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- Table of Contents
Facts about Ephrin type-B receptor 2.
Involved in the guidance of commissural axons, that form a significant interhemispheric connection between the 2 temporal lobes of the cerebral cortex. Also involved in guidance of contralateral inner ear efferent growth cones at the midline and of retinal ganglion cell axons to the optic disk.
Human | |
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Gene Name: | EPHB2 |
Uniprot: | P29323 |
Entrez: | 2048 |
Belongs to: |
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protein kinase superfamily |
CAPB; Cek5; Drt; DRTEphB2; EC 2.7.10; EC 2.7.10.1; EK5; elk-related tyrosine kinase; EPH receptor B2; eph tyrosine kinase 3; EphB2; EPH-like kinase 5; ephrin type-B receptor 2; EPHT3MGC87492; EPTH3; Erk; ERKHek5; Hek5; Nuk; PCBC; protein-tyrosine kinase HEK5; Qek2; Renal carcinoma antigen NY-REN-47; Sek3; Tyro5; Tyrosine-protein kinase receptor EPH-3; Tyrosine-protein kinase TYRO5
Mass (kDA):
117.493 kDA
Human | |
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Location: | 1p36.12 |
Sequence: | 1; NC_000001.11 (22710770..22921500) |
Brain, heart, lung, kidney, placenta, pancreas, liver and skeletal muscle. Preferentially expressed in fetal brain.
Cell membrane; Single-pass type I membrane protein. Cell projection, axon. Cell projection, dendrite.
The EPHB2 protein has many potential uses and is often overlooked by scientists. However, scientists can submit results to gain product credits for their efforts. Researchers from around the world can use this protein to test different samples, species, and applications. Researchers can also submit samples to find out what it means for certain diseases and cancers. This product can be used for all kinds of research, from cancer prevention to drug discovery.
The EPHB2 marker is a highly conserved molecular marker, which is widely used to identify a tumor or protein of interest. It is expressed by SEVs, including endothelial cells. When SEVs express EPHB2, they are able to induce angiogenesis. In addition, it has been shown that the presence of EPHB2 in tumors is associated with poor patient prognosis. The EPHB2 marker promotes angiogenesis, and EV-carried EVs stimulate the ephrin-B phosphorylation.
The EPHB2 marker can be expressed as wild-type (WT) or variant proteins. Human GPVI is stably expressed in the RBL-2H3 cell line. The corresponding EPHB2 variants are phosphorylated in the presence of ephrin and cell-cell contact. The recombinant human GPVI-defias ma R745C mutant is expressed in the medulla but does not exhibit any direct effect on the ephrin-mediated activation process.
The EPHB2 marker is also a candidate gene for mutations that affect the EPHB2 receptor tyrosine kinase gene. This gene is located on chromosome 1 and encodes the EPHB2 receptor tyrosine kinase. Its homozygous c.2233C>T transition is predicted to produce the missense variant, p.R745C. Using PolyPhen-2 software to identify this variant, it also predicted a high degree of damage.
In addition to its role in platelet activation, EPHB2 also acts during the initial step of GPVI signaling. It is also involved in regulating platelet adhesion. These properties have allowed the EPHB2 marker to become the primary candidate for disease markers. There are several other applications for this molecular marker. The EPHB2 gene is highly conserved in humans and is a key factor for diseases such as cardiovascular disease and inflammatory bowel disorders.
KO mice that lack EphB2 expression are commonly used in clinical trials. These mice have been developed by Dr. Henkemeyer of the University of Texas Southwestern Medical Center. They were maintained on the C57BL/6J genetic background and bred in an EphB2+/ heterozygous breeding system. In addition, the mice were genotyped at Dr. Mimche's laboratory at the University of Utah. All procedures were performed under NIH Guidelines for the Care of Laboratory Animals
Moreover, EphB2 is associated with renal damage after IR injury. It may be a key factor in regulating the effects of renal inflammatory and proliferative responses and fibrosis. Its expression in kidney tissue confirms the role of EphB2 in renal injury. And since it is implicated in renal injury, the EphB2 gene is of great importance to research.
EphB1 and EPhB2 are required for proper navigation of caudal thalamic axons in the neocortex. These two proteins act as receptors in axons to allow them to travel through the VTel. Interactions between EphB1 and EPhB2 are involved in this process. The roles of EphB1 and EPhB2 are not fully understood, but they do appear to have distinct roles in brain development.
The interaction between EphB1 and EPhB2 is essential for the development of the dentate gyrus. When mice lacking EphB1 or EphB2 have their missing or defias ma NMDA receptors, the development of the dentate gyrus is severely delayed. EphB2 also mediates phosphorylation of NR2B. EphB2 also stabilizes NMDA receptors on the cell surface.
EphB2-Fc dimers were purchased from R&D Systems and were purified by protein A-Sepharose and p-aminobenzamidine-agarose. EphB2-Fc monomer production was verified using gel electrophoreis/Coomassie stain. EphB2-Fc monomers were then added to NIH3T3 cells 24 h after infection. In addition, they were added at a concentration of 4 mg/ml.
Loss of EphB2 results in a reduction of mature neuronal cells. Mice with EphB2 knockout also show a decrease in granule cell layer. In addition, KO mice display an increase in glial cells. These results suggest that EphB2 has a significant role in adult neurogenesis. Moreover, EphB2 knockout mice lack the ability to regulate their emotional responses.
The expression of EPHB2 in the PDX-derived cell fractions of EwS1 and EwS2 tumors showed a profound decrease in growth and spheroid formation in vitro and in vivo. The tumors from these cells showed expression levels similar to those of control cells. However, they were able to evade the depletion of EPHB2 in vivo, suggesting that these cells can evade EPHB2 knockout and re-colonize the tumor microenvironment.
The EphB2 receptor is an important regulator of the architecture of the neurogenic niche. The EphB2 receptor and its ligands interact with NMDARs. Inactivation of EphB2 results in a reduction in synaptically localized NMDARs. This results in reduced long-term potentiation. The EphB2 knockout mice are also genetically altered, resulting in emotional alterations.
The overexpression of EPHB2 in EwS cancer cells promotes metastasis. Therefore, pharmacological targeting of the EPHB2 pathway may serve as a novel strategy for blunting EwS dissemination. This biomarker is known to be associated with prognosis in cancer patients. This research is a major step in the development of anti-tumor therapies.
Infections of SYT-SSX2 cells have an aberrant cytoskeletal architecture. EphB2 regulates the activation of ephrin signaling. This may explain the development of resistance to systemic cancer therapies. These results also provide insight into the role of EphB2 in synovial sarcoma. However, the effects of EphB2 are not yet fully understood.
Molecular analyses of MICA expression in cancer tissues reveal that this gene is highly expressed in CRCs, compared with uninvolved tissue. The data showed that MICA expression was significantly higher in CRCs than in uninvolved tissue and also increased among men and women with advanced-stage CRCs. The results also showed that MICA expression was elevated in adenocarcinomas, but not in mucinous tumors.
Previous studies have found that patients with low Bax expression are more likely to develop CRC. Although the findings are preliminary, they do show that low levels of Bax expression are associated with worse overall survival in patients with advanced-stage disease. Further research is needed to determine whether Bax expression can be a prognostic marker in CRC patients. It will be useful in clinical trials of patients with advanced-stage disease to identify those with high Bax expression.
The data also suggested that patients with low EphA1 expression had significantly lower survival rates than those with high EphA1 levels. These findings were independent of age, gender, tumour type, and grade. Women had a slightly better overall survival than men. Although it is not clear why this association is strong, these findings suggest that EphA1 may play an important role in colon cancer development. So, it might be a valuable marker for cancer patients.
This study assessed whether the level of Ki67 immunoexpression correlated with outcome in patients with colorectal cancer. Researchers performed immunohistochemistry in tissues from 1800 CRCs to calculate the Ki67 labelling index. They then correlated the results with various clinicopathological and molecular parameters, including the stage and nodal status. In addition, patients with high Ki67 expression showed improved survival. They also had a higher prognosis.
Moreover, there is no correlation between tumor MICA expression and age or race. In CRCs, MICA expression was higher in patients with three distinct nodal metastasis statuses, as well as in tumors without tumor involvement. Age did not seem to play a role in the tumor MICA expression. This study also confirmed that MICA immunoreactivity correlates with T stage in CRCs. And the results are consistent with previous research.
Further study is needed to determine whether MICA can be a discriminant of aggressive and non-aggressive CRC. Molecular analyses of MICA in CRCs will be essential for determining if the gene is involved in the development and progression of CRC. For the time being, however, this study suggests that MICA expression can play a role in CRC progression. There is no consensus as to the role of MICA in the immune system, but future studies will shed more light on the subject.
While CDX2 expression in CRCs is controversial, it has been shown to be an effective prognostic marker in advanced-stage cancers. In fact, chemotherapy-resistant CRCs are often treated with adjuvant chemotherapy, and patients who have metastasized to other organs should be given systemic chemotherapy. However, the effects of chemotherapy on CDX2 expression were unclear, but tumors expressing the gene showed minimal changes in CDX2 expression.
PMID: 8033077 by Kiyokawa E., et al. Overexpression of ERK, an EPH family receptor protein tyrosine kinase, in various human tumors.
PMID: 8589679 by Ikegaki N., et al. Molecular characterization and chromosomal localization of DRT (EPHT3): a developmentally regulated human protein-tyrosine kinase gene of the EPH family.