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- Table of Contents
Facts about CD276 antigen.
May be involved in the development of acute and chronic transplant rejection and in the regulation of lymphocytic action at mucosal surfaces. Could also play a key role in supplying the placenta and fetus with a suitable immunological environment throughout pregnancy.
Human | |
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Gene Name: | CD276 |
Uniprot: | Q5ZPR3 |
Entrez: | 80381 |
Belongs to: |
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immunoglobulin superfamily |
B7H3; B7-H3; B7H34Ig-B7-H3; B7-H3B7 homolog 3; CD276 antigen; CD276 molecule; CD276; Costimulatory molecule
Mass (kDA):
57.235 kDA
Human | |
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Location: | 15q24.1 |
Sequence: | 15; NC_000015.10 (73683966..73714518) |
Ubiquitous but not detectable in peripheral blood lymphocytes or granulocytes. Weakly expressed in resting monocytes. Expressed in dendritic cells derived from monocytes. Expressed in epithelial cells of sinonasal tissue. Expressed in extravillous trophoblast cells and Hofbauer cells of the first trimester placenta and term placenta.
Membrane; Single-pass type I membrane protein.
The immunocheckpoint protein CD276 is an immunocheckpoint marker which performs several important functions. It has the potential to limit the proliferation of tumor cells and their invasion. This molecule can be found on T cells. Read on to discover more. We take a look at some of its most commonly used uses. This article will focus on the functions of CD276 and its significance in cancer treatment. It could also be useful for researchers in oncology.
Scientists have recently discovered that CD276, a drug that is new, can target cancer cells. The drug triggers the NFKB pathway, which increases VEGF expression and IL-8 levels. This can encourage tumor invasion and angiogenesis by increasing VEGF and the expression of IL-8. It has potential to become a key treatment option for treating tumor angiogenesis.
Although CD276 was initially described as a co-stimulatory molecule involved in the activation of T cells recent studies have shown it to have an immunosuppressive effect upon immune cells. Furthermore, up-regulated CD276 can inhibit the release of cytokines and promote the immune removal of cancerous cells. Although CD276's mechanism remains elusive, evidence is mounting that it is working in conjunction with other immune checkpoint molecules such as CTLA4 or PDZFlag.
Although CD276's function characteristics are complex, there is potential for anti-tumor treatments. The regulation of this gene has been studied over the past two decades and is closely linked to tumor growth invading, metastasis and immune escape. It also is expressed in tumors, but not in healthy tissues, which suggests that it is an ideal immunotherapeutic target. Its clinical value requires further study.
One study revealed that CD276-targeted CAR T cells had a high activity rate against bladder cancer cells. This suggests that CD276-targeted CD276 T cells could be an interesting immunotherapy option. However the current treatment used to treat cancer cells has proved ineffective. The future of immune checkpoint molecule therapies is dependent on the effectiveness.
To study the expression of CD276 in bladder cancer in humans, researchers utilized tissue microarrays. The researchers stained the cells with an anti-CD276 antibody in order to identify cancer cells. The result was a significant reduction of the CD276 protein in the tumors. The CD276 protein is also associated with poor prognosis. These findings are further supported by Boster Bio's CD276, an immune checkpoint molecule.
The CD276 protein encoded by boster bio is an innovative antigen for tumors. The peptide stimulates activation of NFKB signaling through TLR-4. Furthermore, CD276 promotes the upregulation of VEGF and the IL-8. These elevated levels are linked to angiogenesis and tumor invasion. These factors are related to the formation of tumors. The targeting of CD276 can offer new treatment options.
CD276 binds to Nutlin-3 which can trigger its expression on cells' surfaces. Nutlin-3 increases the interaction of CD276 with MDM2. It is believed to depend on p53 for CD276 induction. Additionally, CD276 expression in null cells was not elevated. Thus, the CD276 siRNA is a novel T cell antigen that inhibits T cell activation. It also allows researchers to identify the potential mechanisms of its anti-inflammatory effects.
While the function of CD276 is a bit nebulous however, research on its function has been ongoing for more than two decades. The molecules that regulate CD276 have close associations with the immune system's escape, invasion, and growth. Additionally, CD276 is highly expressed in many tumors, but its levels are low in normal tissues. These findings suggest that CD276 is an attractive immunotherapeutic target. However, more research is needed to confirm its clinical significance.
CD276 is a molecule that attaches to extracellular vessels, and has a costimulatory function. It could affect bone growth and also inhibit T and NK cell function. It is also expressed in a variety of malignant tumors. It is a useful immune-therapy agent for tumors, and also research into cancer.
CD276 is a new biomarker for angiogenesis in anti-tumor cells that stimulates the NF-kB signaling pathway in a TLR-4-dependent manner. CD276 increases the stability of the transcription factor HIF-1a and blocks stress-activated transcription factor NRF2, which is vital to activate antioxidants. Recent research has shown that CD276 can enhance the amount of glucose absorbed and encourage the growth of tumors in mice model of breast cancer xenograft. These findings offer a new treatment option for tumor angiogenesis.
Nutlin-3 induces the cell surface expression of CD276. Nutlin-3 can also trigger the expression of CD276. This could indicate an intermediate in the CD276 degradation pathway. Further, Nutlin-3 treatment decreased basal CD276 levels. This suggests that CD276 siRNA may increase Nutlin-3's impact on the proliferation of tumor cells.
CD276 is a potent gene target, however it needs to be studied to determine its function. Although CD276 is a stimulatory molecule that activates T cells, it is a powerful immunosuppressive molecule which inhibit the growth of T cells. Furthermore, up-regulated CD276 promotes immune escape of tumor cells through the inhibition of the production of cytokines. Although it isn't clear what CD276's receptor-mediated mechanism is, there is increasing evidence that CD276 functions in conjunction with other immune checkpoints.
CD276 is a genetically modified protein that contains 28AA signal the peptide, which is a two-component external region, and an immunoglobulin constant (IgC) and variable (IgV) structure. The CD276 gene is composed of ten exons, with four to seven exons coding for the extracellular IgV–C domain. Re-expression of CD276 in mice inhibited the growth of tumor cells.
Researchers discovered that CD276 is a new cancer biomarker, is able to inhibit the invasion of tumor cells. The marker stimulates NFKB signaling via a TLR-4-dependent process. It also blocks Nrf2, an antioxidant that is implicated in a variety of cancers. These findings suggest CD276 could be a potential target for anti-tumor therapies.
CD276 is a newly discovered immunocheckpoint protein, functions as an inhibitor of T cells and is linked to the EMT pathway. While CD276's role in tumor formation and invasion is not fully understood however, research has revealed that upregulated CD276 promotes immune removal of tumor cells and reduces the secretion of cytokines. Although the exact mechanism behind CD276's actions is not clear however, evidence is mounting to suggest that the molecule may interact with other immune checkpoints which allows it to have synergistic effects on tumor cells.
The primary role of B7-H3's gene in the reprogramming of glucose metabolism is performed by cancer cells. A rise in lactate and glycolysis production in cancer cells, also called the Warburg effect confers a survival advantage for the tumor cells by supplying the cells with energy and biosynthetic blocks. To know how CD276 fights cancer cells, a biomarker targeting B7-H3 is an excellent choice.
The CD276 marker has shown significant anti-tumor properties against human and murine cancerous ones. Boster Bio's CD276 marker blocks the growth of tumor cells.
CD276 is an oncogene that regulates the proliferation and differentiation of tumor cells. Its knockout blocks cancer cell migration through upregulating the expression of SMAD6, SMAD4 and MYC. This gene regulates DNA double-strand breaks and cell cycle, as well as radiotherapy. CD276 is likely to be an exciting therapeutic target.
Despite playing a significant role in malignancy cell proliferation, invasion, and migration, CD276 expression is low in normal tissues. It could be a great target for cancer immunotherapy. However, further studies are needed to validate its clinical value. However, there is a lot of potential in the CD276 gene. This novel drug has an extensive therapeutic spectrum. It can be used to treat a variety of kinds of cancers as well as those that cause metastasis.
CD276 expression on tumor cells was studied using flow cytometry in UCCL and NUC. The cells were grown until they reached confluence and then washed with cold water. The cells were incubated with anti CD276 mAb in order to detect CD276 expression on the cell's surface. To determine the presence of proteins, cells were stained with KLH-mAb. In each experiment, the average intensity of the cells stained with anti-CD276mAb were determined and compared to levels of the control antibody.
A sample of benign tissue revealed a strong correlation between stage of cancer and the CD276 expression. In actual fact the CD276 score in the T2a sample of cancerous urothelial cells was substantially lower than the ones in the samples of the tumor. In the case of bladder tumors CD276 expression was also low in the benign tissues surrounding the tumor.
PMID: 11224528 by Chapoval A.I., et al. B7-H3: a costimulatory molecule for T cell activation and IFN-gamma production.
PMID: 14764704 by Steinberger P., et al. Molecular characterization of human 4Ig-B7-H3, a member of the B7 family with four Ig-like domains.