell-promoting gene SOX9 (By similarity). Has apoptotic activity in ovarian cells.
Human | |
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Gene Name: | FOXL2 |
Uniprot: | P58012 |
Entrez: | 668 |
Belongs to: |
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No superfamily |
BPES; BPES1; BPES1PINTO; forkhead box L2; forkhead box protein L2; forkhead transcription factor FOXL2; FOXL2; PFRK; PINTO; POF3
Mass (kDA):
38.772 kDA
Human | |
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Location: | 3q22.3 |
Sequence: | 3; NC_000003.12 (138944224..138947137, complement) |
In addition to its expression in the developing eyelid, it is transcribed very early in somatic cells of the developing gonad (before sex determination) and its expression persists in the follicular cells of the adult ovary.
Nucleus.
FOXL2 (Forkhead box protein L2) is a transcription factor that regulates expression of a variety of proteins. STAT3 regulates the protein, as well as HMGA2. HMGA2 is a crucial transcription factor that regulates the production of FOXL2. HMGA2 is also a major regulator of FOXL2 expression. The posttranslational modifications of FOXL2 are responsible for its expression and also play a role in its transcription.
A lot of debate surrounds the purpose of Stat3 for DNA replication. While Stat proteins are linked to specific pathways within the genome, STAT3 is not. It appears to be a classic transcription factor. This result is a surprising result. Let's examine this possibility. We will demonstrate how Stat3 regulates FOXL2 transcription in Boster Bio.
The function of Stat3 has been extensively researched in cell-culture systems. The activation of Stat3 is associated with distinct cell responses. Stat3's presence in a variety of roles suggests that it's a major signal transmitter downstream of the gp130-like receptors. This raises the question as to how a specific transcription factor can be involved in contradictory cell responses.
The identity of Stat3's serine kinase remains a mystery. The activation signals of Stat3 can be phosphorylated through a variety kinases, including the ERK1, p38, JNK and H-7-sensitive kinase. Incredibly, the majority of evidence points to a positive role for Stat3 phosphorylation in Stat3 transcriptional activation. However, there is also an adverse role for Stat3 serine phosphorylation. The mechanism behind this isn't yet understood.
While Stat3 is involved in a variety of aspects of cell differentiation, growth and survival, it also has an important role in the regulation of keratin5 and FOXL2 expression. Stat3 has been demonstrated to influence the survival of T cells by altering the microenvironment in which T cells live. These functions are indirect , but play an important part in the control of FOXL2's function within Boster Bio.
IL-6 activated STAT3 and led to an increase in the phospho-receptor adaptor molecule (PRLR) levels. In addition, the increased replication of DNA was also a result of an increase in STAT3 levels in response to IL-6. This effect is evident in the lower right corner. This results suggests that STAT3 could play a part in protecting the motoneurons from injury.
Additionally, STAT3 targeting siRNA is delivered via nanoparticulate delivery systems. Because nanoparticulate delivery systems are less harmful than traditional methods of administration they are more suitable for use in clinical trials. To determine if these methods can be adopted mainstream strategies further research is required. The development of a drug which targets STAT3 and FOXL2 is just one of the improvement.
The treatment of FOXL2 in mice is long-lasting and lasts for approximately a week in cells that have split. Gene knockdown is only temporary in cells that have not split. Moreover, it is applicable for scientists from all over the world. If you require blocking peptides it is also possible to purchase one. For more details on this, contact Boster Bio at [188073].
The FOXL2 gene outlines instructions for making an RNA protein that binds to specific regions of DNA to regulate the activity of specific genes. It is known as a transcription factor and its polyalanine tract isn't completely understood. This region is believed to play an important role in pituitary tumorigenesis. Here are some potential uses of FOXL2 as an indicator.
One study showed that FOXL2 was significantly higher in patients suffering from metastatic gastric cancer compared to healthy subjects. The study also showed an important correlation between the levels of FOXL2 and HMGA2, FOXL2 ITGA2, and the stages. It also correlates with T, N, or M staging. While numerous studies are required to determine its clinical relevance This marker could be a helpful diagnostic tool in the treatment of gastric cancer.
In a recent study, researchers found that the FOXL2 marker was associated with chemoresistance and the epithelial-to-mesenchymal transition (EMT). The study examined the mechanism of EMT and metastasis in chemoresistant gastric cancer. The authors identified a key molecular pathway by bioinformatics and gene profiling. Through loss-of function and gain-of function experiments, the functions of FOXL2 and HMGA2 were established in cancer cell lines.
The exogenous expression of FOXL2 reduced the effects of HMGA2 knockdown in cancerous cells in the liver and lung, and reduced E-cadherin expression. Additionally, FOXL2 increased vimentin expression in cancer cells. This suggests that FOXL2 could be used to identify cancerous cells. The marker can also be useful in identifying tumors which are susceptible to metastatic disease.
The findings of the study suggest the expression of FOXL2 is controlled by STAT3 and this pathway may be involved in the suppression of cancerous cells. The marker was also believed to be controlled by STAT3 within the FOXL2 promoter area. Further research is required to confirm the results of this study. Finally, the researchers have found that STAT3 inhibitors can reduce the viability of He La cells. This is a promising discovery that will be further investigated.
Genetic studies have shown that FOXL2 regulates ITGA2, a downstream affector of FOXL2. The knockdown of ITGA2 diminished E-cadherin and vimentin levels, which could have implications for the EMT and metastasis of gastric cancer. It also reduced the high potential for the gastric cancer cells and reduced their overall survival.
The FOXL2 gene is vital for embryogenesis, differentiation of cells, and tumorigenesis. It has multiple target genes involved in a range of processes including cell cycle control and Apoptosis. The Gen Bank cloned FOXL2's promoter and dual luciferase reporter analysis confirmed its role. A molecular genetic test using FOXL2 could also help to discover the role of FOXL2 in blepharophimosis.
During translation, Focal adhesion mole FOXL2 will be subject to both processive and focused modifications. The pathway to subsequent PTMs is defined by the protein's phosphorylation residue S33. An asterisk denotes nonspecific bands, while the rest of the residues are conserved. Posttranslational modifications to FOXL2 are crucial for its cellular function and the process of ubiquitination.
This study looked into the effects of various variations on the stability of FOXL2 on its expression in cell culture. Specifically, FOXL2 overexpression resulted in increased transcriptional activity, which increased cell death. Additionally, the overexpression of FOXL2 was associated with an increase in cell death activity in both KGN and GSK3b-specific siRNA cells. FOXL2 expression was also observed to be increased in cells treated with AR-A014418 which inhibited S33 phosphorylation.
FOXL2 can also be subject to different posttranslational modifications. We used immunoprecipitation and Western blotting to determine the ubiquitination status of FOXL2 in this study. We performed statistical analysis based on the C134W mutation model, where the FOXL2 C134W mutation triggers GCT through the hyperphosphorylation of S33.
FOXL2 is a nucleus-based protein that encodes an elongated winged helix/forkhead transcription factors. It is expressed in the eyelids as well as the fetal ovarian foollicles in the early stages of development. Incredibly, FOXL2 can play multiple roles throughout the fetal development process and also in the fertile age of the female adult. Its posttranslational modifications have been linked to an ovarian failure in mice.
In FOXL2, UBiquitination happens as an exchange process. Ubiquitin and SUMOylation are controlled by the presence of phosphorylated S33 in FOXL2. UBC9 overexpressions of FOXL2 did however not affect the ubiquitination. SUMOylation can't be reduced by the force of ubiquitination, even though it is linked with ubiquitination.
Several studies have implicated the role of posttranslational modifications of FOXL2 in the development of the ovarian. In goats, FOXL2 protein is expressed in the gonad and eyelid tissues. FOXL2 protein is abundantly present in germ cells, surface epithelium as well as follicular cells of women who are pregnant for 36 days. FOXL2 is absent from the testis after 90-dpc.
The study also showed the correlation between mutations in FOXL2 BPES. In addition an in vitro kinase assay showed that FOXL2 physically interacts with active GSK3b and inactive GSK3b does not. These results support the function FOXL2 is playing in BPES. Further research is needed to determine whether it affects the BPES syndrome.
Lysine acetylation can be described as one of the types of posttranslational modification for FOXL2. Phosphorylation occurs on the side chains of amino acids and neutralizes a negative charge bound to carboxylic acids. The lysate of cells that have been starved of serum displays the presence of phosphoproteins that are present on the protein. This kind of alteration is caused by serine residues in FOXL2 and is controlled by a large variety of enzymes.
PMID: 11175783 by Crisponi L., et al. The putative forkhead transcription factor FOXL2 is mutated in blepharophimosis/ptosis/epicanthus inversus syndrome.
PMID: 16153597 by Lee K., et al. Transcriptional factor FOXL2 interacts with DP103 and induces apoptosis.
*More publications can be found for each product on its corresponding product page