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1 rom ADP-ribosylation of elongation factor 2 (EF-2).
2 croM), and no Ca(2+) binding was detected at EF-2.
3 ep, via phosphorylation/dephosphorylation of EF-2.
4 tase-2A, the principal phosphatase acting on EF-2.
5 enzymes such as elongation factor 1alpha and EF-2.
6 ti-EF-3 interaction by EF-1 alpha but not by EF-2.
7 nition of the ADP-ribose acceptor substrate, EF-2.
8 h appears to be presented for recognition by EF-2.
9             The apparent competition between EF-2 and EF-3 may represent binding of these two protein
10 lcium ions to the second and third EF-hands (EF-2 and EF-3) of recoverin leads to the extrusion of th
11 the calcium ion binds to EF-4 in addition to EF-2 and EF-3.
12  dependent both on the ratio of ribosomes to EF-2 and on the nature of the ribosomes.
13 ell-shaped dose-response curve, whereas when EF-2 and ribosomes were in equimolar concentrations sord
14  to abolish high-affinity calcium binding to EF-2 and thereby trap the myristoylated protein with cal
15 otes phosphorylation of elongation factor-2 (EF-2) and prostacyclin production, but not phosphorylati
16 EF-4) binds calcium first, followed by EF-3, EF-2, and EF-1 and determined the four affinity constant
17 nd that DTM has no ability to ADP-ribosylate EF-2 at 18 or 30 degrees C.
18 ed to be a regulatory region for the chicken EF-2 basal promoter activity.
19  for EF-2, it is demonstrated that DB blocks EF-2 binding to pre-translocative ribosome.EF-1alpha com
20 or both wild-type and D150N, suggesting that EF-2 binds constitutively to Mg(2+).
21  GTPase-activation center inhibit binding of EF-2 but not of EF-3 to yeast ribosomes.
22                                              EF-2 competes with EF-3 for the ribosomal binding sites
23  binding to each of the functional EF-hands (EF-2: D150N; EF-3: E186Q; and EF-4: E234Q).
24 cal/mol), EF-4 (DeltaH = +5.2 kcal/mol), and EF-2 (DeltaH = +1 kcal/mol).
25 and it was shown previously that DB prevents EF-2-dependent translocation in partial reaction models
26              In parallel with the effects on EF-2 dephosphorylation, addition of high glucose to 832/
27              The slower rephosphorylation of EF-2 during the transition from high to low glucose may
28 ositive cooperativity between EF-4, EF-3 and EF-2, EF-1 and allostery involving the four EF-hands.
29  for protein synthesis (elongation factor-2 [EF-2], eukaryotic initiation factor-4AII, and transcript
30                           When the amount of EF-2 exceeded that of ribosomes sordarin inhibited the G
31 on the ribosome-dependent GTPase activity of EF-2 from Candida albicans in the absence of any other c
32 ich specifically impair elongation factor 2 (EF-2) function.
33 eate functional domains that control chicken EF-2 gene transcription, the 5'-flanking region of the c
34 d elongation factor (EF-G in prokaryotes and EF-2 in eukaryotes).
35 F-G) in prokaryotes and elongation factor 2 (EF-2) in eukaryotes].
36 NAD to elongation factor-2 (EF-2), rendering EF-2 inactive.
37 toxin-mediated ADP-ribosylation to assay for EF-2, it is demonstrated that DB blocks EF-2 binding to
38 m high to low glucose may involve effects on EF-2 kinase activity.
39                                      Because EF-2 kinase is chaperoned by Hsp90, we investigated the
40  and in vivo and suggest that destruction of EF-2 kinase may be an important cytotoxic mechanism of t
41 viability of glioma cells, the expression of EF-2 kinase protein, and the interaction between Hsp90 a
42 ein phosphatase-1 nor calmodulin kinase III (EF-2 kinase) activity was affected under these condition
43 MP kinase activity in low glucose stimulates EF-2 kinase.
44 otein, and the interaction between Hsp90 and EF-2 kinase.
45 glioma cells was abrogated by overexpressing EF-2 kinase.
46                         Elongation factor-2 (EF-2) kinase (calmodulin kinase III) is a unique protein
47  lines for 24-48 h of GA or 17-AAG disrupted EF-2-kinase/Hsp90 interactions as measured by coimmunopr
48 h of hydrophobic residues formed by EF-1 and EF-2 (Leu24, Trp27, Phe31, Phe45, Phe48, Phe49, Tyr81, V
49            We propose that Mg(2+) binding at EF-2 may structurally bridge DREAM to DNA targets and th
50   Neomycin relieves the inhibitory effect of EF-2 on EF-3 function.
51 lucose resulted in a progressive increase in EF-2 phosphorylation that was maximal by 1-2 h.
52                         Histamine-stimulated EF-2 phosphorylation was not inhibited and prostacyclin
53  high glucose led to a marked stimulation of EF-2 phosphorylation, consistent with the possibility th
54                         Elongation factor 2 (EF-2) plays a key role in the essential process of prote
55               8-bromo-cAMP increased chicken EF-2 promoter activity (-700/+102) in Rat 1 HIR fibrobla
56 ption, the 5'-flanking region of the chicken EF-2 promoter was analyzed.
57 e basal level promoter activity as the whole EF-2 promoter.
58 provide a novel regulatory mechanism for the EF-2 promoter.
59        This report demonstrates that chicken EF-2 protein levels are dependent on transcription in 8-
60                                              EF-2 regulates the outcome of protein synthesis in mamma
61 -ribose group of NAD to elongation factor-2 (EF-2), rendering EF-2 inactive.
62 lucose promoted a rapid dephosphorylation of EF-2 that was complete in 10 min and maintained over the
63 ds NAD and catalyzes the ADP-ribosylation of EF-2, the crystal structure of DT in complex with NAD ha
64 ingly, glucose-mediated dephosphorylation of EF-2 was completely blocked by the mitochondrial respira