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1 tion through tonic stimulation of alpha-cell EphA receptors.
2 ligands, to retinal growth cones, expressing EphA receptors.
5 ntagonist) or the ligand binding site of the EphA receptor (agonist) and thus target EphA function.
8 , through LIM homeodomain protein control of EphA receptors and ephrin-A ligands in motor neurons and
10 that in the chicken olivocerebellar system, EphA receptors and ephrin-As are expressed with distinct
11 Here we review recent data indicating that EphA receptors and glycosylphosphatidylinositol (GPI)-an
12 signaling activities exerted by coexpressed EphA receptors and GPI-linked ephrin-A ligands in spinal
15 al to low nasal gradient in RGCs, similar to EphA receptors, and that balanced FAK activation is nece
18 LMC axons also express ephrinAs, while their EphA receptors are expressed in the limb mesenchyme.
21 n limb innervation is being established, and EphA receptors are present on growth cones of both NGF-d
22 A6 binds with high affinity to several other EphA receptors as well and causes growth cone collapse i
25 ypothesis by using gene targeting to elevate EphA receptor expression in a subset of mouse ganglion c
26 g paradigm to a transgenic mouse lacking the EphA receptor family ligands ephrin-A2 and ephrin-A5 res
27 is well established that EphA7, a member of EphA receptor family, is involved in the topographic map
29 observations suggest critical functions for EphA receptor in establishing callosal connections durin
30 ow the functional requirement for endogenous EphA receptors in retinotectal mapping, show that the re
32 ur data suggest that prolonged activation of EphA receptors is as efficient in recruiting Slap and NM
34 iments, exploiting a combinatorial series of EphA receptor knock-in and knockout mice, confirm the sa
36 ch can be predicted as a function of the net EphA receptor level that a given ganglion cell expresses
37 tition is not based on comparisons of axonal EphA receptor levels but rather relies on the optimizati
40 Ephrin-A1 and ephrin-A4 selectively bind to EphA receptors on neurons restricted to the matrix compa
41 ar maps in mice in which the distribution of EphA receptors over the retina has been modified by knoc
45 mpetition that is governed by comparisons of EphA receptor signalling intensity, which are made using
46 the individual roles played by the multiple EphA receptors that make up the retinal EphA gradient.
47 ciation of ephrin-A cell surface ligands and EphA receptor tyrosine kinases (RTKs) with the organizat
48 expression of members of the EphA family-the EphA receptor tyrosine kinases and the ephrin-A ligands-
49 this map requires complementary gradients of EphA receptor tyrosine kinases and their ephrin-A ligand
52 are no pharmacological agents available for EphA receptors, we designed recombinant immunoadhesins t
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