コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ly are the neuronal proteins spinophilin and neurabin.
2 sponses by a neural tissue-specific protein, neurabin.
3 GS4 interact with the overlapping regions of neurabin.
4 isoforms contributed to their recognition by neurabins.
5 d suggested that PP1 mediated I-2 binding to neurabins.
6 P1 inhibitor, also attenuated I-2 binding to neurabins.
7 ted RhoGEF), RGS3 and RGS12, spinophilin and neurabin-1, SRC homology 3 domain and multiple ankyrin r
10 ant peptides representing central regions of neurabins also preferentially bound PP1gamma1 and PP1alp
11 fractionation of rat brain demonstrates that neurabin and p70(S6k) both localize to the soluble fract
13 ruitment and catalytic efficiency of the PP1-Neurabin and PP1-Spinophilin fusions is primarily determ
15 or subunits suggests that the PDZ domains of neurabin and spinophilin are important for targeting PP1
17 binding data also allowed us to classify the neurabin and spinophilin PDZ domains as the first identi
19 However, thus far, it is still unknown how neurabin and spinophilin themselves are targeted to thes
20 lso outline the required targeting of PP1 by neurabin and spinophilin to achieve substrate specificit
22 493) proteins identified residues 473-479 of neurabin as containing a crucial PP1gamma1-selectivity d
31 1 selectively interacts with spinophilin and neurabin, F-actin-targeting proteins, whereas PP1beta se
36 4 of G(M)/R(GL) fused to residues 457-493 of neurabin (GST-G(M)/Nb) selectively bound to and inhibite
37 sion proteins containing residues 146-493 of neurabin (GST-Nb-(146-493)) or residues 1-240 of G(M)/R(
38 ely interact with one neurabin molecule in a neurabin homo-oligomer to form a ternary complex, repres
42 vity was confirmed by immunoprecipitation of neurabin I and II from brain extracts from wild type and
47 il and sterile alpha motif domains abolished neurabin I dimerization and induced filopodium extension
52 n N-terminal F-actin-binding domain dictated neurabin I localization at actin cytoskeleton and promot
54 tions that attenuated PP1 binding to I-2 and neurabin I suggested distinct and overlapping sites for
59 sights into the assembly and regulation of a neurabin I/PP1 complex that controls actin rearrangement
63 ociation of protein phosphatase-1 (PP1) with neurabin-I through a canonical KIXF motif inhibited filo
65 ted by a fragment of the PP1-binding protein neurabin-I, Nb-(146-493), because of the selective inhib
66 - and protein phosphatase-1-binding protein, neurabin-I, promotes filopodia in neurons and nonneurona
67 on, they impaired the ability of PP1 to bind neurabin-I, the neuronal regulatory subunit, and G(M), t
68 d hippocampal neurons showed that endogenous neurabin II and I-2 colocalized at actin-rich structures
69 n phosphatase 1 catalytic subunit (PP1) with neurabin II and inactivate PP1 and block mitosis during
70 on of the phosphorylated DCX and spinophilin/neurabin II from DCX-synthesizing glioma cells indicated
71 o a block of anchorage-independent growth as neurabin II is a synergistic inhibitor of anchorage-inde
72 Interaction between phosphorylated DCX and neurabin II may induce the association of the protein ph
73 binding proteins neurabin I and spinophilin (neurabin II) also bind PP1, their role in PP1 isoform se
78 lective targeting of PP1gamma1 to F-actin by neurabins in intact cells requires both the canonical PP
79 erely attenuated PP1gamma1 interactions with neurabins in vitro and in cells and disrupted PP1gamma1
84 , A1R and RGS4 each likely interact with one neurabin molecule in a neurabin homo-oligomer to form a
87 death in wild-type (WT) mice did not affect neurabin-null mice or WT mice cotreated with an RGS4 inh
92 t disrupting the functions of a cytoskeletal neurabin/PP1 complex enhanced filopodia and impaired sur
93 Spinophilin residues 427-470, or homologous neurabin residues 436-479, were sufficient to bind PP1 i
95 rid analysis using the coiled-coil domain of neurabin revealed an interaction with Lfc, a Rho GEF.
97 Moreover, these findings implicate the A1R/neurabin/RGS4 complex as a valid therapeutic target for
98 ive effect achieved by disruption of the A1R/neurabin/RGS4 complex is elicited by the on-site and on-
99 ation are essential for formation of the A1R/neurabin/RGS4 ternary complex, as well as for stable loc
101 anslational regulators as substrates for the Neurabin/Spinophilin PIPs, implicated in neuronal plasti
104 A) holoenzymes containing spinophilin and/or neurabin target specific neuronal PP1 isoforms, facilita
105 el PP1gamma1-selective interaction domain in neurabin that may allow for selective regulation and/or
106 me of the structural determinants in PP1 and neurabins that together contribute to preferential targe
107 M)/R(GL) severely compromised the ability of neurabin to bind and inhibit both isoforms but did not a
109 h structures, consistent with the ability of neurabins to target the PP1.I-2 complex to actin cytoske
110 pinophilin: conserved as residues 473-479 in neurabin) to VKDYDTW severely attenuated PP1gamma1 inter
112 s efficiently coprecipitated spinophilin and neurabin, whereas PP1beta immunoprecipitation did not.
113 PP1 binding, facilitated PP1 recruitment by neurabins, which also targeted I-2 to polymerized F-acti