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- Table of Contents
1 Citations
Facts about Transcription factor jun-D.
Human | |
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Gene Name: | JUND |
Uniprot: | P17535 |
Entrez: | 3727 |
Belongs to: |
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bZIP family |
activator protein 1; AP-1; jun D proto-oncogene; JunD; JunD-FL isoform; transcription factor jun-D
Mass (kDA):
35.174 kDA
Human | |
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Location: | 19p13.11 |
Sequence: | 19; NC_000019.10 (18279694..18281622, complement) |
Nucleus.
The JUND Marker is utilized in a number of biological assays. The JUND molecule is identified by antibodies, either monoclonal or polyclonal. They react with samples from various animal species. Boster Bio uses mouse and rabbit as its model species for the development of JUND antibodies. Boster Bio has developed antibodies that are specific for JUND. This is critical for many tests.
Many biochemical tests can detect JUND using antibodies. These antibodies can be monoclonal as well as polyclonal and react with JUND in a wide range of animal specimens. Boster Bio utilizes rabbits and mouse to create antibodies that recognize JUND. This technique is particularly useful for studies on the disease because these models are not representative of human. The JUND marker can be used to identify JUND in human samples and as a test for the toxicity of an antibody.
We transfected cells containing HEK293 that have the Gcm1 promoter to see if mutants of JunD might affect the expression of the respective genes. We also transfected Nfe2kdtrophoblast cells with reporter constructs and JunD oligonucleotide probe. These cells showed an increase in the activity of JunD. Further, we performed supershift analysis to show that the JunD protein connects to the promoter area of Gcm1 (mGcm1).
JunD and Nfe2 interact in a significant way for the development of the placenta. This interaction will help us to understand the functions of bZip transcription elements during the development of the placenta. It will also demonstrate how these genes play an important role during different stages of the development of the placenta. To avoid miscarriages in the future it is important to understand and recognize JunD's role in the development of the placenta.
In the same way, JunD is necessary for the formation of syncytiotrophoblasts. In the absence of Nfe2 The increased JunD expression resulted in an increase in syncytiotrophoblast development. The cross-talk between JunD and Nfe2 is essential to create syncytiotrophoblasts. If you're seeking a treatment using a gene, the use of JUND as a marker in Boster Bio might be the best choice.
The Nfe2 gene inhibits JunD binding activity in murine placenta cells. These cells are inhibited by Curcumin as well as HAT inhibitor curcumin. Nfe2 can be eliminated from the Nfe2-/placenta and Nfe2ctrophoblast cells to increase JunD acetylation , both in vitro, and in the vivo.
It is crucial to develop antibodies against the JUND marker in order to create an effective immunotherapy for cancer. In this study, we employed the HeLa cervical epithelial cells and the mouse embryonic fibroblast cell line to identify JunD. After treating the cells with JunD antibodies, we then reprobed the surface of the cell with an additional, p21-biotin labeled antibody.
We discovered that JunD expression was elevated in immortalized menin-null cells. This suggests a regulating role for menin in the expression of JunD. The increased levels of JunD contribute to the menin-null phenotype. However, it is important to be cautious when developing antibodies against the JUND marker. As long as the results of this study are confirmed the research will remain an important step in developing an anticancer treatment.
In the vivo, JunD hinders normal intestinal epithelial growth. In addition it plays an important role in epithelial cell renewal. The inhibition of epithelial growth caused by JunD is also linked to an increase in polyamine levels. These findings suggest that JunD has an antimitogenic effect. This antisense treatment is effective in preventing the growth of intestinal tumors because JunD is expressed in the colon.
JunD and HBZ promoter functions were found to be synergistic. JunD and HBZ promote hTERT expression when they are cotransfected with the HBZ expression Vector. Both proteins are necessary to increase hTERT expression within HeLa cells. In this study, JunD and HBZ cotransfected into Jurkat cells did not increase the amount of hTERT.
JunD and c–junA belong to the Jun family. They dimerize and form the AP1 transcript factor. There are many proteins within the Jun family which share structural similarities with one another, including activator protein-1. These proteins have dimerization domains as well as DNA binding domains that are enriched in basic residues. In addition, they are involved in the process of repression of transcription.
These two studies also demonstrated an inverse relationship between the expression of mJunD in cJun. The cells with cJun overexpression have shown an increase in their proliferation in comparison to the cells that were transfected with mJunD. Men1-NULL-17 cells had lower levels of JUNA overexpression than mJunD-transfected cells. These cells also showed greater resistance and accumulated in foci in soft-agar, while Men1-NULL-17 and cJun-21 showed no inhibition.
In addition to JunD and HBZ the Sp1 gene also encodes Sp1 and HBZ. In addition to this, the Sp1 protein was cotransfected within HeLa cells. Western Blot analysis of the whole cell lysates of HeLa cells was carried out using an anti-Sp1 rabbit polyclonal antibody. To analyze Sp1 expression, HBZ was used and anti-sp1 antibodies were used.
The development of antibodies against the JUND marker is an essential step in the development of a tumor immunotherapy. JunD mutations block menin-binding which is crucial for tumor growth. The JunD mutation is found in various types of tumors, including tumors of the endocrine system, non-MEN1 parathyroid gastrinomas, tumors, and insulinomas. It is important to know that both JunD and Men1 are tested separately to determine if JunD is a risk factor in endocrine cancers.
PMID: 1903194 by Berger I., et al. Structure and function of human jun-D.
PMID: 2112242 by Nomura N., et al. Isolation of human cDNA clones of jun-related genes, jun-B and jun- D.
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