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1 e UBC-9 through its evolutionarily conserved SAM domain.
2 egion, a PEST domain, and a carboxy-terminal SAM domain.
3 lays a substantial drop after removal of the SAM domain.
4 cient PRE recruitment requires an intact Scm SAM domain.
5 6 N-terminal tyrosines (3Y) dependent on the SAM domain.
6 h a reaction that requires an intact radical SAM domain.
7 clusters was impaired by the deletion of the SAM domain.
8 eract with both Yan and Pnt-P2 through their SAM domains.
9 zosaccharomyces pombe and interact via their SAM domains.
10 Yan and Mae interact through their SAM domains.
11 egion of interaction to their respective SPM/SAM domains.
12 dules when searching for binding partners of SAM domains.
13 ng a new mode of oligomeric organization for SAM domains.
14 o study the behavior of phosphorylated EphA2 SAM domains.
15 coiled-coil domains followed by three tandem SAM domains.
16 iated by the N-terminal sterile alpha motif (SAM) domain.
17 elta and eta, contain a sterile alpha motif (SAM) domain.
18 ity of its intraluminal sterile alpha-motif (SAM) domain.
19 tumor domain (MBT) and sterile alpha motif (SAM) domains.
20 racted from the substrate by the two radical SAM domains, (2) the second tyrosine-derived product, (3
22 ructure reveals an unusual makeup in which a SAM domain, a common protein-protein interaction module,
24 In this context, dNTP triphosphohydrolase SAM domain and HD domain-containing protein 1 (SAMHD1) h
26 those required for viral cDNA synthesis by a SAM domain and HD domain-containing protein 1 (SAMHD1)-i
28 ild-type EphA4 and a mutant lacking both the SAM domain and PDZ binding motif were constitutively tyr
30 in part to the nucleotidase activity of the SAM-domain and HD-domain containing protein (SAMHD1), wh
32 id substitutions in the sterile alpha motif (SAM) domain, and are predicted to affect protein--protei
35 a four-helix bundle (H2-H5), resembling the SAM domain, appended with two additional helices (H0-H1)
37 ein interaction studies demonstrate that the SAM domains are necessary and sufficient to mediate SARM
38 lex interactions between the coiled-coil and SAM domains are thought to create liprin scaffolds, but
41 ce, reduces self-association of the isolated SAM domain as well as high molecular mass complex format
42 tingly, deletion of the sterile alpha motif (SAM) domain at the N terminus dramatically reduced the u
46 he resulting transformants indicate that the SAM domain but not the RA domain is essential for the fu
47 ive-helix-bundle architecture of traditional SAM domains, but has additional short helices at N and C
55 acterize the Drosophila sterile alpha-motif (SAM) domain-containing protein Caskin, which shares homo
57 ur results also suggest a mechanism by which SAM domains could mediate the spreading of transcription
62 tion and abrogated by the deletion of SLP-76 SAM domain (DeltaSAM) or mutation of Tyr-113, Tyr-128, a
63 tations on Mae that specifically disrupt its SAM domain-dependent interactions with Yan disable the d
66 ins green fluroscent protein (GFP) or EphB2 (SAM domain) displayed markedly increased growth rates wi
67 horylation levels upon deletion of the EphA2 SAM domain (EphA2DeltaS) in DU145 and PC3 prostate cance
68 been taken over by a different branch of the SAM domain family during the evolution of nematodes.
69 n EphB2-SAM domain that has the same overall SAM domain fold yet has no substantial intermolecular co
78 dissociation process of the EphA2-SHIP2 SAM-SAM domain heterodimer complex using unrestrained all-at
79 at of dNumb developmental regulators and two SAM domains homologous to those in the C-terminal tail o
80 tantly, aberrant C-terminal extension of the SAM domain in bpk mutant Bicc1 phenocopied these defects
83 identified for the first time a role for the SAM domain in mediating SLP-76 self-association for T-ce
87 tirely different from that of the equivalent SAM domain in SRF and MCM1, accounting for the absence o
88 ins that become ordered upon binding, the EF-SAM domain in the stromal interaction molecule (STIM) 1
93 binding, the solution structure of the Vts1 SAM domain, in the presence of a specific target RNA, ha
95 on these results, we conclude that the EphA2 SAM domain inhibits kinase activity by reducing receptor
97 via a heterotypic sterile alpha motif (SAM)-SAM domain interaction, leading to regulation of EphA2 i
98 Altogether, our data demonstrated that the SAM domain is indispensable for optimal SLP-76 signaling
99 hening of Mtrm::Polo binding mediated by the SAM domain is necessary to prevent meiotic catastrophe a
102 G proteins, but not those in which the SOP-2 SAM domain is replaced with the SAM domains of non-PcG p
103 1 are associated with its HD domain, but the SAM domain is required for maximal activity and nucleic
106 modulated by their evolutionarily conserved SAM domain, is essential to their physiological repressi
107 ires the Scm C-terminal sterile alpha motif (SAM) domain, is crucial for the efficient sumoylation of
108 in vivo, we show that a sterile alpha-motif (SAM) domain located at the C terminus of Mtrm increases
109 loses Ca(2+) from EF hand, its intraluminal SAM domain may change conformation, and via glycosylatio
110 induce these phenotypes, suggesting that the SAM domain may negatively regulate some aspects of EphA4
114 n of messenger RNA encoding the Elp3 radical SAM domain mutant, but not the HAT domain mutant, into M
119 unction alleles indicate that the N-terminal SAM domain of Ckn mediates its interaction with Lar.
121 hermal titration calorimetry) studies on the Sam domain of Ship2 revealing its three-dimensional stru
122 that glycosylation sites in the ER-resident SAM domain of STIM1 are essential for initiation of CIF
123 ts fuse a potent oligomerization module, the SAM domain of TEL, to a variety of tyrosine kinases or t
124 Taken together, our studies suggest that the SAM domain of the EPHA2 protein plays critical roles in
127 ydG showed that the highly conserved radical-SAM domains of both HydE and HydG and the GTPase domain
128 ch the SOP-2 SAM domain is replaced with the SAM domains of non-PcG proteins, confer appropriate in v
131 Here we examine the interaction between the SAM domains of the polycomb group proteins polyhomeotic
132 ions in the cytoplasmic sterile-alpha-motif (SAM) domain of human EPHA2 on chromosome 1p36 have been
134 ted by mutations in the sterile alpha-motif (SAM) domain of p63 that are associated with ankyloblepha
135 that the N-terminal sterile alpha motif (or SAM) domain of SMSr drives self-assembly of the protein
137 the SAMHD1 N-terminal tail and the adjacent SAM domain or the C-terminal tail proceeding the HD doma
141 regulated enhancer controls expression of an SAM domain protein that confers survival in anemia.
143 ure, the N-terminal peptide arm of the EphB2-SAM domain protrudes out from the core of the molecule,
144 Moreover, a mutant DGKdelta containing a SAM domain refractory to zinc binding diminishes the for
145 cted structure modeling and then mutated the SAM domain residues which in this model were predicted t
146 nt microscale thermophoresis of the isolated SAM domain (residues 1-78) revealed evidence of dimers a
149 merizing TNKS and TNKS2 sterile alpha motif (SAM) domains, revealing versatile head-to-tail interacti
150 8 to Ala-8 mutation and found that the EphB2-SAM domain structure and stability were only slightly al
151 leucine zipper (Ste4-LZ) domain as well as a SAM domain, suggesting that Byr2-SAM and Ste4-SAM may fo
152 the catalytic [Fe4S4] cluster in the radical SAM domain, surprisingly, does not abolish the inhibitor
153 solved a new crystal form of the human EphB2-SAM domain that has the same overall SAM domain fold yet
154 nd genetic analysis that it is primarily the SAM domain that interacts specifically with the appropri
155 a structural model of the Ca(2+)-unbound EF-SAM domain that is consistent with a wide range of evide
157 nd that the interface maps to regions of the SAM domains that are known to be important for the forma
159 a small protein with a sterile alpha motif (SAM) domain that can physically interact with the scaffo
160 us of Shank3 contains a sterile alpha motif (SAM) domain that is essential for its postsynaptic local
161 ere, we examine the response of the STIM1 EF-SAM domain to changes in Ca(2+) concentration using math
162 that full-length Yan self associates via its SAM domain to form higher-order complexes in living cell
165 l activity of viperin depends on its radical SAM domain, which contains conserved motifs to coordinat
168 93F, Y587E/Y593E), kinase domain (Y734F), or SAM domain (Y929F) inhibited ephrin-A1-induced vascular
169 is trimeric and, when included with the Ste4-SAM domain, yields a 3:1 Ste4-LZ-SAM:Byr2-SAM complex wi
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