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1  that human retina expressed all GRKs except GRK4.
2 46 codons in the carboxyl-terminal domain of GRK4.
3 s explaining the generally low expression of GRK4.
4 f the three GRK subgroups (GRK1, GRK2/3, and GRK4/5/6) shares even a single intron in common, indicat
5 duced receptor phosphorylation by 77%, while GRK4-6-specific mAbs have no effect.
6               In contrast, overexpression of GRK4 and -6 led mainly to agonist-independent phosphoryl
7            Interestingly, similar regions in GRK4 and GRK6 appear to be palmitoylated (and involved i
8     For example, two members of this family, GRK4 and GRK6, contain C-terminal cysteine residues that
9                              Coexpression of GRK4 and the D1 receptor in a heterologous system induce
10 -activated D1R is regulated by both SNX5 and GRK4, and that SNX5 is critical to the recycling of the
11 through G-protein-coupled receptor kinase 4 (GRK4), comparatively little is known about other aspects
12 n this article, we present data showing that GRK4 constitutively phosphorylates the D1 receptor in th
13 lation resulting from mutationally activated GRK4 contributes to the heritable component of human ess
14 least, the G protein-coupled receptor kinase GRK4 does not display a preference for the agonist-occup
15              The genomic organization of the GRK4 gene is completely distinct from that of the human
16                                    The human GRK4 gene is composed of 16 exons extending over 75 kilo
17 istinguishes the betaARK (GRK2 and GRK3) and GRK4 (GRK4, GRK5, and GRK6) subfamilies.
18 uishes the betaARK (GRK2 and GRK3) and GRK4 (GRK4, GRK5, and GRK6) subfamilies.
19 erved between members of the GRK4 subfamily (GRK4, GRK5, and GRK6).
20 in binding sites, and is highly conserved in GRK4, GRK5, and GRK6.
21  bind PIP2, betaARK (GRK2), betaARK2 (GRK3), GRK4, GRK5, and GRK6.
22 pecifically react with GRK2 and GRK3 or with GRK4, GRK5, and GRK6.
23  conservation, whereas GRK1 and particularly GRK4 have accumulated amino acid changes at extremely ra
24 d beta2-adrenergic receptor, indicating that GRK4 is a functional protein kinase.
25                                              GRK4 is capable of augmenting the desensitization of the
26                                              GRK4 is implicated in the regulation of blood pressure,
27 amily (GRKs 4, 5, and 6) suggests that mouse GRK4 is not alternatively spliced in a manner analogous
28                                    Thus, the GRK4 mRNA and the GRK4 protein can exist as four distinc
29                                        Human GRK4 mRNA is expressed highly only in testis, and both a
30  regions undergo alternative splicing in the GRK4 mRNA, resulting from the presence or absence of exo
31  the regulation of blood pressure, and three GRK4 polymorphisms (R65L, A142V, and A486V) are associat
32                  Thus, the GRK4 mRNA and the GRK4 protein can exist as four distinct variant forms.
33                                     The four GRK4 proteins have been expressed, and all incorporate [
34 , is highly conserved between members of the GRK4 subfamily (GRK4, GRK5, and GRK6).
35                     Examination of the mouse GRK4 subfamily (GRKs 4, 5, and 6) suggests that mouse GR
36               Indeed, all the members of the GRK4 subfamily exhibit PIP2-dependent receptor kinase ac
37                      GRK6 is a member of the GRK4 subfamily of GRKs, which is represented in most, if
38  and 6 genes reveals that all members of the GRK4 subfamily share an identical gene structure, in whi
39 mediated exclusively by the alpha isoform of GRK4; the beta, gamma, and delta isoforms are ineffectiv
40 pliced in a manner analogous to human or rat GRK4, whereas GRK6 undergoes extensive alternative splic
41 a system incorporating constitutively active GRK4 will be prone to dysregulation, perhaps explaining
42 arison of the deduced amino acid sequence of GRK4 with those of the closely related GRK5 and GRK6 sug
43 sion of G-protein-coupled receptor kinase 4 (GRK4) with wild type receptor resulted in an increase in

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