Is a protein encoded by EPH receptor A4 is by gene EphA4 of (ephrin, receptor 4) in human. This gene belongs to the ephrin receptor subfamily of protein tyrosine kinase. In the central nervous system, EPH-related receptors EPH is involved in mediating a particular developmental event. Usually, EPH subfamily receptors, have an extracellular region containing two fibronectin type III repeats and cysteine-rich domain and kinase domain of the single. Are divided into two groups based on the similarity of their affinity for the ligand ephrin binding and ephrin-AB extracellular domain sequence of the ephrin receptor. In 2012, can live significantly longer compared to patients with the gene intact ALS patients is defective genes published in Nature Medicine journal, wherein, amyotrophic lateral sclerosis and neurodegenerative diseases EphA4 I discloses the connection between the (ALS). This will open for the development of treatments for incurable diseases of this current.
This gene belongs to the ephrin receptor subfamily of protein tyrosine kinase. In the central nervous system, EPH-related receptors EPH is involved in mediating a particular developmental event. Usually, EPH subfamily receptors, have an extracellular region containing two fibronectin type III repeats and cysteine-rich domain and kinase domain of the single. Are divided into two groups based on the similarity of their affinity for the ligand ephrin binding and ephrin-AB extracellular domain sequence of the ephrin receptor.
Due to the rapid pace of discovery of ligand and receptor in different species, the scientific community general it is difficult, you are to monitor developments in this exciting field, different names of many, these It is used to specify the product. To address this problem, “Molecular Biology of orientation Axon” workshop representatives of the laboratory more than 20 involved in research Ephesians family was held EMBL in September, in Heidelberg, the extensive discussion in 1996 began. Ephesians naming committee was elected for the improvement of the proposal in consultation with the society as a whole as a result, the proposal, and, out to standardize the nomenclature of ligands and receptors of these, and organize. Scientists more than 70, named, creation of this letter, and to determine a gene nomenclature committee human and mouse nomenclature results are approved by most to contribute exclusively .
This gene belongs to the ephrin receptor subfamily of protein tyrosine kinase. In the central nervous system, EPH-related receptors EPH is involved in mediating a particular developmental event. The receptor in EPH Subfamily has an extracellular region containing two fibronectin type III repeats and a cysteine-rich domain and the kinase domain of a single, typically. Are divided into two groups based on the similarity of their affinity for the ligand ephrin binding and ephrin-AB extracellular domain sequence of the ephrin receptor.
Membrane-bound ephrin ligands family receptor tyrosine kinase that binds a contact-dependent bidirectional signaling devices in neighboring cells, resulting to exist in a cell adjacent. Downstream between signaling pathways ligand ephrin reverse signaling is called downstream signaling the first signaling path of the receptor. Has the unique properties of Ephesus receptor while the highly promiscuous, to bind it, and is activated by transmembrane ephrin-B ligand, including EFNB3 and GPI-anchored ephrin EFNA1 both physiologically. Activation of ephrin ligand by Rac and morphology of the cells, to regulate Rho GTP-ase activity of the lap, to regulate cell adhesion integrin-dependent. Plays an important role in the development of the nervous system control Various stages of axon guidance, including the creation of the corticospinal projection,. It is possible to control the release of the motor and sensory axons during the development of neural circuits. To play the role of synaptic plasticity in addition to its role in axon guidance. Activated by CDK5 in the “Tyr-15 of” EFNA1 phosphorylation phosphorus NGEF regulation of morphogenesis of RhoA Noto dendritic spines in order. After prevented plays a role in blood vessel formation in the central nervous system and in the nervous system, angiogenesis damage and axonal regeneration plays the role of repair. Further, for example, its non-uniformity that is involved in cell-cell signaling various causes regulate the development of thymic epithelial
Four hetero ligand binding. I consists of ephrin receptor dimer and tetramer hetero. Oligomerization, it is necessary to induce a biological response probably. Phosphorylation of CDK5 kinase interact with CHN1 activation of NGEF EFNA1 is induced; effector of axon guidance of EphA4 in the activation of EphA4 connection of .. RAC1 regulatory dialogue (through Tyr-602 CDK5, CDK5R1 of ( PDZ motif and (via PDZ domain) SIPA1L1 control by adjusting the phosphorus interaction neuronal morphology at a position interacts with FYN and NGEF) and (RAP2A, RAP2C or RAP2B) of ATPase RAP2 and (RAP1B or RAP1A) of Rap1
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting motor neurons. By decades month survival rate is different, but the onset and progression of the disease, it is variable. Factors underlying this variation may represent a target for therapeutic intervention. It is a zebra pattern of ALS, were identified in the repellent system EphA4, ephrin receptor axon as a modifier of disease phenotype of human fish, rodents and here. Save the phenotype of SOD1 mutant in zebrafish, pharmacological inhibition and genetic signaling of EphA4, improve the survival rate in the rat model mice and ALS. Motor neurons most susceptible to degeneration of the ALS, re-expression of innervation of axotomy motor neurons and high levels of EphA4 that was inhibited by the presence of the EphA4. In people with ALS, the onset of disease and survival, and expression of EphA4 correlates with loss of function mutations in the EphA4 associated with the long-term survival in reverse. In addition, another protein, mutant TAR DNA binding protein 43 was found to save that axons fault that was also induced knockdown of the EphA4 of the expression (TDP-43) is, of knock-down motor neuron 1, we atrophy of the spinal cord that causes muscle axonopathy and familial ALS, due to the survival rate of the model for. This suggests that there may represent new targets for therapeutic intervention generic modulation vulnerability EphA4 with axonal degeneration (motor) neurons.