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anti-Mouse (Murine) Ephrin A5 Antibodies:
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Human Polyclonal Ephrin A5 Primary Antibody for ICC, IF - ABIN5076560
Andretta, Cartón-García, Martínez-Barriocanal, de Marcondes, Jimenez-Flores, Macaya, Bazzocco, Bilic, Rodrigues, Nieto, Landolfi, Ramon Y Cajal, Schwartz, Brown, Dopeso, Arango: Investigation of the role of tyrosine kinase receptor EPHA3 in colorectal cancer. in Scientific reports 2017
Human Polyclonal Ephrin A5 Primary Antibody for ELISA, WB - ABIN560699
Beauchamp, Lively, Mintz, Gibo, Wykosky, Debinski: EphrinA1 is released in three forms from cancer cells by matrix metalloproteases. in Molecular and cellular biology 2012
that Epha2 and Efna5 participate in the complex, global patterning of lens fiber cells that is necessary for maximal optical quality
This study demonstrated for a role of ephrinA signaling for the selective targeting of serotonergic raphe nuclei. We show that EphA5 is differentially expressed across the different hindbrain raphe nuclei, and that this correlates with a different repulsive action of ephrinA on 5-HT axon growth.
these results suggest that the basic helix-loop-helix transcription factorsbinding site in ECR1 is involved in the positive regulation of ephrin-A5 gene expression during the development of the mesencephalon.
During urogenital development, different modes of Eph/Ephrin signaling occur at several sites with EphrinB2 and EphrinA5 acting in concert.
dissociations of N-cadherin and adherens junctions in the associated interlocking domains may result in the formation of isolated globules and nuclear opacities in the ephrin-A5(-/-) mice.
Overexpression of Ephrin-A5 in mice results in decreasing the size of progenitor pool through inducing apoptosis.
Ephrin-A5 interacts with Ephrin-A4 to modulate neurogenesis and angiogenesis in a model of temporal lobe epilepsy.
Data show the effects of genetic loss of ephrin-A5, Eph receptors EphA4, and EphA7 on the development of medulloblastoma tumors in the smoothened (Smo) transgenic mouse model.
the unique cross-subclass interaction of EphB2 with ephrin A5 has evolved to function upstream of JNK signaling for the purpose of maintaining an adequate pool of progenitor cells to ensure proper closure of the optic fissure.
Female mice lacking EFNA5 are subfertile, exhibit a compromised response to LH, and display abnormal ovarian histology after superovulation.
NF-kappaB in NG2(+) cells promotes myoblast migration to the tips of myofibers through cell-cell contact through expression of ephrinA5 from NG2(+) cells
The reduced nuclear size and diminished gene expression mirrors subtle changes in ephrin A5 expression evident in P1 and P4 enucleated neocortex, 11 and 8 days prior to natural eye opening, respectively.
These data support the hypothesis that the retinocollicular projection is a superimposition of a number of individual two-dimensional topographic maps that originate from specific types of RGCs, require ephrin-A signaling.
The results of this study suggested that majority of the changes observed ephrin-A2 and ephrin-A5 KO mice appear to be mediated by the effects on motor neurons and their muscle targets, rather than changes in auditory sensitivity.
Ephrin A2 and Ephrin-A5 are important for the functional development of cutaneous innervation.
ephrin A5 ligands imported by invading thalamic axons interact with EphA4-expressing radial glial cells.
data show that ephrinA5 drives repellent interactions between temporal and nasal axons within the superior colliculus, and demonstrates for the first time that target-independent mechanisms play an essential role in retinocollicular map formation in vivo.
At high frequencies, the ephrin-A2A5(-/-) mice exhibited thresholds that were significantly lower than in wild-type mice by approximately 20 dB, suggesting ephrin-A2 and ephrin-A5 may have frequency-specific effects on the auditory system.
multi-protein complex comprising ephrinA5, EphA7, and TNFR1 may constitute a platform for inducing caspase-dependent apoptotic cell death
Data show that Dlx5 and Msx2 play a critical role in controlling cranial neural tube morphogenesis by regulating cell adhesion via the ephrinA5 and EphA7 pathway.
These results indicate a novel mechanism of ephrin-Eph signaling independent of direct cell contact and proteolytic cleavage and suggest the participation of EphB2(+) extracellular vesicles in neural development and synapse physiology.
MiR-96 and miR-182 are upregulated in hepatocellular carcinoma and negatively associated with ephrin A5 expression.
the structure of the ligand-binding domain of the EphA3 receptor in complex with its preferred ligand, ephrin-A5, is reported.
The genetic variations c.668C>T (rs201008479), c.102C>T (rs199980747) and c.-27C>G (rs200187971) may present an additional genetic risk factor for age-related cataract in the Chinese population.
Data indicate that ephrin-A5 binding directly facilitates the formation of Eph/ephrin clusters by inducing conformational changes in the ligand-binding domain (LBD) of EphA4.
Transgenic ephrin-A5 plays a critical role in postnatal lens fiber organization to maintain lens transparency: cells in the ephrin-A5-deficient lens are severely disorganized
EphrinA5, especially ephrinA5S, acts as a tumor suppressor in hepatocarcinogenesis.
This study presented that EFNA5 showed strong associations with alcohol withdrawal symptoms.
Data suggest that ephrinA5 mRNA/protein levels are reduced in colon adenocarcinoma compared to normal colon tissue; staging/grading indicates that ephrinA5 inhibits colon adenocarcinoma progression via c-Cbl-mediated EGFR ubiquitination/degradation.
analysis of molecular surfaces in ephrin-A5 essential for a functional interaction with EphA3
ephrin-A5-induced cell-morphologic changes of EphA3-positive LK63 pre-B acute lymphoblastic leukemia cells
These observations indicate that only a subset of signal transduction pathways is required for ephrin-A5-induced growth cone collapse.
ephrinA5 acted as a tumor suppressor in glioma, and its negative regulation of EGFR contributed to the suppressive effects.
EFNA5 down-regulation is a consistent finding in chondrosarcomas
Treatment of the bovine satellite cells (BSC) with ephrin-A5 causes a reduction in velocity with a concomitant increase in directed migration. Treatment of BSC with hepatocyte growth factor had no immediate effect on cell motility or migration.
Ephrin-A5, a member of the ephrin gene family, prevents axon bundling in cocultures of cortical neurons with astrocytes, a model of late stage nervous system development and differentiation. The EPH and EPH-related receptors comprise the largest subfamily of receptor protein-tyrosine kinases and have been implicated in mediating developmental events, particularly in the nervous system. EPH receptors typically have a single kinase domain and an extracellular region containing a Cys-rich domain and 2 fibronectin type III repeats. The ephrin ligands and receptors have been named by the Eph Nomenclature Committee (1997). Based on their structures and sequence relationships, ephrins are divided into the ephrin-A (EFNA) class, which are anchored to the membrane by a glycosylphosphatidylinositol linkage, and the ephrin-B (EFNB) class, which are transmembrane proteins. The Eph family of receptors are similarly divided into 2 groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands.
, ephrin A5
, EPH-related receptor tyrosine kinase ligand 7
, eph-related receptor tyrosine kinase ligand 7
, repulsive axon guidance signal protein