EPHB2

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EPHB2

A gene on chromosome 1p36.1-p35 that encodes a member of the ephrin-B receptor subfamily of receptor tyrosine kinases, which “promiscuously” bind membrane-bound ephrin-B family ligands residing on adjacent cells, leading to contact-dependent bidirectional signalling into neighbouring cells. EPHB2 functions in axon guidance during development, guiding commissural axons and forming a major interhemispheric connection between the two temporal lobes of the cerebral cortex. EPHB2 is also involved in the guidance of contralateral inner ear efferent growth cones at the midline, and of retinal ganglion cell axons to the optic disk. It also regulates dendritic spines development and maturation, and it stimulates the formation of excitatory synapses.

Activation of EPHB2 by EFNB1 abolishes the ARHGEF15-mediated negative regulation on excitatory synapse formation. EPHB2 also controls other aspects of development, including angiogenesis, palate development, as well as inner ear development by regulating endolymph production. It may act as a tumour suppressor.

Molecular pathology
Defects in EPHB2 have been linked to prostate cancer.
References in periodicals archive ?
Previous studies indicated that the activation of ERK or CHOP might result in the damage of podocytes, Anzai et al, proved that the endoplasmic reticulum stress effector, CHOP, could regulate chronic kidney disease-induced vascular calcification [20], Zhang et al, showed that the ERK activation resulted in the RPC6 up-regulation in angiotensin Il-induced podocyte apoptosis [34], Also, Fujita et al, demonstrated that ERK mediated the high-glucose-induced hypertrophy in renal tubular cells [35], In this study, the p-ERK and CHOP expression was up-regulated by the TM treatment in the [MPC.
We assumed that ghrelin would promote INS-1 cell survival by increasing ERK activation and decreasing p38MAPK expression after dexamethasone treatment.
This was not due to a defect in Fc[gamma]RIIa signaling because the same cross-linking procedure led to robust activation of ERK (Figure 6).
The primary antibodies and dilutions were as follows: primary antibodies against phosphorylated ERK1/2 (number 9101,1: 1000), ERK 1/2 (number 4695, 1:1000), and GAPDH (number 5174, 1: 1000) were purchased from Cell Signaling Technology (Danvers, MA), and caspase-3 (1 [micro]g/mL, number ab32351, 1:1000), Bax (number ab7977; 1:1000), and Bcl-2 (number ab7973; 1: 100) were purchased from Abcam Plc, Cambridge, UK.
ERK phosphorylation, gene expression changes, and cell migration in CAFs treated with vehicle (-), 1 nmol/L E2, or 1 [micro]mol/L atrazine (Atr).
7 B7-H1 expression was shown to be dependent on the ERK and p38 mitogen-activated protein kinase (MAPK) signaling pathways in colon cancer8 in anaplastic large cell lymphoma and Hodgkin lymphoma.
Citation: "Genome-wide Kinase-Chromatin Inter-actions Reveal the Regulatory Network of ERK Signaling in Human Embryonic Stem Cells"; Jonathan Goke et al.
ERK and cell death: mechanisms of ERK-induced cell death-apoptosis, autophagy and senescence.
In this study, we demonstrate that Ras activation, MEK phosphorylation, and ERK phosphorylation exhibit circadian rhythms in mouse liver and ERK phosphorylation rhythms are controlled by circadian core clock components.
However, Engelman and colleagues discovered that although mutant KRAS activates ERK signaling in human KRAS mutant colorectal cancers, receptor tyrosine kinases control PI3K signaling.
In the mouse studies, losartan shut down the excess ERK signaling, while enalapril had no effect on this pathway.
In the mouse studies, losartan shut down the excess ERK signaling, while enalapril had no effect on this pathway This lends further support to the idea that ARB may be superior to ACE inhibitors as a clinical treatment.