EPHA5

EPHA5

A gene on chromosome 4q13.1 that encodes a member of the ephrin-A receptor subfamily of receptor tyrosine kinases, which “promiscuously” bind membrane-bound ephrin-A family ligands residing on adjacent cells, leading to contact-dependent bidirectional signalling into neighbouring cells. EPNA5 is thought to constitute the cognate/functional ligand for EPHA5, acting as an axon guidance molecule during development. EPHA5 may be involved in the development of retinotectal, entorhino-hippocampal and hippocamposeptal pathways; with EFNA5 it also play a role in synaptic plasticity in adult brain by regulating synaptogenesis. In addition to its role in the nervous system, the EPHA5/EFNA5 interaction mediates communication between pancreatic islet cells to regulate glucose-stimulated insulin secretion.
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One gene, EPHA5, has been linked to neuronal development, in particular synapse formation in mouse models [1].
Zhou, "EphA5 and EphA6: Regulation of neuronal and spine morphology," Cell and Bioscience, vol.
EphA1, EphA4, and EphA7 are expressed at the crypt bottom, while EphA2, EphA5, and the ephrin-A1 ligand are enriched at the upper colonic crypts [20].
In our prediction list, five genes can be classified in such subfamily: EPHA3, EPHA4, EPHA5, EPHA7, and EPHB2.
Overall, genes with which DM sites were associated include (but are not limited to) those having functions in chromatin compaction (NAT15; HDAC4; UHRF1); DNA damage/repair or chromosomal segregation (SOD3; UHRF1; NAT15); muscle contraction (NR4A3; HDAC4; FEZ1; PRKG1; KCNH7); axonal bundling/outgrowth (FEZ1); cell signaling in muscle (NR4A3; PRKG1); neuronal excitability/synaptic transmission (BDNF; BZRAP1; EPHA5; KCNH7); muscle maturation (HDAC4); response to oxidative stress (SOD3); and inflammatory processes (AXL; SH2B2).
A TaqMan [R] probe/primer set was designed for real-time reverse transcription-PCR (RT-PCR) for the detection and quantification of gene expression of all currently known human members of the Eph receptor and ephrin family except for EphA5 and EphA10.
All currently known human Eph receptors and ephrins were investigated except EphA5 (assay design failed repeatedly) and EphA10 (sequence only recently reported) (20).
Expression in glioblastomas has been reported only for EphA5 (34).
Based on GO_BP and KEGG pathway enrichment analysis (Table 2), we found genes related to MAPK signaling pathway, insulin signaling pathway, axon guidance, focal adhesion, and energy pathways dysregulated in blood and brain, such as AKT1, TGFBR1, IGF1R, EPHA5, VCAM1, and L1CAM.
Term Count P value Genes MAPK signaling pathway 13 0.0062 RPS6KA5, AKT1, MAP4K4, MAP3K5, PLA2G4A, DUSP2, FGF9, TGFBR1, MAP2K4, MKNK2, PPP3R1, FGF12, DUSP6 Endocytosis 10 0.010 IGF1R, ADRB3, FLT1, TGFBR1, PSD3, VPS4B, DNAJC6, PSD2, ARAP2, LDLRAP1 Axon guidance 7 0.042 EPHA5, SEMA6A, PLXNA1, PPP3R1, SEMA4C, L1CAM, SRGAP1 Insulin signaling 6 0.0076 AKT1, L1CAM, IGF1R, IRS2, pathway SOCS7, RHOQ Focal adhesion 4 0.021 VCAM1, L1CAM, ITGA4, CERCAM Table 2: Small molecules which might reverse the dysregulation of AD in EC and HIP regions.