Ephrin type B-6 receptor is a protein encoded by a gene EPHB6 in humans. And its ligand ephrin receptor, ephrin, many processes of development of the nervous system in particular mediation,. Based on the sequence context and their structure, ephrins are divided into (EFNA) Class ephrin-A, which is fixed to the membrane by (EFNB) Class ephrin-B is a transmembrane protein and glycosylphosphatidylinositol linkage. Eph family of receptors are divided into two groups based on the similarity of their affinity for ephrin ligand binding and ephrin-AB extracellular domain sequence thereof. I comprises a subgroup of the maximum ephrin receptor tyrosine kinase (RTK) family. Lacks kinase activity of the receptor tyrosine kinase most ephrin receptor encoded by this gene, and is connected to the ephrin-B ligands.
And its ligand ephrin receptor, ephrin, many processes of development of the nervous system in particular mediation,. Based on the sequence context and their structure, ephrins are divided into (EFNA) Class ephrin-A, which is fixed to the membrane by (EFNB) Class ephrin-B is a transmembrane protein and glycosylphosphatidylinositol linkage. Eph family of receptors are divided into two groups based on the similarity of their affinity for ephrin ligand binding and ephrin-AB extracellular domain sequence thereof. I comprises a subgroup of the maximum ephrin receptor tyrosine kinase (RTK) family. Lacks kinase activity of the receptor tyrosine kinase most ephrin receptor encoded by this gene, and is connected to the ephrin-B ligands.
Is a family of the largest known receptor tyrosine kinase Eph receptors. First, all of them are identified as orphan receptors Zu known ligands, certain features of which are not well understood. In recent years, the family ligand was identified named ephrins, certain features are identified in the nervous generated accordingly. It is possible to guide the development Eph receptors and ephrins, nerve topographic As it has been implicated as a position tag. They also axon guidance and cell migration, and has been involved in the route selection in the creation of regional model of the nervous system. Ligand is fixed to the cell surface, most of the features found so far, it can be interpreted as an accurate axon guidance or cell migration. This large family of ligands and receptors, there is a potential to contribute significantly to the exact space modeling of cell location and connection of the nervous system.
Was used in order to further express Kaplan-Meier analysis, to examine the predicted relationship between the expression of EFNB3 or EPHB6, EFNB2 TrkA is NB. ; The TrkA and EFNB2; the TrkA and TrkA and EPHB6 of EFNB3: Study groups were divided into groups based on the expression level of the gene combination, the following. ; The high / low EPHB6 TrkA, TrkA / EPHB6 in the low altitude; EPHB6 TrkA of high / low, high TrkA / low EPHB6: For example, there was a combination of TrkA and EPHB6 groups of four. The pattern of the probability distribution of the survival of each of the four groups and patient, I was next examined.
One third of the NB, expressed low low EPHB6 both bets TrkA. Third of another, expressed high TrkA, the high EPHB6 both. The third and the last is TrkA high door of low-TrkA but EPHB6 high NB express, expression who were included low EPHB6. Show the group of positive and negative presence of NB and 3 Group 2, is different by expressing the (or vice versa) of TrkA identification EPHB6 by the expression. Therefore, regardless of the expression of NB TrkA, EPHB6 formula to predict the outcome of the disease. NB individual in the group defined by the combination of these three variables will vary. Together TrkA/EFNB3 combination with TrkA/EFNB2 is obtained, regardless EFNB3 formula data that these EPHB6, EFNB2, Similar results demonstrate that to predict the outcome of the disease from NB expression TrkA.
Incomplete kinase receptor for members of the ephrin-B family. I will bind to ephrin-B2 and ephrin-B1. Regulate the migration and cell adhesion by the effect of both positive and negative upon stimulation by ephrin-B2. Inhibitory activity of JNK, the expression of CD25 and IL-2 secretion induced by T cell receptor stimulation by ephrin-B2
First to evaluate the role of blood pressure Ephb6 (BP) regulation. We its ligand EphB6 Efnb All three have observed that expressed vascular smooth muscle cells in mice (VSMC). We found castrated the shrinkable men Ephb6 gene KO is increased compared to the corresponding WT those small arteries, the activation of RhoA, and shown by ex vivo phosphorylation of constitutive myosin light chain . According to this finding, Ephb6 KO mice presented BP reinforcing castrated compared to castrated WT controls. In experiments in vitro, the Ephb6 reduced VSMC contraction, crosslinking Efnbs is, VSMC that revealed that suggest that it is the responsibility of the phenotypic BP reverse signaling has been observed through Efnbs. Reverse signaling is mediated by GRIP1 adapter protein. As a compensatory mechanism, 24 hours, reduction was shown from Ephb6 KO urinary catecholamine in male mice for feedback to maintain BP within the normal range probably additional experiment. To castration, however, that compensation is canceled in Ephb6 KO mouse, BP is a reason for increase was detected in these animals probably. In addition to regulation of testosterone, which suggests that it is an object nervous / endocrine According VSMC, the catecholamines correction mechanism Ephb6. Extended FNS and method with EPHS and testosterone, can play an important role in the regulation of BP and contraction of the small arteries revealed in our study.
For example, Eph receptors belong to the large class of receptor tyrosine kinases involved in various processes such as angiogenesis rear modeling, and axon guidance. Further These molecules are involved in several cancers, significant work has been done to understand the biological significance of their tumor formation. Eph receptor number and are transferred silence cell, the invasive breast cancer in addition to EphB6 representation of variants of ephrin ligand. In transcriptional silencing of EphB6 due to methylation of the CpG dinucleotide in the gene promoter specific. Gene transcription EphB6 was not detected in MDA-MB-231 cells, transfection of EphB6 expression construction reduces the invasiveness of the in vitro these cells significantly. Perhaps, the yeast two-hybrid system is referred to as reaction EphB6 with intracellular proteins other mediating EphB6 phenotypic expression cells. It was found to affect proteins involved in the metabolism of various or indirectly EphB6 direct comparison proteome analysis of the MDA-MB-231 cells, signal transduction, the expression of energy homeostasis and cytoskeleton.
I have shown that proteome changes seen in cells expressing EphB6 breast cancer may be a direct effect of EphB6 changes in the level of specific proteins. However, most of the change in the level of protein appears to be an indirect effect of EphB6. Major mechanism for these changes, you can include a change of translatable richness of transcript specific, and stability. Of a variety of regulatory molecules that control the expression of genes encoded by the human genome, has emerged as an important class of regulators miRNA. To enhance preventing the transfer and degradation of RNA or small molecule of 21 to 23 nucleotides in length, transcripts and was obtained caused a change in the level of protein in this manner. This is assumed to be a sequence that can be targeted by the miRNA that 2/3rd over gene to be encoded in the human genome are different. diseases appropriate miRNA can be seen from the different levels of these molecules in various types of cancer. The introduction of the miRNA construction of certain tumor cells, inhibiting tumor phenotype miRNA was assigned an important regulatory role thereby is shown. Given a number, miRNA for the purpose intended by the particular miRNA will be able to influence the presence of a large number of proteins and mRNA.
The EphB6 transfection can affect the protein profile due to the abundance of modulating miRNA addition of cells was assumed probably based on proteomic profile was altered EphB6 transfected MDA-MB-231 cells. In response to this opportunity, using nucleic acid locked (LNA) miRCURY platform link between miRNA and cell phenotype, to establish a hybridization array-based strategies. I will provide a link between the biological significance of the change in phenotype of cancer cells and expression status EphB6 MDA-MB-231 cells with the miRNA of here.