Ephrin type-B receptor 3 Antibodies

Ephrin type-B receptor 3 (EPHB3)

Receptor tyrosine kinase which binds promiscuously transmembrane ephrin-B family ligands residing on adjacent cells, leading to contact-dependent bidirectional signaling into neighboring cells. The signaling pathway downstream of the receptor is known as forward signaling while the signaling pathway downstream of the ephrin ligand is known as reverse signaling.

Like EPHB2, functions in axon guidance during development regulating for instance the neurons forming the corpus callosum and the anterior commissure, 2 important interhemispheric connections between the temporal lobes of the cerebral cortex. In addition to its role in axon guidance plays an important redundant role with other ephrin-B receptors in development and maturation of dendritic spines as well as the formation of excitatory synapses.

Gene Information

Human
Gene Name:	EPHB3
Uniprot:	P54753
Entrez:	2049

Family

Belongs to:
protein kinase superfamily

Alternative Names

Cek10; EC 2.7.10; EC 2.7.10.1; EK2; EPH receptor B3; EphB3; EPH-like kinase 2; EPH-like tyrosine kinase-2; ephrin type-B receptor 3; ETK2Hek2; Hek2; human embryo kinase 2; Mdk5; Sek4; Tyro6; Tyrosine-protein kinase TYRO6

Molecular Weight

Mass (kDA):
110.33 kDA

Genomic Context

Human
Location:	3q27.1
Sequence:	3; NC_000003.12 (184561785..184582408)

Tissue Specificity

Ubiquitous.

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein. Cell projection, dendrite.

Diseases

• Malignant Neoplasms
• Neoplasms
• Tissue Adhesions
• Nervousness
• Cell Transformation, Neoplastic
• Colorectal Cancer
• Carcinoma
• Neoplasm Metastasis
• Malignant Paraganglionic Neoplasm
• Crest Syndrome
• Tumor Angiogenesis
• Colorectal Neoplasms
• Congenital Abnormality

• Prostatic Neoplasms
• Malignant Neoplasm Of Lung
• Malignant Neoplasm Of Prostate
• Inflammation
• Carcinogenesis
• Lung Neoplasms
• Adenocarcinoma

Pathways

• Cell Migration
• Axon Guidance
• Cell Adhesion
• Cell Proliferation
• Pathogenesis
• Angiogenesis
• Cell Differentiation
• Localization
• Methylation
• Segmentation
• Cell-cell Adhesion
• Regeneration
• Neurogenesis

• Palate Development
• Inflammatory Response
• Epithelial Cell Proliferation
• Contact Inhibition
• Synaptic Transmission
• Locomotion
• Osteoblast Differentiation

PTMs

• Phosphorylation
• Methylation

• Dephosphorylation
• Biotinylation

• Reduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/EPHB3

Best Uses Of The EPHB3 Marker

The EPHB3Marker is a genetic marker that can be used to identify and track a specific gene. This article will examine how EphB3 acts in Papillary Thyroid Cancer as a tumor-promoter. We also look at how this gene regulates Rho, Vav2 GTPases activities that are involved with cell signaling and receptivity of various proteins.

EphB3 acts in Papillary Thyroid Cancer as a tumor stimulator

EPHB3 is eliminated by the SNAIL1 proteins, which are a crucial cellular guide element in intestinal epithelium. EPHB3 has been found to be a tumor-suppressor in colorectal and is often silenced by the body during adenoma/carcinoma transition. The molecular mechanisms underlying EPHB3 silencing are still unclear, but the protein exhibits a strong anticorrelation with induced epithelial-mesenchymal transition (EMT). SNAIL1 competes in binding to the Ebox motif with ASCL2, a stem cell factor.

EphB3 regulates Ecadherin, vimentin expression, and is associated to shorter survival rates in GCs. Hence, the protein may be a prognostic biomarker for GC. Therefore, treatment targeting EphB3 in Papillary Thyroid Cancer is crucial in the management of this disease. This protein performs many functions.

MiR-124 targets the Notch2 signalling pathway and inhibits cell growth and invasion. AURKA, a regulator, is also targeted by miR125a. It regulates expression of the mRNA HSA-mir-126-5p, which is involved in the development of gastric cancer. This regulates invasion and promotes apoptosis.

The findings suggest that EphB3 may act as a tumor promoter in this disease, which is more common than previously thought. The study revealed several mutations in EphB3, including APC1 and ADAMTS9 which affect EphB3. These mutations are likely to cause EphB3 to inhibit endocrine activity. These findings will need to be confirmed by further research.

Thyroid cancer has become more common in recent years. Thanks to modern imaging technology, doctors can detect small cancers earlier in the disease's progression. Fortunately, incidental Thyroid Cancers are rare and often respond well to treatment. A doctor should be consulted if you experience symptoms of thyroid carcinoma. The free Thyroid Cancer Guide includes information on how to cope with the disease and how to get a second opinion. You can unsubscribe at anytime.

The authors did a retrospective clinic/pathological review on 19 patients undergoing spinal EPN and MEPN resections. In addition, they investigated whether EPhB3 upregulation affected genes in stromal cell-derived factor-1 (SDGF-1) and Down syndrome critical region family. The study also found several new cases for Papillary Thyroid Cancer.

MiRNA-123 prevents cell proliferation and migration, invasion, cell cycle progression, and cell cycle progression in gastric carcinoma cells. It also targets the tumor suppressor FSCN1 and inhibits growth of gastric cancer cell lines. This miRNA targets FSCN1 but also inhibits cell proliferation and invasion in gastric cancer cells.

EphB3 regulates Vav2 & Rho GTPases

The EPHB3 gene can be used to study how the ephrin receptor affects cell proliferation, differentiation, migration. Ephrin B3 also regulates neurogenesis, cell growth, and synaptic flexibility. This protein is found in various parts of the human body, including the hippocampal Synapse.

The EPHB3 protein binds to Ephrin B2 in the postnatal pipitary gland. The two proteins interact in cis- and trans ways depending on which cell type they are. These two proteins are made by endothelial cells, and corticotropes. The interactions between EphB3 and ephrin-B2 were confirmed by double immunohistochemistry.

The immune system detects the EPHB3 protein in cells. This protein is present in both human and animal cells and serves a variety of functions. It is a critical component in regulating hormone production in the body. By detecting EPHB3 proteins, the immune system recognizes certain proteins. This protein is a good indicator about the health of a particular cell. The EPHB3 genes can be found in almost every tissue, including skin and other organs.

EphB3Fc treatment results in an increase in the expression of the reelin pathway when compared with Fc-control treatments. Fc treatment didn't affect the hippocampal-region total level of Dab1 protein or reelin. This marker has no effect at all on the level of p–Dab1 found in the hippocampus. The EphB3Fc therapy did not affect levels of reelin or other proteins.

The EPHB3 gene products is a potent tumor inducer in Papillary Thyroid Cancer. EphB3 is a hormone that promotes tumor growth. It is also associated with adipocytes. It also regulates Rho and Vav2 GTPases. Although EphB3 cannot be identified in human tumors, it plays an important role in the progression.

Recent research on rats treated with EphB3Fc revealed that the treatment decreased the number of cells with DCX labeled dendrites and reduced neurite outgrowth. Fc control treatment resulted in a decrease in the number or dendritic growth in the control group and a reduction of the number/number of neurons. It also reduced abnormal dendrite growth.

Epilepsy can be described as a condition in that seizures are of high frequency and duration, last for up to 10 second, and are long-lasting. EphB3–Fc reduced spontaneous seizures in Ep rats by reducing their frequency and duration. It did not decrease seizure severity or duration. EphB3Fc does not detect epilepsy in humans.

The Eph/ephrin-receptors are members the largest family of receptor Tyrosine Kinases. They control cell-cell adhesion as well as morphology. They also control cell positioning in similar populations. Eph-mediated tissue formation relies on the delicate balance of cell adhesion reaction. These interactions determine the patterning of tissues. If they are not working properly, the immune system may respond to the immunosuppressive effects Eph receptors.