This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
1 Citations 4 Q&As
3 Citations 5 Q&As
Facts about Zinc finger E-box-binding homeobox 1.
Enhances or represses the promoter activity of this ATP1A1 gene based on the quantity of cDNA and on the cell type. Represses E-cadherin promoter and causes an epithelial-mesenchymal transition (EMT) by recruitment SMARCA4/BRG1.
Human | |
---|---|
Gene Name: | ZEB1 |
Uniprot: | P37275 |
Entrez: | 6935 |
Belongs to: |
---|
delta-EF1/ZFH-1 C2H2-type zinc-finger family |
AREB6; AREB6MGC133261; BZP; delta-crystallin enhancer binding factor 1; DELTAEF1; FECD6; Negative regulator of IL2; NIL-2-A zinc finger protein; NIL2A; NIL-2-A; posterior polymorphous corneal dystrophy 3; PPCD3; TCF8; TCF-8; TCF8BZP; transcription factor 8 (represses interleukin 2 expression); Transcription factor 8; ZEB; ZEB1; ZFHEP; ZFHX1A; zinc finger E-box binding homeobox 1; zinc finger E-box-binding homeobox 1; zinc finger homeodomain enhancer-binding protein
Mass (kDA):
124.074 kDA
Human | |
---|---|
Location: | 10p11.22 |
Sequence: | 10; NC_000010.11 (31318417..31529814) |
Colocalizes with SMARCA4/BRG1 in E-cadherin- negative cells from established lines, and stroma of normal colon as well as in de-differentiated epithelial cells at the invasion front of colorectal carcinomas (at protein level). Expressed in heart and skeletal muscle, but not in liver, spleen, or pancreas.
Nucleus.
Antibodies to the ZEB1 gene are used in many biological assays. These antibodies can be monoclonal or polyclonal and react with the protein in many animal samples. Boster Bio uses mouse and rabbit as models to create its antibodies. These antibodies target ZEB1's role as a transcriptional repressor. Inhibiting the expression of the interleukin-2 gene and E-cadherin promoter are two of the main roles of ZEB1 in the epithelial-mesenchymal transition.
The Boster Bio cDNA library contains a new transcriptional repressor called ZEB1. It inhibits gene expression through its association with other genes. The ZEB1/miR-200s loop is a novel regulator of ZEB1. It is also important in breast cancer, where reduced estrogen receptor-alpha (ER-a) expression may cause resistance to antiestrogen therapy.
A number of biological assays use antibodies against ZEB1. These antibodies may be monoclonal or polyclonal and react with the ZEB1 protein in several animal samples. Boster Bio used rabbit and mouse to produce antibodies against ZEB1. In a variety of biological assays, ZEB1 inhibits the expression of interleukin-2 gene and represses E-cadherin promoter, which causes the epithelial-mesenchymal transition.
ZEB1 promotes mammary epithelial tumors. In addition, it regulates p53 signaling. By interfering with ZEB1 activity, it inhibits the production of VEGF and FGF. These factors regulate cell biology, including proliferation and angiogenesis. As a result, the ZEB1/miR-200 axis is involved in the promotion of mammary epithelial tumors.
In a recent study, the role of long non-coding RNAs (lncRNAs) in epithelial-mesenchymal transformation was found to be linked with cell invasion and motility. These RNAs were also identified as potential candidates for transforming growth factor beta (TGF-beta) signaling. In the study, the lncRNA PVT1 was found to promote the proliferation and invasion of EC cells by increasing the expression of AKT1, and it induced the expression of lncRNA EIF3J-AS1 and microRNA-373-3p.
The results showed that microRNA-21 is significantly increased in lung epithelial cells during bleomycin-induced pulmonary fibrosis. MicroRNA-21 regulates the expression of alpha-smactin and vimentin, two markers of the epithelial transition. However, this effect was reversed when the microRNA-21 inhibitor was added. RNA was isolated from cultured cells and used in RNA-seq assays.
In addition to targeting pro-inflammatory cytokines, Boster Bio ZEB1 inhibitors have anti-cancer properties. By targeting the expression of interleukin-2, these drugs inhibit p53 signaling, which promotes the progression of breast cancer. These agents have additional effects that are not yet known. Further investigations will help determine the role of various tumor microenvironmental factors in the development and progression of cancer.
In addition to regulating pro-inflammatory cytokines, ZEB1 also regulates the DDR and p53 status of cells. These effects of ZEB1 may be beneficial for combined therapy of DNA-damaging drugs, which decreases unwanted side effects and enhances patient response. But the drug needs to be more specific and able to target the whole range of functions regulated by this pathway.
The ZEB1 protein is a core EMT-TF of the ZEB family that is implicated in cellular plasticity, dissemination, and the dormant-to-proliferative switch. In fact, it is implicated in the poor clinical outcome of most cancers, including lung cancer, prostate cancer, and melanoma. Furthermore, its activation contributes to resistance to anticancer drugs. In addition, ZEB1 protein expression increases through the progression of tumor progression, including metastatic and castration-resistant PCa.
The ZEB1 protein functions as a transcriptional regulator of several intracellular processes, including the ATR-CHK1 axis, DNA repair machinery, and p53 status. Because of its role in regulating DDR, it is a promising target for drug combinations against cancer. This could result in fewer unwanted side effects and improved treatment outcomes. The ZEB1 marker will help researchers understand how this pathway regulates tumor growth and metastasis.
The differentiation of pre-cDCs by differentiation of cDCs requires certain signature genes. These genes are not fully expressed in pre-cDCs. Hence, identifying these cells requires a detailed analysis of their global transcriptome. However, we can make a start by isolating pre-cDCs by using a gene-expression analysis. After the identification of the signature gene, we can proceed further to identify the subpopulation of pre-cDCs.
The phenotypic expression patterns of pre-cDCs show that their IRF8/IRF4 ratios correlate with their commitment to their respective subsets. However, a gene named CD172a (SIRPA) has been identified that distinguishes pre-cDCs from each other. Cells that express this gene show higher pre-commitment to cDC2 than to cDC1. Cluster C1 contains more CD172a cells than cluster C3, which suggests a connection between these two subsets.
Scientists worldwide are studying COVID-19, a virus that causes SARS. Researchers have identified a protein spike that interacts with a receptor called ACE2 and primed by the TMPRSS2 enzyme. Boster Bio provides antibodies to detect this protein spike. The company also provides custom services and BeNeLux delivery. The researchers are excited to learn how this biomarker will help them understand the disease.
A high-sensitivity ELISA kit can detect biomarkers in different tissue samples, such as skin and adipose tissue. This method is highly sensitive, and Boster Bio's antibody kits are validated for many sample types. The company's proprietary ELISA platform, PicoKine(tm), provides high-sensitivity ELISA kits. Researchers can also use the Boster Bio antibodies for a wide range of applications, including immunoassay, ELISA, and flow cytometry.
ZEB1 promotes metastasis and predicts poor prognosis in hepatocellular carcinoma. It is also known as HBx-related long non-coding RNA. The gene is regulated by PI3K. The ZEB1 protein has a wide range of functions in the body, including regulation of cell proliferation and survival. Oncotarget is an online resource for scientific research.
The ZEB1 gene is closely related to miR-200a-3p, miR-200c-3p, and miR-141-3p. These molecules are involved in the ATRA-induced effects on cell proliferation and parallel migration. They also regulate other genes, including Pou4f, Ets1, and Jun. Further, ZEB1 is regulated by PI3K, and inhibition of its activity inhibits this signaling pathway.
The effect of EPDR1 on PI3K/AKT/mTOR pathway was investigated by overexpressing this gene in A2780 cells. Interestingly, both A2780 and EPDR1 inhibited PI3K/AKT signaling. Similarly, the PI3K/AKT/mTOR pathway inhibited EMT. Western blotting demonstrated that PtoxDpt downregulated both E-cadherin and N-cadherin expression.
In non-small cell lung cancer, the ZEB1 marker suppresses the expression of the miR-200 family, which upregulates PD-L1 (programmed cell death protein). Scientists suspect that the ZEB1/miR-200 axis may affect the immune system's recognition of cancer cells. This research has led to new therapeutic strategies for metastatic breast cancer.
In cancer, ZEB1 downregulates expression of E-cadherin, a cell-selective adhesion protein that promotes tumor growth. It also recruits histone deacetylases, HDAC1 and HDAC2, and inhibits PI3K activity. Deubiquitinated ZEB1 is a potential biomarker of poor clinical outcomes.
The stability of EMT-related transcription factors is important for initiating cellular EMT. Deubiquitinating enzymes counteract polyubiquitination and stabilize ZEB1. Other proteins that interact with ZEB1 include USP51 and CSN5. In response to DNA damage, the ATM kinase phosphorylates and stabilizes ZEB1 by reducing its activity. Deubiquitinases provide an alternative pathway to treat breast cancer by inhibiting DNA damage.
In tumors, the ZEB1 marker is coexpressed with nuclear b-catenin. This suggests that it regulates b-catenin expression. The ZEB1 marker is stabilized by IGF2BP2.
The ZEB1 gene controls several pathways in the tumor microenvironment, including EMT. The expression of ZEB1 in tumors promotes EMT. Besides controlling cell polarity, ZEB1 also controls the expression of other genes involved in the process. It represses Pals1 (a component of adherent junctions) and Crumbs3 (a regulator of cell polarity). It also activates metalloproteinases, including MT1-MMP.
In another study, ZEB1 is required for efficient transendothelial migration of PC-3 cells. It has been shown that loss of ZEB1 leads to a reduced migration of these cells. This finding supports the hypothesis that ZEB1 regulates epithelial properties. The loss of ZEB1 decreases migration of PC-3 cells in other contexts. In contrast, loss of ZEB1 in PC-3 cells enables enhanced invasive properties.
PMID: 8138542 by Watanabe Y., et al. Transcription factors positively and negatively regulating the Na,K- ATPase alpha 1 subunit gene.
PMID: 1840704 by Williams T.M., et al. Identification of a zinc finger protein that inhibits IL-2 gene expression.
*More publications can be found for each product on its corresponding product page