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1 tion through tonic stimulation of alpha-cell EphA receptors.
2 ligands, to retinal growth cones, expressing EphA receptors.
3                           We also found that EphA receptor activation by ephrin-A ligands in neurons
4                          Ephrin-A3-dependent EphA receptor activation is reduced in mutant cells that
5 ntagonist) or the ligand binding site of the EphA receptor (agonist) and thus target EphA function.
6                   The induced association of EphA receptor and Vav proteins modulates the activity of
7 n between complementary gradients of retinal EphA receptors and collicular ephrin-A ligands.
8 , through LIM homeodomain protein control of EphA receptors and ephrin-A ligands in motor neurons and
9 eved to involve graded repulsion mediated by EphA receptors and ephrin-A ligands.
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
13                                        Thus, EphA receptors and their ligands are implicated as media
14                                 There are 10 EphA receptors, and six EphB receptors, distinguished on
15 al to low nasal gradient in RGCs, similar to EphA receptors, and that balanced FAK activation is nece
16                        In addition, multiple EphA receptors are expressed in callosal neurons and eph
17                        We show that multiple EphA receptors are expressed in DRGs when limb innervati
18 LMC axons also express ephrinAs, while their EphA receptors are expressed in the limb mesenchyme.
19              In the embryonic visual system, EphA receptors are expressed on both temporal and nasal
20                                          The EphA receptors are generally thought to become activated
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
23 niculate projections that suggest defects in EphA receptor-dependent axon guidance.
24 hemistry revealed the expression of multiple EphA receptors (EphARs) in astrocytes.
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
28 glion cell populations that express distinct EphA receptor gradients.
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
31 , we describe a loss-of-function analysis of EphA receptors in retinotectal mapping.
32 ur data suggest that prolonged activation of EphA receptors is as efficient in recruiting Slap and NM
33  but that in cell culture, expression of the EphA receptors is predominant.
34 iments, exploiting a combinatorial series of EphA receptor knock-in and knockout mice, confirm the sa
35                                 Of the eight EphA receptors known to be expressed in mice (A1-A8), RT
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
38                                          The EphA receptor-mediated angiogenic response is dependent
39                      Ephrin-A stimulation of EphA receptors modulates the activity of ephexin leading
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
42  branching is mediated by relative levels of EphA receptor repellent signaling.
43                            Here we show that EphA receptor signaling remodels spines by triggering a
44 ls (HUVECs), demonstrating a requirement for EphA receptor signaling.
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
50         Ephrin-A1, the prototypic ligand for EphA receptor tyrosine kinases, is overexpressed in vasc
51                                        Thus, EphA receptors utilize discrete cellular and molecular p
52  are no pharmacological agents available for EphA receptors, we designed recombinant immunoadhesins t

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